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Neuroscientists say they have uncovered genetic differences between radiation-induced meningiomas (RIMs) and sporadic meningiomas (SMs).
Their work suggests RIMs have a different “mutational landscape” from SMs, a finding that may have “significant therapeutic implications” for childhood cancer survivors who undergo cranial radiation.
Gelareh Zadeh, MD, PhD, of the University of Toronto in Ontario, Canada, and her colleagues reported these findings in Nature Communications.
“Radiation-induced meningiomas appear the same [as SMs] on MRI and pathology, feel the same during surgery, and look the same under the operating microscope,” Dr Zadeh said.
“What’s different is they are more aggressive, tend to recur in multiples, and invade the brain, causing significant morbidity and limitations (or impairments) for individuals who survive following childhood radiation. By understanding the biology, the goal is to identify a therapeutic strategy that could be implemented early on after childhood radiation to prevent the formation of these tumors in the first place.”
To better understand the biology, Dr Zadeh and her colleagues analyzed 31 RIMs. This included 18 tumors from 16 patients with childhood cancers, 9 with leukemia.
The researchers found NF2 gene rearrangements in 12 of the RIMs and noted that such rearrangements have not been observed in SMs.
On the other hand, recurrent mutations characteristic of SMs—AKT1, KLF4, TRAF7, and SMO—were not found in the RIMs.
The researchers also noted that, overall, chromosomal aberrations in RIMs were more complex than those observed in SMs. And combined loss of chromosomes 1p and 22q was common in RIMs (16/18).
“Our research identified a specific rearrangement involving the NF2 gene that causes radiation-induced meningiomas,” said Kenneth Aldape, MD, of University Health Network in Toronto.
“But there are likely other genetic rearrangements that are occurring as a result of that radiation-induced DNA damage. So one of the next steps is to identify what the radiation is doing to the DNA of the meninges.”
“In addition, identifying the subset of childhood cancer patients who are at highest risk to develop meningioma is critical so that they could be followed closely for early detection and management.” 
Neuroscientists say they have uncovered genetic differences between radiation-induced meningiomas (RIMs) and sporadic meningiomas (SMs).
Their work suggests RIMs have a different “mutational landscape” from SMs, a finding that may have “significant therapeutic implications” for childhood cancer survivors who undergo cranial radiation.
Gelareh Zadeh, MD, PhD, of the University of Toronto in Ontario, Canada, and her colleagues reported these findings in Nature Communications.
“Radiation-induced meningiomas appear the same [as SMs] on MRI and pathology, feel the same during surgery, and look the same under the operating microscope,” Dr Zadeh said.
“What’s different is they are more aggressive, tend to recur in multiples, and invade the brain, causing significant morbidity and limitations (or impairments) for individuals who survive following childhood radiation. By understanding the biology, the goal is to identify a therapeutic strategy that could be implemented early on after childhood radiation to prevent the formation of these tumors in the first place.”
To better understand the biology, Dr Zadeh and her colleagues analyzed 31 RIMs. This included 18 tumors from 16 patients with childhood cancers, 9 with leukemia.
The researchers found NF2 gene rearrangements in 12 of the RIMs and noted that such rearrangements have not been observed in SMs.
On the other hand, recurrent mutations characteristic of SMs—AKT1, KLF4, TRAF7, and SMO—were not found in the RIMs.
The researchers also noted that, overall, chromosomal aberrations in RIMs were more complex than those observed in SMs. And combined loss of chromosomes 1p and 22q was common in RIMs (16/18).
“Our research identified a specific rearrangement involving the NF2 gene that causes radiation-induced meningiomas,” said Kenneth Aldape, MD, of University Health Network in Toronto.
“But there are likely other genetic rearrangements that are occurring as a result of that radiation-induced DNA damage. So one of the next steps is to identify what the radiation is doing to the DNA of the meninges.”
“In addition, identifying the subset of childhood cancer patients who are at highest risk to develop meningioma is critical so that they could be followed closely for early detection and management.”
Neuroscientists say they have uncovered genetic differences between radiation-induced meningiomas (RIMs) and sporadic meningiomas (SMs).
Their work suggests RIMs have a different “mutational landscape” from SMs, a finding that may have “significant therapeutic implications” for childhood cancer survivors who undergo cranial radiation.
Gelareh Zadeh, MD, PhD, of the University of Toronto in Ontario, Canada, and her colleagues reported these findings in Nature Communications.
“Radiation-induced meningiomas appear the same [as SMs] on MRI and pathology, feel the same during surgery, and look the same under the operating microscope,” Dr Zadeh said.
“What’s different is they are more aggressive, tend to recur in multiples, and invade the brain, causing significant morbidity and limitations (or impairments) for individuals who survive following childhood radiation. By understanding the biology, the goal is to identify a therapeutic strategy that could be implemented early on after childhood radiation to prevent the formation of these tumors in the first place.”
To better understand the biology, Dr Zadeh and her colleagues analyzed 31 RIMs. This included 18 tumors from 16 patients with childhood cancers, 9 with leukemia.
The researchers found NF2 gene rearrangements in 12 of the RIMs and noted that such rearrangements have not been observed in SMs.
On the other hand, recurrent mutations characteristic of SMs—AKT1, KLF4, TRAF7, and SMO—were not found in the RIMs.
The researchers also noted that, overall, chromosomal aberrations in RIMs were more complex than those observed in SMs. And combined loss of chromosomes 1p and 22q was common in RIMs (16/18).
“Our research identified a specific rearrangement involving the NF2 gene that causes radiation-induced meningiomas,” said Kenneth Aldape, MD, of University Health Network in Toronto.
“But there are likely other genetic rearrangements that are occurring as a result of that radiation-induced DNA damage. So one of the next steps is to identify what the radiation is doing to the DNA of the meninges.”
“In addition, identifying the subset of childhood cancer patients who are at highest risk to develop meningioma is critical so that they could be followed closely for early detection and management.”