Frederik Joelving

It was déjà vu last month when a university in Belgium stripped Egyptian physician Hatem Abu Hashim of his doctorate after he was found to have fabricated data in his thesis. 

Just weeks earlier, another Egyptian doctor, Ahmed Badawy, lost the PhD degree he had earned at a Dutch university in 2008. Abu Hashim and Badawy are both professors in the department of obstetrics and gynecology at Mansoura University in Egypt.

According to an investigation by the Vrije Universeit Brussel (VUB), which awarded Abu Hashim his PhD in 2013, the researcher was in “serious violation of scientific integrity” based on “overwhelming evidence of fabrication of statistical outcomes” and “clear lack of statistical proficiency.” 

Ben Mol of Monash University in Australia, a researcher turned data sleuth who alerted VUB and Utrecht University to problems with Abu Hashim and Badawy ‘s research in 2021 and 2020, respectively, told Retraction Watch by email, “The good news is obviously that there is a firm conclusion from both universities after a robust process independent of the complaint.” 

Mol also laid out his concerns in a study published with then-PhD student Esmée Bordewijk and others in 2020, as Retraction Watch reported that year. 

“Yes, it could have been a bit faster, but on the other hand we have this conversation because they took the right decision,” he added.

Abu Hashim’s PhD thesis is based on 11 randomized controlled trials, all of which have been published. Ostensibly, the studies were done at Mansoura University before Abu Hashim enrolled as an external PhD candidate at VUB. 

A report from the Flemish Commission for Scientific Integrity, which gave a second opinion on the VUB findings following a request from Abu Hashim, offers a “credible” scenario for how the 11 papers came about, suggesting “that Abu Hashim had learned to write medical papers by reading others, that he made up all reported values and that he wrote more papers by adapting previous papers, copying results between articles and applying small alterations (+1 or -1 in some digits).”

The commission agreed with VUB that “complete (or virtually complete) fabrication is the only reasonable explanation for the findings.” It also noted that “strikingly,” the researcher did not address any of the allegations against him:

“To the contrary, his defence consists mainly of accusing those bringing forward the complaint of misconduct and questioning their work and methods.”

Neither Abu Hashim nor Mansoura University responded to requests for comment.

The school, however, has known about Abu Hashim’s fraudulent research for a decade. In an internal investigation from 2014, then-head of department Nasser El Lakany and five other professors found that one of the researcher’s trials had never been done; six trials included an impossibly large number of women with polycystic ovary syndrome; and two reported 366 ovarian-drilling procedures while records were found to exist only for 94. The latter two groups of studies formed part of Abu Hashim’s PhD thesis.

“There is no excuse for the researcher’ [sic] misconduct (fabricating imaginary data and studies not done at all, or studies with doubtful cases not in records),” the Mansoura professors wrote, according to an English translation of the original Arabic report.   

In 2021, sleuth Nick Brown also began poring over the Egyptian researchers’ work after a Dutch journalist requested his opinion. 

“People don’t read papers. They read the abstract. They say, congratulations, great paper. And then they go back to what they were doing the rest of their day because reading a paper is quite hard,” Brown told Retraction Watch. “I’m not very good at statistics, but I can read a table and things jump out at me.”

Brown quickly realized that Badawy and Abu Hashim’s publications were littered with “fatal flaws.” Virtually all of the P-values were wrong. In some cases, they exceeded 1 – a mathematical impossibility. In others, vastly different values were given for identical statistical tests that by definition should have yielded the same results. 

“I assume the authors were just making up ‘likely-looking’ numbers in a hurry and didn’t realise that these needed to be identical,” Brown said in an email. “We often find that people who cheat are not very good at knowing what genuine numbers should look like.” 

Brown, who himself has an external PhD from a Dutch university, noted that institutions receive the same amount of money from the government whether a PhD candidate is external or internal:

“So someone comes along with some papers already done. They need to write a top and tail of a thesis. They’re probably not going to need a whole lot of supervision.  Exactly how many questions do you ask?” 

A spokesperson for Utrecht University told Retraction Watch by email:

“We have asked ourselves the question how this could have happened. Why did the supervisor and the Doctoral Examination Committee not notice this? The articles that were the basis for the thesis, were published in peer reviewed journals. Only much later it came to light that the data underlying these articles had been compromised.”

She added that the rules for external PhD candidates have been tightened since 2008, when Badawy obtained his degree (the changes are described here). 

Sam Jaspers, a VUB press officer, told us, “the Vrije Universiteit Brussel is updating its PhD regulations. External PhD students working with existing datasets created at a university other than the VUB and publications reviewed by scientific journals will soon (this spring) be fully audited by the VUB.”

Meanwhile, Mol, whose work on various cases recently featured in The Economist, worries about all the fake studies that have not yet been retracted, and the impact they might have on patient care. 

“I cannot understand that ... three years after our publication of the Bordewijk study, still half of the Badawy and Abu Hashim studies are out there even without an expression of concern,” he said. “What ideally should happen is that there should be a mechanism that all the journals and publishers bundle their investigation.”

A version of this article first appeared on retractionwatch.com.

It was déjà vu last month when a university in Belgium stripped Egyptian physician Hatem Abu Hashim of his doctorate after he was found to have fabricated data in his thesis. 

Just weeks earlier, another Egyptian doctor, Ahmed Badawy, lost the PhD degree he had earned at a Dutch university in 2008. Abu Hashim and Badawy are both professors in the department of obstetrics and gynecology at Mansoura University in Egypt.

According to an investigation by the Vrije Universeit Brussel (VUB), which awarded Abu Hashim his PhD in 2013, the researcher was in “serious violation of scientific integrity” based on “overwhelming evidence of fabrication of statistical outcomes” and “clear lack of statistical proficiency.” 

Ben Mol of Monash University in Australia, a researcher turned data sleuth who alerted VUB and Utrecht University to problems with Abu Hashim and Badawy ‘s research in 2021 and 2020, respectively, told Retraction Watch by email, “The good news is obviously that there is a firm conclusion from both universities after a robust process independent of the complaint.” 

Mol also laid out his concerns in a study published with then-PhD student Esmée Bordewijk and others in 2020, as Retraction Watch reported that year. 

“Yes, it could have been a bit faster, but on the other hand we have this conversation because they took the right decision,” he added.

Abu Hashim’s PhD thesis is based on 11 randomized controlled trials, all of which have been published. Ostensibly, the studies were done at Mansoura University before Abu Hashim enrolled as an external PhD candidate at VUB. 

A report from the Flemish Commission for Scientific Integrity, which gave a second opinion on the VUB findings following a request from Abu Hashim, offers a “credible” scenario for how the 11 papers came about, suggesting “that Abu Hashim had learned to write medical papers by reading others, that he made up all reported values and that he wrote more papers by adapting previous papers, copying results between articles and applying small alterations (+1 or -1 in some digits).”

The commission agreed with VUB that “complete (or virtually complete) fabrication is the only reasonable explanation for the findings.” It also noted that “strikingly,” the researcher did not address any of the allegations against him:

“To the contrary, his defence consists mainly of accusing those bringing forward the complaint of misconduct and questioning their work and methods.”

Neither Abu Hashim nor Mansoura University responded to requests for comment.

The school, however, has known about Abu Hashim’s fraudulent research for a decade. In an internal investigation from 2014, then-head of department Nasser El Lakany and five other professors found that one of the researcher’s trials had never been done; six trials included an impossibly large number of women with polycystic ovary syndrome; and two reported 366 ovarian-drilling procedures while records were found to exist only for 94. The latter two groups of studies formed part of Abu Hashim’s PhD thesis.

“There is no excuse for the researcher’ [sic] misconduct (fabricating imaginary data and studies not done at all, or studies with doubtful cases not in records),” the Mansoura professors wrote, according to an English translation of the original Arabic report.   

In 2021, sleuth Nick Brown also began poring over the Egyptian researchers’ work after a Dutch journalist requested his opinion. 

“People don’t read papers. They read the abstract. They say, congratulations, great paper. And then they go back to what they were doing the rest of their day because reading a paper is quite hard,” Brown told Retraction Watch. “I’m not very good at statistics, but I can read a table and things jump out at me.”

Brown quickly realized that Badawy and Abu Hashim’s publications were littered with “fatal flaws.” Virtually all of the P-values were wrong. In some cases, they exceeded 1 – a mathematical impossibility. In others, vastly different values were given for identical statistical tests that by definition should have yielded the same results. 

“I assume the authors were just making up ‘likely-looking’ numbers in a hurry and didn’t realise that these needed to be identical,” Brown said in an email. “We often find that people who cheat are not very good at knowing what genuine numbers should look like.” 

Brown, who himself has an external PhD from a Dutch university, noted that institutions receive the same amount of money from the government whether a PhD candidate is external or internal:

“So someone comes along with some papers already done. They need to write a top and tail of a thesis. They’re probably not going to need a whole lot of supervision.  Exactly how many questions do you ask?” 

A spokesperson for Utrecht University told Retraction Watch by email:

“We have asked ourselves the question how this could have happened. Why did the supervisor and the Doctoral Examination Committee not notice this? The articles that were the basis for the thesis, were published in peer reviewed journals. Only much later it came to light that the data underlying these articles had been compromised.”

She added that the rules for external PhD candidates have been tightened since 2008, when Badawy obtained his degree (the changes are described here). 

Sam Jaspers, a VUB press officer, told us, “the Vrije Universiteit Brussel is updating its PhD regulations. External PhD students working with existing datasets created at a university other than the VUB and publications reviewed by scientific journals will soon (this spring) be fully audited by the VUB.”

Meanwhile, Mol, whose work on various cases recently featured in The Economist, worries about all the fake studies that have not yet been retracted, and the impact they might have on patient care. 

“I cannot understand that ... three years after our publication of the Bordewijk study, still half of the Badawy and Abu Hashim studies are out there even without an expression of concern,” he said. “What ideally should happen is that there should be a mechanism that all the journals and publishers bundle their investigation.”

A version of this article first appeared on retractionwatch.com.

It was déjà vu last month when a university in Belgium stripped Egyptian physician Hatem Abu Hashim of his doctorate after he was found to have fabricated data in his thesis. 

Just weeks earlier, another Egyptian doctor, Ahmed Badawy, lost the PhD degree he had earned at a Dutch university in 2008. Abu Hashim and Badawy are both professors in the department of obstetrics and gynecology at Mansoura University in Egypt.

According to an investigation by the Vrije Universeit Brussel (VUB), which awarded Abu Hashim his PhD in 2013, the researcher was in “serious violation of scientific integrity” based on “overwhelming evidence of fabrication of statistical outcomes” and “clear lack of statistical proficiency.” 

Ben Mol of Monash University in Australia, a researcher turned data sleuth who alerted VUB and Utrecht University to problems with Abu Hashim and Badawy ‘s research in 2021 and 2020, respectively, told Retraction Watch by email, “The good news is obviously that there is a firm conclusion from both universities after a robust process independent of the complaint.” 

Mol also laid out his concerns in a study published with then-PhD student Esmée Bordewijk and others in 2020, as Retraction Watch reported that year. 

“Yes, it could have been a bit faster, but on the other hand we have this conversation because they took the right decision,” he added.

Abu Hashim’s PhD thesis is based on 11 randomized controlled trials, all of which have been published. Ostensibly, the studies were done at Mansoura University before Abu Hashim enrolled as an external PhD candidate at VUB. 

A report from the Flemish Commission for Scientific Integrity, which gave a second opinion on the VUB findings following a request from Abu Hashim, offers a “credible” scenario for how the 11 papers came about, suggesting “that Abu Hashim had learned to write medical papers by reading others, that he made up all reported values and that he wrote more papers by adapting previous papers, copying results between articles and applying small alterations (+1 or -1 in some digits).”

The commission agreed with VUB that “complete (or virtually complete) fabrication is the only reasonable explanation for the findings.” It also noted that “strikingly,” the researcher did not address any of the allegations against him:

“To the contrary, his defence consists mainly of accusing those bringing forward the complaint of misconduct and questioning their work and methods.”

Neither Abu Hashim nor Mansoura University responded to requests for comment.

The school, however, has known about Abu Hashim’s fraudulent research for a decade. In an internal investigation from 2014, then-head of department Nasser El Lakany and five other professors found that one of the researcher’s trials had never been done; six trials included an impossibly large number of women with polycystic ovary syndrome; and two reported 366 ovarian-drilling procedures while records were found to exist only for 94. The latter two groups of studies formed part of Abu Hashim’s PhD thesis.

“There is no excuse for the researcher’ [sic] misconduct (fabricating imaginary data and studies not done at all, or studies with doubtful cases not in records),” the Mansoura professors wrote, according to an English translation of the original Arabic report.   

In 2021, sleuth Nick Brown also began poring over the Egyptian researchers’ work after a Dutch journalist requested his opinion. 

“People don’t read papers. They read the abstract. They say, congratulations, great paper. And then they go back to what they were doing the rest of their day because reading a paper is quite hard,” Brown told Retraction Watch. “I’m not very good at statistics, but I can read a table and things jump out at me.”

Brown quickly realized that Badawy and Abu Hashim’s publications were littered with “fatal flaws.” Virtually all of the P-values were wrong. In some cases, they exceeded 1 – a mathematical impossibility. In others, vastly different values were given for identical statistical tests that by definition should have yielded the same results. 

“I assume the authors were just making up ‘likely-looking’ numbers in a hurry and didn’t realise that these needed to be identical,” Brown said in an email. “We often find that people who cheat are not very good at knowing what genuine numbers should look like.” 

Brown, who himself has an external PhD from a Dutch university, noted that institutions receive the same amount of money from the government whether a PhD candidate is external or internal:

“So someone comes along with some papers already done. They need to write a top and tail of a thesis. They’re probably not going to need a whole lot of supervision.  Exactly how many questions do you ask?” 

A spokesperson for Utrecht University told Retraction Watch by email:

“We have asked ourselves the question how this could have happened. Why did the supervisor and the Doctoral Examination Committee not notice this? The articles that were the basis for the thesis, were published in peer reviewed journals. Only much later it came to light that the data underlying these articles had been compromised.”

She added that the rules for external PhD candidates have been tightened since 2008, when Badawy obtained his degree (the changes are described here). 

Sam Jaspers, a VUB press officer, told us, “the Vrije Universiteit Brussel is updating its PhD regulations. External PhD students working with existing datasets created at a university other than the VUB and publications reviewed by scientific journals will soon (this spring) be fully audited by the VUB.”

Meanwhile, Mol, whose work on various cases recently featured in The Economist, worries about all the fake studies that have not yet been retracted, and the impact they might have on patient care. 

“I cannot understand that ... three years after our publication of the Bordewijk study, still half of the Badawy and Abu Hashim studies are out there even without an expression of concern,” he said. “What ideally should happen is that there should be a mechanism that all the journals and publishers bundle their investigation.”

A version of this article first appeared on retractionwatch.com.

Catching all solid cancers before they metastasize could prevent 26% to 32% of cancer deaths in women and 18% to 24% in men within 10 years of diagnosis, researchers in Australia estimate.

Those figures translate to 2,064 to 2,677 fewer cancer deaths annually in the state of New South Wales between 2005 and 2014, the most recent period studied.

“While it is well established that diagnosing cancers at an earlier stage is ‘better,’ our study is unique in that it quantifies what that ‘better’ might look like in terms of how many deaths would be avoided within 10 years of diagnosis,” the authors write in an article published online Jan. 17 in the International Journal of Cancer. “By doing so, it is hoped that these results will provide continued motivation to develop more effective strategies to diagnose cancers at an earlier stage.”

Of course, achieving such a “stage-shift in practice is difficult,” study author Xue Qin Yu, PhD, of The Daffodil Centre in Sydney and colleagues, acknowledge. First, Dr. Yu and colleagues note, “diagnosis at an earlier stage can be challenging due to the nonspecific nature of many common symptoms which may not be recognized by either patients or doctors.” Plus, they add, a challenge for diagnosing cancers at an earlier stage “is the overall low uptake of screening.”

For their study, the researchers used data from a cohort of more than 716,000 people aged 15 to 89 years diagnosed with a solid cancer in New South Wales between 1985 and 2014 and followed through 2015.

To estimate how many deaths could be avoided if tumors were caught earlier, the authors looked at two scenarios. In scenario 1, they assumed all known cases of distant cancer were instead diagnosed at the regional stage, and in scenario 2, they assumed half of the cases were diagnosed as regional and half as localized disease.

Under the conservative scenario 1, about 18% of the observed cancer deaths in males and 26% in females could be avoided. In total, this corresponded to 21% of observed deaths.

Colorectal cancer topped the list of avoidable deaths in both men (27%) and women (33%), followed by prostate cancer in men (19%), breast cancer in women (18%), and melanoma in women (16%) and men (13%).

Under scenario 2, 24% of cancer deaths in males and 32% in females – or 28% overall – were avoidable.

The researchers caution that their study is limited by a high proportion of cases of unknown stage. Still, they say their findings are consistent with results from the United States indicating 15% to 25% of cancer-related deaths were potentially avoidable if tumors were detected before metastasizing.

“Given our study cohort was sourced from a population-based cancer registry with complete enumeration of cancers diagnosed during the study period, it is likely that our study findings, particularly in terms of the population rate of avoidable deaths, would be generalizable to other populations with similar characteristics,” Dr. Yu and colleagues write. “However, results may be different in countries that have a different mix of cancer types or distribution of stage at diagnosis.”

A version of this article first appeared on Medscape.com.

Catching all solid cancers before they metastasize could prevent 26% to 32% of cancer deaths in women and 18% to 24% in men within 10 years of diagnosis, researchers in Australia estimate.

Those figures translate to 2,064 to 2,677 fewer cancer deaths annually in the state of New South Wales between 2005 and 2014, the most recent period studied.

“While it is well established that diagnosing cancers at an earlier stage is ‘better,’ our study is unique in that it quantifies what that ‘better’ might look like in terms of how many deaths would be avoided within 10 years of diagnosis,” the authors write in an article published online Jan. 17 in the International Journal of Cancer. “By doing so, it is hoped that these results will provide continued motivation to develop more effective strategies to diagnose cancers at an earlier stage.”

Of course, achieving such a “stage-shift in practice is difficult,” study author Xue Qin Yu, PhD, of The Daffodil Centre in Sydney and colleagues, acknowledge. First, Dr. Yu and colleagues note, “diagnosis at an earlier stage can be challenging due to the nonspecific nature of many common symptoms which may not be recognized by either patients or doctors.” Plus, they add, a challenge for diagnosing cancers at an earlier stage “is the overall low uptake of screening.”

For their study, the researchers used data from a cohort of more than 716,000 people aged 15 to 89 years diagnosed with a solid cancer in New South Wales between 1985 and 2014 and followed through 2015.

To estimate how many deaths could be avoided if tumors were caught earlier, the authors looked at two scenarios. In scenario 1, they assumed all known cases of distant cancer were instead diagnosed at the regional stage, and in scenario 2, they assumed half of the cases were diagnosed as regional and half as localized disease.

Under the conservative scenario 1, about 18% of the observed cancer deaths in males and 26% in females could be avoided. In total, this corresponded to 21% of observed deaths.

Colorectal cancer topped the list of avoidable deaths in both men (27%) and women (33%), followed by prostate cancer in men (19%), breast cancer in women (18%), and melanoma in women (16%) and men (13%).

Under scenario 2, 24% of cancer deaths in males and 32% in females – or 28% overall – were avoidable.

The researchers caution that their study is limited by a high proportion of cases of unknown stage. Still, they say their findings are consistent with results from the United States indicating 15% to 25% of cancer-related deaths were potentially avoidable if tumors were detected before metastasizing.

“Given our study cohort was sourced from a population-based cancer registry with complete enumeration of cancers diagnosed during the study period, it is likely that our study findings, particularly in terms of the population rate of avoidable deaths, would be generalizable to other populations with similar characteristics,” Dr. Yu and colleagues write. “However, results may be different in countries that have a different mix of cancer types or distribution of stage at diagnosis.”

A version of this article first appeared on Medscape.com.

Catching all solid cancers before they metastasize could prevent 26% to 32% of cancer deaths in women and 18% to 24% in men within 10 years of diagnosis, researchers in Australia estimate.

Those figures translate to 2,064 to 2,677 fewer cancer deaths annually in the state of New South Wales between 2005 and 2014, the most recent period studied.

“While it is well established that diagnosing cancers at an earlier stage is ‘better,’ our study is unique in that it quantifies what that ‘better’ might look like in terms of how many deaths would be avoided within 10 years of diagnosis,” the authors write in an article published online Jan. 17 in the International Journal of Cancer. “By doing so, it is hoped that these results will provide continued motivation to develop more effective strategies to diagnose cancers at an earlier stage.”

Of course, achieving such a “stage-shift in practice is difficult,” study author Xue Qin Yu, PhD, of The Daffodil Centre in Sydney and colleagues, acknowledge. First, Dr. Yu and colleagues note, “diagnosis at an earlier stage can be challenging due to the nonspecific nature of many common symptoms which may not be recognized by either patients or doctors.” Plus, they add, a challenge for diagnosing cancers at an earlier stage “is the overall low uptake of screening.”

For their study, the researchers used data from a cohort of more than 716,000 people aged 15 to 89 years diagnosed with a solid cancer in New South Wales between 1985 and 2014 and followed through 2015.

To estimate how many deaths could be avoided if tumors were caught earlier, the authors looked at two scenarios. In scenario 1, they assumed all known cases of distant cancer were instead diagnosed at the regional stage, and in scenario 2, they assumed half of the cases were diagnosed as regional and half as localized disease.

Under the conservative scenario 1, about 18% of the observed cancer deaths in males and 26% in females could be avoided. In total, this corresponded to 21% of observed deaths.

Colorectal cancer topped the list of avoidable deaths in both men (27%) and women (33%), followed by prostate cancer in men (19%), breast cancer in women (18%), and melanoma in women (16%) and men (13%).

Under scenario 2, 24% of cancer deaths in males and 32% in females – or 28% overall – were avoidable.

The researchers caution that their study is limited by a high proportion of cases of unknown stage. Still, they say their findings are consistent with results from the United States indicating 15% to 25% of cancer-related deaths were potentially avoidable if tumors were detected before metastasizing.

“Given our study cohort was sourced from a population-based cancer registry with complete enumeration of cancers diagnosed during the study period, it is likely that our study findings, particularly in terms of the population rate of avoidable deaths, would be generalizable to other populations with similar characteristics,” Dr. Yu and colleagues write. “However, results may be different in countries that have a different mix of cancer types or distribution of stage at diagnosis.”

A version of this article first appeared on Medscape.com.

People with bipolar disorder as well as their unaffected siblings appear to be at increased risk for cancer, particularly of the breast, according to new research from Taiwan.

“To our knowledge, our study is the first to report an increased overall cancer risk as well as increased risks of breast and ectodermal cancer among the unaffected siblings aged < 50 years of patients with bipolar disorder,” Ya-Mei Bai, MD, PhD, of National Yang-Ming University, Taipei, Taiwan, and colleagues write in an article published online in the International Journal of Cancer.

Most, but not all, previous studies have shown a link between bipolar disorder and cancer. Whether the elevated risk of malignancy extends to family members without the mental health condition has not been elucidated.

To investigate, the researchers turned to the National Health Insurance Research Database of Taiwan. They identified 25,356 individuals diagnosed with bipolar disorder by a psychiatrist between 1996 and 2010 and the same number of unaffected siblings, as well as more than 100,000 age-, sex-, income-, and residence-matched controls without severe mental illness.

Compared with the control group, people with bipolar disorder (odds ratio, 1.22) and their unaffected siblings (OR, 1.17) both had a higher risk of developing malignant cancer of any kind. The researchers also found that both groups were at higher risk for breast cancer, with odds ratios of 1.98 in individuals with bipolar disorder and 1.73 in their unaffected siblings.

However, the risk of skin cancer was only high in people with bipolar disorder (OR, 2.70) and not in their siblings (OR, 0.62). And conversely, the risk of kidney cancer was significantly increased in unaffected siblings (OR, 2.45) but not in people with bipolar disorder (OR, 0.47).

When stratified by the embryonic developmental layer from which tumors had originated – ectodermal, mesodermal, or endodermal – the authors observed a significantly increased risk for only ectodermal cancers. In addition, only people under age 50 in both groups (OR, 1.90 for those with bipolar disorder; OR, 1.65 for siblings) were more likely to develop an ectodermal cancer, especially of the breast, compared with the control group. The risks remained elevated after excluding breast cancer but were no longer significant.

When stratified by age, the risk of developing any cancer in both groups also only appeared to be greater for those under age 50 (OR, 1.34 in people with bipolar disorder; OR, 1.32 in siblings) compared with those aged 50 and over (OR, 0.97 and 0.99, respectively). The authors highlighted these figures in the supplemental data set but did not discuss it further in the study beyond a brief mention that “younger patients with bipolar disorder and younger unaffected siblings (< 50 years), but not older ones (≥ 50 years), were more likely to develop any malignancy during the follow-up than matched controls.”

“This paper essentially finds what we have found in our previous work – that people with bipolar disorder have a greater risk of cancer,” said Michael Berk, MBBCh, PhD, a professor of psychiatry at the Deakin University School of Medicine in Geelong, Australia, who published a systematic review and meta-analysis last spring on cancer risk and the role of lithium treatment in bipolar disorder.

“The interesting finding in our work,” Dr. Berk told this news organization, “is that this risk is attenuated by use of lithium but not other agents.”

The Taiwanese researchers propose a “biopsychosocial explanation” for their results, noting that both the nervous system and the breast and skin develop from the ectoderm, and that cancer risk factors such as smoking and obesity are more common in people with bipolar disorder and their unaffected siblings.

“The findings,” they write, “imply a genetic overlap in neurodevelopment and malignancy pathogenesis and may encourage clinicians to closely monitor patients with bipolar disorder and their unaffected siblings for cancer warning signs.”

The authors, however, caution that their study needs validation and had several limitations, including lack of adjustment for drug treatment and lifestyle and environmental factors.

“Our findings may persuade clinicians and researchers to reevaluate the cancer risk among the unaffected siblings of patients with schizophrenia and bipolar disorder because these two severe mental disorders may have a common biopsychosocial pathophysiology,” the team writes.

The study was supported by a grant from Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and the Ministry of Science and Technology, Taiwan.

A version of this article first appeared on Medscape.com.

People with bipolar disorder as well as their unaffected siblings appear to be at increased risk for cancer, particularly of the breast, according to new research from Taiwan.

“To our knowledge, our study is the first to report an increased overall cancer risk as well as increased risks of breast and ectodermal cancer among the unaffected siblings aged < 50 years of patients with bipolar disorder,” Ya-Mei Bai, MD, PhD, of National Yang-Ming University, Taipei, Taiwan, and colleagues write in an article published online in the International Journal of Cancer.

Most, but not all, previous studies have shown a link between bipolar disorder and cancer. Whether the elevated risk of malignancy extends to family members without the mental health condition has not been elucidated.

To investigate, the researchers turned to the National Health Insurance Research Database of Taiwan. They identified 25,356 individuals diagnosed with bipolar disorder by a psychiatrist between 1996 and 2010 and the same number of unaffected siblings, as well as more than 100,000 age-, sex-, income-, and residence-matched controls without severe mental illness.

Compared with the control group, people with bipolar disorder (odds ratio, 1.22) and their unaffected siblings (OR, 1.17) both had a higher risk of developing malignant cancer of any kind. The researchers also found that both groups were at higher risk for breast cancer, with odds ratios of 1.98 in individuals with bipolar disorder and 1.73 in their unaffected siblings.

However, the risk of skin cancer was only high in people with bipolar disorder (OR, 2.70) and not in their siblings (OR, 0.62). And conversely, the risk of kidney cancer was significantly increased in unaffected siblings (OR, 2.45) but not in people with bipolar disorder (OR, 0.47).

When stratified by the embryonic developmental layer from which tumors had originated – ectodermal, mesodermal, or endodermal – the authors observed a significantly increased risk for only ectodermal cancers. In addition, only people under age 50 in both groups (OR, 1.90 for those with bipolar disorder; OR, 1.65 for siblings) were more likely to develop an ectodermal cancer, especially of the breast, compared with the control group. The risks remained elevated after excluding breast cancer but were no longer significant.

When stratified by age, the risk of developing any cancer in both groups also only appeared to be greater for those under age 50 (OR, 1.34 in people with bipolar disorder; OR, 1.32 in siblings) compared with those aged 50 and over (OR, 0.97 and 0.99, respectively). The authors highlighted these figures in the supplemental data set but did not discuss it further in the study beyond a brief mention that “younger patients with bipolar disorder and younger unaffected siblings (< 50 years), but not older ones (≥ 50 years), were more likely to develop any malignancy during the follow-up than matched controls.”

“This paper essentially finds what we have found in our previous work – that people with bipolar disorder have a greater risk of cancer,” said Michael Berk, MBBCh, PhD, a professor of psychiatry at the Deakin University School of Medicine in Geelong, Australia, who published a systematic review and meta-analysis last spring on cancer risk and the role of lithium treatment in bipolar disorder.

“The interesting finding in our work,” Dr. Berk told this news organization, “is that this risk is attenuated by use of lithium but not other agents.”

The Taiwanese researchers propose a “biopsychosocial explanation” for their results, noting that both the nervous system and the breast and skin develop from the ectoderm, and that cancer risk factors such as smoking and obesity are more common in people with bipolar disorder and their unaffected siblings.

“The findings,” they write, “imply a genetic overlap in neurodevelopment and malignancy pathogenesis and may encourage clinicians to closely monitor patients with bipolar disorder and their unaffected siblings for cancer warning signs.”

The authors, however, caution that their study needs validation and had several limitations, including lack of adjustment for drug treatment and lifestyle and environmental factors.

“Our findings may persuade clinicians and researchers to reevaluate the cancer risk among the unaffected siblings of patients with schizophrenia and bipolar disorder because these two severe mental disorders may have a common biopsychosocial pathophysiology,” the team writes.

The study was supported by a grant from Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and the Ministry of Science and Technology, Taiwan.

A version of this article first appeared on Medscape.com.

People with bipolar disorder as well as their unaffected siblings appear to be at increased risk for cancer, particularly of the breast, according to new research from Taiwan.

“To our knowledge, our study is the first to report an increased overall cancer risk as well as increased risks of breast and ectodermal cancer among the unaffected siblings aged < 50 years of patients with bipolar disorder,” Ya-Mei Bai, MD, PhD, of National Yang-Ming University, Taipei, Taiwan, and colleagues write in an article published online in the International Journal of Cancer.

Most, but not all, previous studies have shown a link between bipolar disorder and cancer. Whether the elevated risk of malignancy extends to family members without the mental health condition has not been elucidated.

To investigate, the researchers turned to the National Health Insurance Research Database of Taiwan. They identified 25,356 individuals diagnosed with bipolar disorder by a psychiatrist between 1996 and 2010 and the same number of unaffected siblings, as well as more than 100,000 age-, sex-, income-, and residence-matched controls without severe mental illness.

Compared with the control group, people with bipolar disorder (odds ratio, 1.22) and their unaffected siblings (OR, 1.17) both had a higher risk of developing malignant cancer of any kind. The researchers also found that both groups were at higher risk for breast cancer, with odds ratios of 1.98 in individuals with bipolar disorder and 1.73 in their unaffected siblings.

However, the risk of skin cancer was only high in people with bipolar disorder (OR, 2.70) and not in their siblings (OR, 0.62). And conversely, the risk of kidney cancer was significantly increased in unaffected siblings (OR, 2.45) but not in people with bipolar disorder (OR, 0.47).

When stratified by the embryonic developmental layer from which tumors had originated – ectodermal, mesodermal, or endodermal – the authors observed a significantly increased risk for only ectodermal cancers. In addition, only people under age 50 in both groups (OR, 1.90 for those with bipolar disorder; OR, 1.65 for siblings) were more likely to develop an ectodermal cancer, especially of the breast, compared with the control group. The risks remained elevated after excluding breast cancer but were no longer significant.

When stratified by age, the risk of developing any cancer in both groups also only appeared to be greater for those under age 50 (OR, 1.34 in people with bipolar disorder; OR, 1.32 in siblings) compared with those aged 50 and over (OR, 0.97 and 0.99, respectively). The authors highlighted these figures in the supplemental data set but did not discuss it further in the study beyond a brief mention that “younger patients with bipolar disorder and younger unaffected siblings (< 50 years), but not older ones (≥ 50 years), were more likely to develop any malignancy during the follow-up than matched controls.”

“This paper essentially finds what we have found in our previous work – that people with bipolar disorder have a greater risk of cancer,” said Michael Berk, MBBCh, PhD, a professor of psychiatry at the Deakin University School of Medicine in Geelong, Australia, who published a systematic review and meta-analysis last spring on cancer risk and the role of lithium treatment in bipolar disorder.

“The interesting finding in our work,” Dr. Berk told this news organization, “is that this risk is attenuated by use of lithium but not other agents.”

The Taiwanese researchers propose a “biopsychosocial explanation” for their results, noting that both the nervous system and the breast and skin develop from the ectoderm, and that cancer risk factors such as smoking and obesity are more common in people with bipolar disorder and their unaffected siblings.

“The findings,” they write, “imply a genetic overlap in neurodevelopment and malignancy pathogenesis and may encourage clinicians to closely monitor patients with bipolar disorder and their unaffected siblings for cancer warning signs.”

The authors, however, caution that their study needs validation and had several limitations, including lack of adjustment for drug treatment and lifestyle and environmental factors.

“Our findings may persuade clinicians and researchers to reevaluate the cancer risk among the unaffected siblings of patients with schizophrenia and bipolar disorder because these two severe mental disorders may have a common biopsychosocial pathophysiology,” the team writes.

The study was supported by a grant from Taipei Veterans General Hospital, Yen Tjing Ling Medical Foundation, and the Ministry of Science and Technology, Taiwan.

A version of this article first appeared on Medscape.com.

Nearly 1 in 5 women who receive the recommended 10 biennial screening rounds for breast cancer in Norway will get a false positive result, and 1 in 20 women will receive a false positive result that leads to an invasive procedure, a new analysis shows.

While the risk may seem high, it is actually much lower than what researchers have reported in the U.S., the study authors note in their paper, published online Dec. 21 in Cancer.

“I am proud about the low rate of recalls we have in Norway and Europe – and hope we can keep it that low for the future,” said senior author Solveig Hofvind, PhD, head of BreastScreen Norway, a nationwide screening program that invites women aged 50 to 69 to mammographic screening every other year.

“The double reading in Europe is probably the main reason for the lower rate in Europe compared to the U.S., where single reading is used,” she said in an interview.

Until now, Dr. Hofvind and her colleagues say, no studies have been performed using exclusively empirical data to describe the cumulative risk of experiencing a false positive screening result in Europe because of the need for long-term follow-up and complete data registration.

For their study, the researchers turned to the Cancer Registry of Norway, which administers BreastScreen Norway. They focused on data from 1995 to 2019 on women aged 50 to 69 years who had attended one or more screening rounds and could potentially attend all 10 screening examinations over the 20-year period.

Women were excluded if they were diagnosed with breast cancer before attending screening, participated in interventional research, self-referred for screening, were recalled due to self-reported symptoms or technically inadequate mammograms, or declined follow-up after a positive screen.

Among more than 421,000 women who underwent nearly 1.9 million screening examinations, 11.3% experienced at least one false positive result and 3.3% experienced at least one false positive involving an invasive procedure, such as fine-needle aspiration cytology, core-needle biopsy, or open biopsy.

The cumulative risk of experiencing a first false positive screen was 18.0% and that of experiencing a false positive that involved an invasive procedure was 5.01%. Adjusting for irregular attendance, age at screening, or the number of screens attended had little effect on the estimates.

The results closely match earlier findings from Norway that have been based on assumptions rather than exclusively empirical data. However, these findings differ from results reported in U.S. studies, which have relied largely on data from the Breast Cancer Surveillance Consortium, the researchers say.

“The latter have indicated that, for women who initiate biennial screening at the age of 50 years, the cumulative risk after 10 years is 42% for experiencing at least one false-positive screening result and 6.4% for experiencing at least one false-positive screening result involving an invasive procedure,” Dr. Hofvind and her colleagues write.

Several principal investigators with the Breast Cancer Surveillance Consortium did not respond or were unavailable for comment when contacted by this news organization.

However, the study authors highlighted several factors that could help explain the discrepancy between the U.S. and European results.

In addition to double mammogram reading, “European guidelines recommend that breast radiologists read 3,500 to 11,000 mammograms annually, whereas 960 every 2 years are required by the U.S. Mammography Quality Standards Act,” the researchers note. They also point out that previous screening mammograms are readily available in Norway, whereas this is not always the case in the U.S.

“False-positive screening results are a part of the screening for breast cancer – and the women need to be informed about the risk,” Dr. Hofvind concluded. “The screening programs should aim to keep the rate as low as possible for the women [given] the costs.”

The study was supported by the Dam Foundation via the Norwegian Breast Cancer Society.

A version of this article first appeared on Medscape.com.

Nearly 1 in 5 women who receive the recommended 10 biennial screening rounds for breast cancer in Norway will get a false positive result, and 1 in 20 women will receive a false positive result that leads to an invasive procedure, a new analysis shows.

While the risk may seem high, it is actually much lower than what researchers have reported in the U.S., the study authors note in their paper, published online Dec. 21 in Cancer.

“I am proud about the low rate of recalls we have in Norway and Europe – and hope we can keep it that low for the future,” said senior author Solveig Hofvind, PhD, head of BreastScreen Norway, a nationwide screening program that invites women aged 50 to 69 to mammographic screening every other year.

“The double reading in Europe is probably the main reason for the lower rate in Europe compared to the U.S., where single reading is used,” she said in an interview.

Until now, Dr. Hofvind and her colleagues say, no studies have been performed using exclusively empirical data to describe the cumulative risk of experiencing a false positive screening result in Europe because of the need for long-term follow-up and complete data registration.

For their study, the researchers turned to the Cancer Registry of Norway, which administers BreastScreen Norway. They focused on data from 1995 to 2019 on women aged 50 to 69 years who had attended one or more screening rounds and could potentially attend all 10 screening examinations over the 20-year period.

Women were excluded if they were diagnosed with breast cancer before attending screening, participated in interventional research, self-referred for screening, were recalled due to self-reported symptoms or technically inadequate mammograms, or declined follow-up after a positive screen.

Among more than 421,000 women who underwent nearly 1.9 million screening examinations, 11.3% experienced at least one false positive result and 3.3% experienced at least one false positive involving an invasive procedure, such as fine-needle aspiration cytology, core-needle biopsy, or open biopsy.

The cumulative risk of experiencing a first false positive screen was 18.0% and that of experiencing a false positive that involved an invasive procedure was 5.01%. Adjusting for irregular attendance, age at screening, or the number of screens attended had little effect on the estimates.

The results closely match earlier findings from Norway that have been based on assumptions rather than exclusively empirical data. However, these findings differ from results reported in U.S. studies, which have relied largely on data from the Breast Cancer Surveillance Consortium, the researchers say.

“The latter have indicated that, for women who initiate biennial screening at the age of 50 years, the cumulative risk after 10 years is 42% for experiencing at least one false-positive screening result and 6.4% for experiencing at least one false-positive screening result involving an invasive procedure,” Dr. Hofvind and her colleagues write.

Several principal investigators with the Breast Cancer Surveillance Consortium did not respond or were unavailable for comment when contacted by this news organization.

However, the study authors highlighted several factors that could help explain the discrepancy between the U.S. and European results.

In addition to double mammogram reading, “European guidelines recommend that breast radiologists read 3,500 to 11,000 mammograms annually, whereas 960 every 2 years are required by the U.S. Mammography Quality Standards Act,” the researchers note. They also point out that previous screening mammograms are readily available in Norway, whereas this is not always the case in the U.S.

“False-positive screening results are a part of the screening for breast cancer – and the women need to be informed about the risk,” Dr. Hofvind concluded. “The screening programs should aim to keep the rate as low as possible for the women [given] the costs.”

The study was supported by the Dam Foundation via the Norwegian Breast Cancer Society.

A version of this article first appeared on Medscape.com.

Nearly 1 in 5 women who receive the recommended 10 biennial screening rounds for breast cancer in Norway will get a false positive result, and 1 in 20 women will receive a false positive result that leads to an invasive procedure, a new analysis shows.

While the risk may seem high, it is actually much lower than what researchers have reported in the U.S., the study authors note in their paper, published online Dec. 21 in Cancer.

“I am proud about the low rate of recalls we have in Norway and Europe – and hope we can keep it that low for the future,” said senior author Solveig Hofvind, PhD, head of BreastScreen Norway, a nationwide screening program that invites women aged 50 to 69 to mammographic screening every other year.

“The double reading in Europe is probably the main reason for the lower rate in Europe compared to the U.S., where single reading is used,” she said in an interview.

Until now, Dr. Hofvind and her colleagues say, no studies have been performed using exclusively empirical data to describe the cumulative risk of experiencing a false positive screening result in Europe because of the need for long-term follow-up and complete data registration.

For their study, the researchers turned to the Cancer Registry of Norway, which administers BreastScreen Norway. They focused on data from 1995 to 2019 on women aged 50 to 69 years who had attended one or more screening rounds and could potentially attend all 10 screening examinations over the 20-year period.

Women were excluded if they were diagnosed with breast cancer before attending screening, participated in interventional research, self-referred for screening, were recalled due to self-reported symptoms or technically inadequate mammograms, or declined follow-up after a positive screen.

Among more than 421,000 women who underwent nearly 1.9 million screening examinations, 11.3% experienced at least one false positive result and 3.3% experienced at least one false positive involving an invasive procedure, such as fine-needle aspiration cytology, core-needle biopsy, or open biopsy.

The cumulative risk of experiencing a first false positive screen was 18.0% and that of experiencing a false positive that involved an invasive procedure was 5.01%. Adjusting for irregular attendance, age at screening, or the number of screens attended had little effect on the estimates.

The results closely match earlier findings from Norway that have been based on assumptions rather than exclusively empirical data. However, these findings differ from results reported in U.S. studies, which have relied largely on data from the Breast Cancer Surveillance Consortium, the researchers say.

“The latter have indicated that, for women who initiate biennial screening at the age of 50 years, the cumulative risk after 10 years is 42% for experiencing at least one false-positive screening result and 6.4% for experiencing at least one false-positive screening result involving an invasive procedure,” Dr. Hofvind and her colleagues write.

Several principal investigators with the Breast Cancer Surveillance Consortium did not respond or were unavailable for comment when contacted by this news organization.

However, the study authors highlighted several factors that could help explain the discrepancy between the U.S. and European results.

In addition to double mammogram reading, “European guidelines recommend that breast radiologists read 3,500 to 11,000 mammograms annually, whereas 960 every 2 years are required by the U.S. Mammography Quality Standards Act,” the researchers note. They also point out that previous screening mammograms are readily available in Norway, whereas this is not always the case in the U.S.

“False-positive screening results are a part of the screening for breast cancer – and the women need to be informed about the risk,” Dr. Hofvind concluded. “The screening programs should aim to keep the rate as low as possible for the women [given] the costs.”

The study was supported by the Dam Foundation via the Norwegian Breast Cancer Society.

A version of this article first appeared on Medscape.com.

Aspirin use was associated with longer overall survival in people with inoperable non–small cell lung cancer (NSCLC), according to a new study from Taiwan.

copyright Darren Hester/Fotolia.com

The analysis, published online Nov. 22 in BMC Cancer , adds another data point to a small and inconsistent evidence base.

“Despite the need for future prospective randomized clinical trials, aspirin may be considered as an additional treatment for inoperable NSCLC patients,” Ming-Szu Hung, MD, of Chang-Gung University, Taoyuan City, and colleagues write.

The current literature suggests that the over-the-counter medication may help ward off various types of cancer, including lung cancer, but the various study findings do not always align. For lung-cancer survival, in particular, a few observational studies have found increased survival among aspirin users while others have not.

To help bring clarity to the literature, Dr. Hung’s team examined data from Taiwan’s National Health Insurance Research Database on more than 38,000 patients diagnosed with NSCLC between 2000 and 2012, almost 5,000 of whom were taking aspirin at the time of diagnosis.

The researchers found that aspirin users survived for a median of 1.73 years, compared with 1.30 years for nonusers. Taking the drug was associated with longer overall survival in time-varying covariate analysis (hazard ratio, 0.83; 95% CI, 0.80-0.86). This finding was confirmed in a propensity-score analysis of 4,932 matched pairs (HR, 0.79; 95% CI, 0.75-0.83).

“These results warrant further randomized clinical trials to evaluate the actual role of aspirin in the treatment of NSCLC patients,” the researchers conclude.

But Úna McMenamin, PhD, a cancer epidemiologist at Queen’s University Belfast, Ireland, was not convinced by the study’s methods.

While she praised its large size and use of population-based health registers, she expressed concern about the potential for reverse causation, “as it is unclear whether authors lagged the aspirin exposure in the cohort of lung cancer patients.”

There is evidence that common medications such as aspirin may be withdrawn from patients who are thought to be near the end of their life, Dr. McMenamin told this news organization. When not factored into the statistical analysis, aspirin may appear “to be spuriously associated with a reduced risk of death when, in fact, no association may be present.”

Previous studies of aspirin use in lung cancer patients that have included a lag, such as one Dr. McMenamin and colleagues conducted in 2015, have found no evidence of a protective effect.

That is why, according to Dr. McMenamin, “additional population-based studies, in diverse populations, are required to investigate the association between aspirin use and survival outcomes in lung-cancer patients to determine whether randomized controlled trials are warranted in this patient group.”

In addition, she noted, “any potential benefit of aspirin in lung cancer patients needs to be balanced against known adverse events associated with prolonged aspirin use, such as gastrointestinal bleeding.”

Dr. Hung did not reply to requests for comment.

The study had no funding, and the researchers report no conflicts of interest.

A version of this article first appeared on Medscape.com.

Aspirin use was associated with longer overall survival in people with inoperable non–small cell lung cancer (NSCLC), according to a new study from Taiwan.

copyright Darren Hester/Fotolia.com

The analysis, published online Nov. 22 in BMC Cancer , adds another data point to a small and inconsistent evidence base.

“Despite the need for future prospective randomized clinical trials, aspirin may be considered as an additional treatment for inoperable NSCLC patients,” Ming-Szu Hung, MD, of Chang-Gung University, Taoyuan City, and colleagues write.

The current literature suggests that the over-the-counter medication may help ward off various types of cancer, including lung cancer, but the various study findings do not always align. For lung-cancer survival, in particular, a few observational studies have found increased survival among aspirin users while others have not.

To help bring clarity to the literature, Dr. Hung’s team examined data from Taiwan’s National Health Insurance Research Database on more than 38,000 patients diagnosed with NSCLC between 2000 and 2012, almost 5,000 of whom were taking aspirin at the time of diagnosis.

The researchers found that aspirin users survived for a median of 1.73 years, compared with 1.30 years for nonusers. Taking the drug was associated with longer overall survival in time-varying covariate analysis (hazard ratio, 0.83; 95% CI, 0.80-0.86). This finding was confirmed in a propensity-score analysis of 4,932 matched pairs (HR, 0.79; 95% CI, 0.75-0.83).

“These results warrant further randomized clinical trials to evaluate the actual role of aspirin in the treatment of NSCLC patients,” the researchers conclude.

But Úna McMenamin, PhD, a cancer epidemiologist at Queen’s University Belfast, Ireland, was not convinced by the study’s methods.

While she praised its large size and use of population-based health registers, she expressed concern about the potential for reverse causation, “as it is unclear whether authors lagged the aspirin exposure in the cohort of lung cancer patients.”

There is evidence that common medications such as aspirin may be withdrawn from patients who are thought to be near the end of their life, Dr. McMenamin told this news organization. When not factored into the statistical analysis, aspirin may appear “to be spuriously associated with a reduced risk of death when, in fact, no association may be present.”

Previous studies of aspirin use in lung cancer patients that have included a lag, such as one Dr. McMenamin and colleagues conducted in 2015, have found no evidence of a protective effect.

That is why, according to Dr. McMenamin, “additional population-based studies, in diverse populations, are required to investigate the association between aspirin use and survival outcomes in lung-cancer patients to determine whether randomized controlled trials are warranted in this patient group.”

In addition, she noted, “any potential benefit of aspirin in lung cancer patients needs to be balanced against known adverse events associated with prolonged aspirin use, such as gastrointestinal bleeding.”

Dr. Hung did not reply to requests for comment.

The study had no funding, and the researchers report no conflicts of interest.

A version of this article first appeared on Medscape.com.

Aspirin use was associated with longer overall survival in people with inoperable non–small cell lung cancer (NSCLC), according to a new study from Taiwan.

copyright Darren Hester/Fotolia.com

The analysis, published online Nov. 22 in BMC Cancer , adds another data point to a small and inconsistent evidence base.

“Despite the need for future prospective randomized clinical trials, aspirin may be considered as an additional treatment for inoperable NSCLC patients,” Ming-Szu Hung, MD, of Chang-Gung University, Taoyuan City, and colleagues write.

The current literature suggests that the over-the-counter medication may help ward off various types of cancer, including lung cancer, but the various study findings do not always align. For lung-cancer survival, in particular, a few observational studies have found increased survival among aspirin users while others have not.

To help bring clarity to the literature, Dr. Hung’s team examined data from Taiwan’s National Health Insurance Research Database on more than 38,000 patients diagnosed with NSCLC between 2000 and 2012, almost 5,000 of whom were taking aspirin at the time of diagnosis.

The researchers found that aspirin users survived for a median of 1.73 years, compared with 1.30 years for nonusers. Taking the drug was associated with longer overall survival in time-varying covariate analysis (hazard ratio, 0.83; 95% CI, 0.80-0.86). This finding was confirmed in a propensity-score analysis of 4,932 matched pairs (HR, 0.79; 95% CI, 0.75-0.83).

“These results warrant further randomized clinical trials to evaluate the actual role of aspirin in the treatment of NSCLC patients,” the researchers conclude.

But Úna McMenamin, PhD, a cancer epidemiologist at Queen’s University Belfast, Ireland, was not convinced by the study’s methods.

While she praised its large size and use of population-based health registers, she expressed concern about the potential for reverse causation, “as it is unclear whether authors lagged the aspirin exposure in the cohort of lung cancer patients.”

There is evidence that common medications such as aspirin may be withdrawn from patients who are thought to be near the end of their life, Dr. McMenamin told this news organization. When not factored into the statistical analysis, aspirin may appear “to be spuriously associated with a reduced risk of death when, in fact, no association may be present.”

Previous studies of aspirin use in lung cancer patients that have included a lag, such as one Dr. McMenamin and colleagues conducted in 2015, have found no evidence of a protective effect.

That is why, according to Dr. McMenamin, “additional population-based studies, in diverse populations, are required to investigate the association between aspirin use and survival outcomes in lung-cancer patients to determine whether randomized controlled trials are warranted in this patient group.”

In addition, she noted, “any potential benefit of aspirin in lung cancer patients needs to be balanced against known adverse events associated with prolonged aspirin use, such as gastrointestinal bleeding.”

Dr. Hung did not reply to requests for comment.

The study had no funding, and the researchers report no conflicts of interest.

A version of this article first appeared on Medscape.com.

A potential new urine biomarker for prostate cancer not only spots the presence of aggressive tumors, it also indicates the amount of these tumors, according to a recent report.

In a study of biopsy and prostatectomy samples, researchers found that the multigene Prostate Urine Risk-4 (PUR-4) signature was strongly associated with the presence and amount of Gleason pattern 4 tumors, but not tumors of less aggressive histology.

Given that increased Gleason pattern 4 tumor burden is associated with disease progression in men at intermediate risk, the results suggest that “PUR can show us which men at intermediate risk may require treatment and which may instead be managed conservatively with surveillance,” said senior author Jeremy Clark, PhD, of the University of East Anglia, Norwich, England. “PUR will also be useful for monitoring disease in men that do not currently require treatment and flag up the emergence and expansion of aggressive disease.”

The study by Dr. Clark and colleagues was published online on Nov. 3, 2021, in Life.

Tests using the traditional blood-based biomarker for prostate cancer – prostate-specific antigen (PSA) – have limited sensitivity and specificity, leading to unnecessary biopsies and overtreatment.

The PUR biomarker, one of several emerging alternatives to PSA, is a four-group classifier based on 36 genes, Dr. Clark and colleagues explained. Its categories correspond to the probabilities of the presence of normal tissue (PUR-1), and D’Amico low-risk (PUR-2), intermediate-risk (PUR-3), and high-risk (PUR-4) prostate cancer.

Dr. Clark’s team found in earlier research that the PUR-4 signature was able to predict disease progression in men on active surveillance for prostate cancer up to 5 years after a single urine sample. For their latest study, they sought to understand the relationship between PUR-4 and the amount and grade of tumor.

On the basis of biopsy samples from 215 men with prostate cancer, the researchers found that PUR-4 signature values correlated significantly with increasing Gleason grade.

There was no significant difference in PSA level by tumor volume for Gleason grade 1, 2, or 3. The same was true for PUR-4 and Gleason grade 1 tumors, which only contain less clinically significant Gleason pattern 3 cancer. However, PUR-4 values in men with Gleason grade 2 tumors larger than the median were significantly greater than for smaller tumors. PUR-4 values for large Gleason grade 3 tumors were also greater than for smaller ones, although the difference did not reach statistical significance.

“Since [Gleason grade] 2 and [Gleason grade] 3 contain both Gleason pattern 3 and 4 cancer these observations suggest that Gleason Pattern 4 cancer may be contributing to PUR-4 status,” the authors wrote.

The researchers also examined radical-prostatectomy specimens from nine men – three with Gleason grade 1, four with Gleason grade 2, and two with Gleason grade 3 tumors, as determined on the basis of presurgical biopsy.

There was no significant correlation between PUR-4 and PSA levels, nor were PUR-4 values linked to total tumor area or Gleason pattern 3 tumor area. But the amount of Gleason pattern 4 tumors showed a strong correlation with PUR-4 values, which did not change after adjusting for total prostate size.

“Our study shows that the PUR test can assess the amount of Gleason pattern 4 without the need for a biopsy,” Dr. Clark said in an interview. “It could therefore be a very useful tool indeed for assessing a man’s risk of dying from prostate cancer.”

Jack Schalken, PhD, a professor of experimental urology at Radboud University Medical Center in Nijmegen, the Netherlands, called PUR “another test” for prostate cancer the performance of which is in the same range as that of existing products.

“In fact, several tests are commercially available, but the clinical use is surprisingly low,” he told this news organization. Dr. Schalken, who was not involved in the new study, has reviewed several biomarkers for prostate cancer.

The PUR test is now undergoing validation in an international study that is expected to last another 2 years, Dr. Clark said. If successful, the test would stand out for several reasons.

First, it is based on many genes, so it is able to spot malignancies that other tests, which rely on just a few genes, may not pick up. In addition, although it is sensitive to the amount of Gleason pattern 4 tumor, it does not seem to detect the clinically less significant Gleason pattern 3 cancers.

“We have an at-home collection kit – the men do not have to come to a hospital to provide a urine sample,” Dr. Clark said.

The study did not receive commercial funding. Dr. Clark and two coauthors have filed a patent application related to their research.
 

A version of this article first appeared on Medscape.com.

A potential new urine biomarker for prostate cancer not only spots the presence of aggressive tumors, it also indicates the amount of these tumors, according to a recent report.

In a study of biopsy and prostatectomy samples, researchers found that the multigene Prostate Urine Risk-4 (PUR-4) signature was strongly associated with the presence and amount of Gleason pattern 4 tumors, but not tumors of less aggressive histology.

Given that increased Gleason pattern 4 tumor burden is associated with disease progression in men at intermediate risk, the results suggest that “PUR can show us which men at intermediate risk may require treatment and which may instead be managed conservatively with surveillance,” said senior author Jeremy Clark, PhD, of the University of East Anglia, Norwich, England. “PUR will also be useful for monitoring disease in men that do not currently require treatment and flag up the emergence and expansion of aggressive disease.”

The study by Dr. Clark and colleagues was published online on Nov. 3, 2021, in Life.

Tests using the traditional blood-based biomarker for prostate cancer – prostate-specific antigen (PSA) – have limited sensitivity and specificity, leading to unnecessary biopsies and overtreatment.

The PUR biomarker, one of several emerging alternatives to PSA, is a four-group classifier based on 36 genes, Dr. Clark and colleagues explained. Its categories correspond to the probabilities of the presence of normal tissue (PUR-1), and D’Amico low-risk (PUR-2), intermediate-risk (PUR-3), and high-risk (PUR-4) prostate cancer.

Dr. Clark’s team found in earlier research that the PUR-4 signature was able to predict disease progression in men on active surveillance for prostate cancer up to 5 years after a single urine sample. For their latest study, they sought to understand the relationship between PUR-4 and the amount and grade of tumor.

On the basis of biopsy samples from 215 men with prostate cancer, the researchers found that PUR-4 signature values correlated significantly with increasing Gleason grade.

There was no significant difference in PSA level by tumor volume for Gleason grade 1, 2, or 3. The same was true for PUR-4 and Gleason grade 1 tumors, which only contain less clinically significant Gleason pattern 3 cancer. However, PUR-4 values in men with Gleason grade 2 tumors larger than the median were significantly greater than for smaller tumors. PUR-4 values for large Gleason grade 3 tumors were also greater than for smaller ones, although the difference did not reach statistical significance.

“Since [Gleason grade] 2 and [Gleason grade] 3 contain both Gleason pattern 3 and 4 cancer these observations suggest that Gleason Pattern 4 cancer may be contributing to PUR-4 status,” the authors wrote.

The researchers also examined radical-prostatectomy specimens from nine men – three with Gleason grade 1, four with Gleason grade 2, and two with Gleason grade 3 tumors, as determined on the basis of presurgical biopsy.

There was no significant correlation between PUR-4 and PSA levels, nor were PUR-4 values linked to total tumor area or Gleason pattern 3 tumor area. But the amount of Gleason pattern 4 tumors showed a strong correlation with PUR-4 values, which did not change after adjusting for total prostate size.

“Our study shows that the PUR test can assess the amount of Gleason pattern 4 without the need for a biopsy,” Dr. Clark said in an interview. “It could therefore be a very useful tool indeed for assessing a man’s risk of dying from prostate cancer.”

Jack Schalken, PhD, a professor of experimental urology at Radboud University Medical Center in Nijmegen, the Netherlands, called PUR “another test” for prostate cancer the performance of which is in the same range as that of existing products.

“In fact, several tests are commercially available, but the clinical use is surprisingly low,” he told this news organization. Dr. Schalken, who was not involved in the new study, has reviewed several biomarkers for prostate cancer.

The PUR test is now undergoing validation in an international study that is expected to last another 2 years, Dr. Clark said. If successful, the test would stand out for several reasons.

First, it is based on many genes, so it is able to spot malignancies that other tests, which rely on just a few genes, may not pick up. In addition, although it is sensitive to the amount of Gleason pattern 4 tumor, it does not seem to detect the clinically less significant Gleason pattern 3 cancers.

“We have an at-home collection kit – the men do not have to come to a hospital to provide a urine sample,” Dr. Clark said.

The study did not receive commercial funding. Dr. Clark and two coauthors have filed a patent application related to their research.
 

A version of this article first appeared on Medscape.com.

A potential new urine biomarker for prostate cancer not only spots the presence of aggressive tumors, it also indicates the amount of these tumors, according to a recent report.

In a study of biopsy and prostatectomy samples, researchers found that the multigene Prostate Urine Risk-4 (PUR-4) signature was strongly associated with the presence and amount of Gleason pattern 4 tumors, but not tumors of less aggressive histology.

Given that increased Gleason pattern 4 tumor burden is associated with disease progression in men at intermediate risk, the results suggest that “PUR can show us which men at intermediate risk may require treatment and which may instead be managed conservatively with surveillance,” said senior author Jeremy Clark, PhD, of the University of East Anglia, Norwich, England. “PUR will also be useful for monitoring disease in men that do not currently require treatment and flag up the emergence and expansion of aggressive disease.”

The study by Dr. Clark and colleagues was published online on Nov. 3, 2021, in Life.

Tests using the traditional blood-based biomarker for prostate cancer – prostate-specific antigen (PSA) – have limited sensitivity and specificity, leading to unnecessary biopsies and overtreatment.

The PUR biomarker, one of several emerging alternatives to PSA, is a four-group classifier based on 36 genes, Dr. Clark and colleagues explained. Its categories correspond to the probabilities of the presence of normal tissue (PUR-1), and D’Amico low-risk (PUR-2), intermediate-risk (PUR-3), and high-risk (PUR-4) prostate cancer.

Dr. Clark’s team found in earlier research that the PUR-4 signature was able to predict disease progression in men on active surveillance for prostate cancer up to 5 years after a single urine sample. For their latest study, they sought to understand the relationship between PUR-4 and the amount and grade of tumor.

On the basis of biopsy samples from 215 men with prostate cancer, the researchers found that PUR-4 signature values correlated significantly with increasing Gleason grade.

There was no significant difference in PSA level by tumor volume for Gleason grade 1, 2, or 3. The same was true for PUR-4 and Gleason grade 1 tumors, which only contain less clinically significant Gleason pattern 3 cancer. However, PUR-4 values in men with Gleason grade 2 tumors larger than the median were significantly greater than for smaller tumors. PUR-4 values for large Gleason grade 3 tumors were also greater than for smaller ones, although the difference did not reach statistical significance.

“Since [Gleason grade] 2 and [Gleason grade] 3 contain both Gleason pattern 3 and 4 cancer these observations suggest that Gleason Pattern 4 cancer may be contributing to PUR-4 status,” the authors wrote.

The researchers also examined radical-prostatectomy specimens from nine men – three with Gleason grade 1, four with Gleason grade 2, and two with Gleason grade 3 tumors, as determined on the basis of presurgical biopsy.

There was no significant correlation between PUR-4 and PSA levels, nor were PUR-4 values linked to total tumor area or Gleason pattern 3 tumor area. But the amount of Gleason pattern 4 tumors showed a strong correlation with PUR-4 values, which did not change after adjusting for total prostate size.

“Our study shows that the PUR test can assess the amount of Gleason pattern 4 without the need for a biopsy,” Dr. Clark said in an interview. “It could therefore be a very useful tool indeed for assessing a man’s risk of dying from prostate cancer.”

Jack Schalken, PhD, a professor of experimental urology at Radboud University Medical Center in Nijmegen, the Netherlands, called PUR “another test” for prostate cancer the performance of which is in the same range as that of existing products.

“In fact, several tests are commercially available, but the clinical use is surprisingly low,” he told this news organization. Dr. Schalken, who was not involved in the new study, has reviewed several biomarkers for prostate cancer.

The PUR test is now undergoing validation in an international study that is expected to last another 2 years, Dr. Clark said. If successful, the test would stand out for several reasons.

First, it is based on many genes, so it is able to spot malignancies that other tests, which rely on just a few genes, may not pick up. In addition, although it is sensitive to the amount of Gleason pattern 4 tumor, it does not seem to detect the clinically less significant Gleason pattern 3 cancers.

“We have an at-home collection kit – the men do not have to come to a hospital to provide a urine sample,” Dr. Clark said.

The study did not receive commercial funding. Dr. Clark and two coauthors have filed a patent application related to their research.
 

A version of this article first appeared on Medscape.com.

Even third-degree relatives of people with early-onset colorectal cancer (CRC) are at elevated risk for the disease, according to a study that researchers say could influence screening recommendations.

Among first-degree relatives, there was a sixfold increased risk of developing the malignancy before age 50 in comparison with the general population. Among second- and third-degree relatives, the risk was 1.5 times higher.

Family history is a recognized risk factor for CRC. Roughly 1 in 10 cases of CRC in the United States occurs in people younger than 50 years. It has not been clear to what extent having relatives with early-onset CRC contributes to risk beyond familial syndromes and whether risk extends beyond first-degree relatives, according to study author Lisa A. Cannon-Albright, PhD, of the University of Utah, Salt Lake City, and colleagues.

The new findings suggest “that extended family history should be part of the discussion when making cancer screening decisions,” the researchers write. Their study appears in the August issue of Cancer Epidemiology.

The authors used the Utah Population Data Base (UPDB) to examine genealogies in which more than three generations were linked to the Utah Cancer Registry. The analysis comprised all CRC cases for which there were linked genealogy data.

Of the 1,510 cases of early-onset CRC that the team identified, the risk for CRC was 6.00, 3.09, and 1.56 times higher than expected on the basis of UPDB disease rates for first-, second-, and third-degree relatives, respectively. All results were statistically significant.

The authors also found that individuals with a first-degree relative with early-onset CRC were at 2.64-fold higher risk for CRC at any age. The risk was 1.96-fold higher risk with a second-degree relative and 1.3-fold higher with a third-degree relative. In other words, “the risk for [early-onset] CRC is higher than the risk for CRC at any age, for all degrees of relatives shown,” the team writes.

“Significantly elevated risk for CRC at both locations (left or right) was observed for all degrees of relationship; however the confidence intervals are overlapping, suggesting no difference in risk of left- vs. right-sided CRC,” they state.

The findings held up when the researchers used a genealogic index of familiality test instead of calculating relative risk. Although the authors were unable to exclude from the analysis people with inherited syndromes, they say that it is not likely that Lynch syndrome is driving the results, given that more than three-quarters of the early-onset CRC cases were left-sided, “and Lynch primarily occurs in the proximal colon.”

The authors caution, however, that the majority of the study population were of Northern European ancestry, which could limit generalizability to other groups.

Currently, there are no screening guidelines for second- or third-degree relatives of persons with early-onset CRC unless Lynch syndrome or another genetic condition is identified, the researchers write.

The authors note that their findings suggest that early colonoscopy screening may be considered not only for first-degree relatives, but also for second- and possibly third-degree relatives of persons who have early-onset CRC and that the findings could “influence future CRC screening recommendations.

“Relatives may also benefit from an evaluation with genetic counseling to assess underlying inherited conditions,” they write. “However, we note that there are important considerations in the need for resources to accomplish earlier population-based CRC screening.”

The study was supported by the Utah Cancer Registry, which is funded by the National Cancer Institute’s SEER Program, and the U.S. Centers for Disease Control and Prevention’s National Program of Cancer Registries. Additional support was provided by the University of Utah and Huntsman Cancer Foundation. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Even third-degree relatives of people with early-onset colorectal cancer (CRC) are at elevated risk for the disease, according to a study that researchers say could influence screening recommendations.

Among first-degree relatives, there was a sixfold increased risk of developing the malignancy before age 50 in comparison with the general population. Among second- and third-degree relatives, the risk was 1.5 times higher.

Family history is a recognized risk factor for CRC. Roughly 1 in 10 cases of CRC in the United States occurs in people younger than 50 years. It has not been clear to what extent having relatives with early-onset CRC contributes to risk beyond familial syndromes and whether risk extends beyond first-degree relatives, according to study author Lisa A. Cannon-Albright, PhD, of the University of Utah, Salt Lake City, and colleagues.

The new findings suggest “that extended family history should be part of the discussion when making cancer screening decisions,” the researchers write. Their study appears in the August issue of Cancer Epidemiology.

The authors used the Utah Population Data Base (UPDB) to examine genealogies in which more than three generations were linked to the Utah Cancer Registry. The analysis comprised all CRC cases for which there were linked genealogy data.

Of the 1,510 cases of early-onset CRC that the team identified, the risk for CRC was 6.00, 3.09, and 1.56 times higher than expected on the basis of UPDB disease rates for first-, second-, and third-degree relatives, respectively. All results were statistically significant.

The authors also found that individuals with a first-degree relative with early-onset CRC were at 2.64-fold higher risk for CRC at any age. The risk was 1.96-fold higher risk with a second-degree relative and 1.3-fold higher with a third-degree relative. In other words, “the risk for [early-onset] CRC is higher than the risk for CRC at any age, for all degrees of relatives shown,” the team writes.

“Significantly elevated risk for CRC at both locations (left or right) was observed for all degrees of relationship; however the confidence intervals are overlapping, suggesting no difference in risk of left- vs. right-sided CRC,” they state.

The findings held up when the researchers used a genealogic index of familiality test instead of calculating relative risk. Although the authors were unable to exclude from the analysis people with inherited syndromes, they say that it is not likely that Lynch syndrome is driving the results, given that more than three-quarters of the early-onset CRC cases were left-sided, “and Lynch primarily occurs in the proximal colon.”

The authors caution, however, that the majority of the study population were of Northern European ancestry, which could limit generalizability to other groups.

Currently, there are no screening guidelines for second- or third-degree relatives of persons with early-onset CRC unless Lynch syndrome or another genetic condition is identified, the researchers write.

The authors note that their findings suggest that early colonoscopy screening may be considered not only for first-degree relatives, but also for second- and possibly third-degree relatives of persons who have early-onset CRC and that the findings could “influence future CRC screening recommendations.

“Relatives may also benefit from an evaluation with genetic counseling to assess underlying inherited conditions,” they write. “However, we note that there are important considerations in the need for resources to accomplish earlier population-based CRC screening.”

The study was supported by the Utah Cancer Registry, which is funded by the National Cancer Institute’s SEER Program, and the U.S. Centers for Disease Control and Prevention’s National Program of Cancer Registries. Additional support was provided by the University of Utah and Huntsman Cancer Foundation. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Even third-degree relatives of people with early-onset colorectal cancer (CRC) are at elevated risk for the disease, according to a study that researchers say could influence screening recommendations.

Among first-degree relatives, there was a sixfold increased risk of developing the malignancy before age 50 in comparison with the general population. Among second- and third-degree relatives, the risk was 1.5 times higher.

Family history is a recognized risk factor for CRC. Roughly 1 in 10 cases of CRC in the United States occurs in people younger than 50 years. It has not been clear to what extent having relatives with early-onset CRC contributes to risk beyond familial syndromes and whether risk extends beyond first-degree relatives, according to study author Lisa A. Cannon-Albright, PhD, of the University of Utah, Salt Lake City, and colleagues.

The new findings suggest “that extended family history should be part of the discussion when making cancer screening decisions,” the researchers write. Their study appears in the August issue of Cancer Epidemiology.

The authors used the Utah Population Data Base (UPDB) to examine genealogies in which more than three generations were linked to the Utah Cancer Registry. The analysis comprised all CRC cases for which there were linked genealogy data.

Of the 1,510 cases of early-onset CRC that the team identified, the risk for CRC was 6.00, 3.09, and 1.56 times higher than expected on the basis of UPDB disease rates for first-, second-, and third-degree relatives, respectively. All results were statistically significant.

The authors also found that individuals with a first-degree relative with early-onset CRC were at 2.64-fold higher risk for CRC at any age. The risk was 1.96-fold higher risk with a second-degree relative and 1.3-fold higher with a third-degree relative. In other words, “the risk for [early-onset] CRC is higher than the risk for CRC at any age, for all degrees of relatives shown,” the team writes.

“Significantly elevated risk for CRC at both locations (left or right) was observed for all degrees of relationship; however the confidence intervals are overlapping, suggesting no difference in risk of left- vs. right-sided CRC,” they state.

The findings held up when the researchers used a genealogic index of familiality test instead of calculating relative risk. Although the authors were unable to exclude from the analysis people with inherited syndromes, they say that it is not likely that Lynch syndrome is driving the results, given that more than three-quarters of the early-onset CRC cases were left-sided, “and Lynch primarily occurs in the proximal colon.”

The authors caution, however, that the majority of the study population were of Northern European ancestry, which could limit generalizability to other groups.

Currently, there are no screening guidelines for second- or third-degree relatives of persons with early-onset CRC unless Lynch syndrome or another genetic condition is identified, the researchers write.

The authors note that their findings suggest that early colonoscopy screening may be considered not only for first-degree relatives, but also for second- and possibly third-degree relatives of persons who have early-onset CRC and that the findings could “influence future CRC screening recommendations.

“Relatives may also benefit from an evaluation with genetic counseling to assess underlying inherited conditions,” they write. “However, we note that there are important considerations in the need for resources to accomplish earlier population-based CRC screening.”

The study was supported by the Utah Cancer Registry, which is funded by the National Cancer Institute’s SEER Program, and the U.S. Centers for Disease Control and Prevention’s National Program of Cancer Registries. Additional support was provided by the University of Utah and Huntsman Cancer Foundation. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.