Mehdi S

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Renal Cell carcinoma (RCC) possesses the ability to metastasize to distant places most commonly lungs, lymph nodes, liver, bone, and brain. While RCC can metastasize potentially to any organ, the gastrointestinal tract involvement is exceedingly rare.

Case Presentation: A 76-year-old male veteran presented with complain of hematuria and was diagnosed initially with stage 3 (pT3cN0M0) clear cell RCC of the right kidney. He underwent right radical nephrectomy with caval thrombectomy. He was then followed for surveillance during which, based on his radiological imaging, he was found to have a mesenteric mass inseparable from the transverse colon, multiple pulmonary nodules, and a large hypo density in the liver. He underwent subsequent biopsy of the mesenteric mass, which confirmed metastatic RCC (clear cell).

He was started on sunitinib 50mg based on NCCN guidelines. He did well on sunitinib for a while, but repeat CT chest, abdomen, and pelvis scans showed progression of his disease. He was started on nivolumab as a second line agent as per the NCCN guidelines. While on nivolumab, he presented in early 2019 with an episode of GI bleeding (melena). He underwent repeat radiological imaging as well as an endoscopy, which showed medium size friable soft tissue mass in the 2nd part of duodenum. Biopsy of that mass con rmed RCC eroding into the duodenal mucosa. His case was discussed at the tumor board, and it was recommended that palliative surgery and radiation were not an option for him. A recommendation for palliative and supportive treatment were made. The patient’s condition was discussed with him, and given that he was asymptomatic and at his general baseline health, he opted to continue with the immunotherapy.

Conclusion: RCC metastasis to GI tract is rare. The duodenum is reported to be the least involved segment of the small intestine. The number of cases reports in literature on duodenal metastasis from RCC is estimated to be around 20-25.Treatment of RCC with duodenal metastases depends upon the location and extent of the tumor as well as patient’s fitness for different modalities.

Background: Renal Cell carcinoma (RCC) possesses the ability to metastasize to distant places most commonly lungs, lymph nodes, liver, bone, and brain. While RCC can metastasize potentially to any organ, the gastrointestinal tract involvement is exceedingly rare.

Case Presentation: A 76-year-old male veteran presented with complain of hematuria and was diagnosed initially with stage 3 (pT3cN0M0) clear cell RCC of the right kidney. He underwent right radical nephrectomy with caval thrombectomy. He was then followed for surveillance during which, based on his radiological imaging, he was found to have a mesenteric mass inseparable from the transverse colon, multiple pulmonary nodules, and a large hypo density in the liver. He underwent subsequent biopsy of the mesenteric mass, which confirmed metastatic RCC (clear cell).

He was started on sunitinib 50mg based on NCCN guidelines. He did well on sunitinib for a while, but repeat CT chest, abdomen, and pelvis scans showed progression of his disease. He was started on nivolumab as a second line agent as per the NCCN guidelines. While on nivolumab, he presented in early 2019 with an episode of GI bleeding (melena). He underwent repeat radiological imaging as well as an endoscopy, which showed medium size friable soft tissue mass in the 2nd part of duodenum. Biopsy of that mass con rmed RCC eroding into the duodenal mucosa. His case was discussed at the tumor board, and it was recommended that palliative surgery and radiation were not an option for him. A recommendation for palliative and supportive treatment were made. The patient’s condition was discussed with him, and given that he was asymptomatic and at his general baseline health, he opted to continue with the immunotherapy.

Conclusion: RCC metastasis to GI tract is rare. The duodenum is reported to be the least involved segment of the small intestine. The number of cases reports in literature on duodenal metastasis from RCC is estimated to be around 20-25.Treatment of RCC with duodenal metastases depends upon the location and extent of the tumor as well as patient’s fitness for different modalities.

Background: Renal Cell carcinoma (RCC) possesses the ability to metastasize to distant places most commonly lungs, lymph nodes, liver, bone, and brain. While RCC can metastasize potentially to any organ, the gastrointestinal tract involvement is exceedingly rare.

Case Presentation: A 76-year-old male veteran presented with complain of hematuria and was diagnosed initially with stage 3 (pT3cN0M0) clear cell RCC of the right kidney. He underwent right radical nephrectomy with caval thrombectomy. He was then followed for surveillance during which, based on his radiological imaging, he was found to have a mesenteric mass inseparable from the transverse colon, multiple pulmonary nodules, and a large hypo density in the liver. He underwent subsequent biopsy of the mesenteric mass, which confirmed metastatic RCC (clear cell).

He was started on sunitinib 50mg based on NCCN guidelines. He did well on sunitinib for a while, but repeat CT chest, abdomen, and pelvis scans showed progression of his disease. He was started on nivolumab as a second line agent as per the NCCN guidelines. While on nivolumab, he presented in early 2019 with an episode of GI bleeding (melena). He underwent repeat radiological imaging as well as an endoscopy, which showed medium size friable soft tissue mass in the 2nd part of duodenum. Biopsy of that mass con rmed RCC eroding into the duodenal mucosa. His case was discussed at the tumor board, and it was recommended that palliative surgery and radiation were not an option for him. A recommendation for palliative and supportive treatment were made. The patient’s condition was discussed with him, and given that he was asymptomatic and at his general baseline health, he opted to continue with the immunotherapy.

Conclusion: RCC metastasis to GI tract is rare. The duodenum is reported to be the least involved segment of the small intestine. The number of cases reports in literature on duodenal metastasis from RCC is estimated to be around 20-25.Treatment of RCC with duodenal metastases depends upon the location and extent of the tumor as well as patient’s fitness for different modalities.

Background: In 2018, a male aged 62 years with a history of squamous cell tonsillar cancer, which was successfully treated by concurrent chemoradiation and selective neck dissection in 2014, was diagnosed with primary right sided lung adenocarcinoma (Stage IV, cT4c cN3 cM1a) after presenting with post-obstructive pneumonia. Molecular analysis was about 100% positive for PDL-1 and negative for EGFR, ALK, BRAF, and ROS. The patient was started on Pembrolizumab. After 5 cycles, he developed worsening dyspnea. A CT scan of his chest revealed a large pericardial effusion and decrease in size of right upper lobe lesion. An echocardiogram confirmed cardiac tamponade physiology. 400 ml of fluid was removed by emergent pericardial window and surgical drain was placed. Cytopathological analysis of pericardial fluid returned negative for malignant cells. The patient was treated with high dose prednisone with tapering, and pembrolizumab was discontinued. Patient responded very well. A repeat CT and ECHO after 3 months of treatment confirmed nearresolution of effusion.

Discussion: Distinguishing immune mediated pericardial effusion from malignant effusion is vital. Development of pericardial effusion with concurrent improvement or stability of malignant lesion, negative cytology and brisk response to corticosteroids indicates an immune etiology.

Pericardiocentesis or pericardial window is the key intervention in acute management. The critical step in immune mediated pericardial effusions is initiation of high-dose corticosteroids (1-2 mg/kg of Prednisone) with tapering of at least 4 weeks in severe cases. In unresponsive cases, corticosteroids at transplant rejection dose (1 g methylprednisone daily) and addition of mycophenolate mofetil, in iximab or antithymocyte globulin should be considered. As per ‘ASCO Practice Guideline’, any grade of cardiotoxicity above grade 1 warrants holding or permanently discontinuing the immunotherapy. For pericardial effusions secondary to pseudoprogression, immunotherapy can be continued.

Based on our literature review, concurrence of other immune related adverse events and recurrence of effusions with discontinuation of corticosteroids is reported with immune mediated pericardial effusions.

Conclusion: Early identification of immune related adverse events is very important. In immune mediated pericardial effusion, pericardial fluid should be drained, and corticosteroids should be started promptly. Permanent discontinuation of immunotherapy is recommended for grade 3 and 4 cardiotoxicity. Re-challenge of immunotherapy after treating the adverse event is a subject that needs further research.

Background: In 2018, a male aged 62 years with a history of squamous cell tonsillar cancer, which was successfully treated by concurrent chemoradiation and selective neck dissection in 2014, was diagnosed with primary right sided lung adenocarcinoma (Stage IV, cT4c cN3 cM1a) after presenting with post-obstructive pneumonia. Molecular analysis was about 100% positive for PDL-1 and negative for EGFR, ALK, BRAF, and ROS. The patient was started on Pembrolizumab. After 5 cycles, he developed worsening dyspnea. A CT scan of his chest revealed a large pericardial effusion and decrease in size of right upper lobe lesion. An echocardiogram confirmed cardiac tamponade physiology. 400 ml of fluid was removed by emergent pericardial window and surgical drain was placed. Cytopathological analysis of pericardial fluid returned negative for malignant cells. The patient was treated with high dose prednisone with tapering, and pembrolizumab was discontinued. Patient responded very well. A repeat CT and ECHO after 3 months of treatment confirmed nearresolution of effusion.

Discussion: Distinguishing immune mediated pericardial effusion from malignant effusion is vital. Development of pericardial effusion with concurrent improvement or stability of malignant lesion, negative cytology and brisk response to corticosteroids indicates an immune etiology.

Pericardiocentesis or pericardial window is the key intervention in acute management. The critical step in immune mediated pericardial effusions is initiation of high-dose corticosteroids (1-2 mg/kg of Prednisone) with tapering of at least 4 weeks in severe cases. In unresponsive cases, corticosteroids at transplant rejection dose (1 g methylprednisone daily) and addition of mycophenolate mofetil, in iximab or antithymocyte globulin should be considered. As per ‘ASCO Practice Guideline’, any grade of cardiotoxicity above grade 1 warrants holding or permanently discontinuing the immunotherapy. For pericardial effusions secondary to pseudoprogression, immunotherapy can be continued.

Based on our literature review, concurrence of other immune related adverse events and recurrence of effusions with discontinuation of corticosteroids is reported with immune mediated pericardial effusions.

Conclusion: Early identification of immune related adverse events is very important. In immune mediated pericardial effusion, pericardial fluid should be drained, and corticosteroids should be started promptly. Permanent discontinuation of immunotherapy is recommended for grade 3 and 4 cardiotoxicity. Re-challenge of immunotherapy after treating the adverse event is a subject that needs further research.

Background: In 2018, a male aged 62 years with a history of squamous cell tonsillar cancer, which was successfully treated by concurrent chemoradiation and selective neck dissection in 2014, was diagnosed with primary right sided lung adenocarcinoma (Stage IV, cT4c cN3 cM1a) after presenting with post-obstructive pneumonia. Molecular analysis was about 100% positive for PDL-1 and negative for EGFR, ALK, BRAF, and ROS. The patient was started on Pembrolizumab. After 5 cycles, he developed worsening dyspnea. A CT scan of his chest revealed a large pericardial effusion and decrease in size of right upper lobe lesion. An echocardiogram confirmed cardiac tamponade physiology. 400 ml of fluid was removed by emergent pericardial window and surgical drain was placed. Cytopathological analysis of pericardial fluid returned negative for malignant cells. The patient was treated with high dose prednisone with tapering, and pembrolizumab was discontinued. Patient responded very well. A repeat CT and ECHO after 3 months of treatment confirmed nearresolution of effusion.

Discussion: Distinguishing immune mediated pericardial effusion from malignant effusion is vital. Development of pericardial effusion with concurrent improvement or stability of malignant lesion, negative cytology and brisk response to corticosteroids indicates an immune etiology.

Pericardiocentesis or pericardial window is the key intervention in acute management. The critical step in immune mediated pericardial effusions is initiation of high-dose corticosteroids (1-2 mg/kg of Prednisone) with tapering of at least 4 weeks in severe cases. In unresponsive cases, corticosteroids at transplant rejection dose (1 g methylprednisone daily) and addition of mycophenolate mofetil, in iximab or antithymocyte globulin should be considered. As per ‘ASCO Practice Guideline’, any grade of cardiotoxicity above grade 1 warrants holding or permanently discontinuing the immunotherapy. For pericardial effusions secondary to pseudoprogression, immunotherapy can be continued.

Based on our literature review, concurrence of other immune related adverse events and recurrence of effusions with discontinuation of corticosteroids is reported with immune mediated pericardial effusions.

Conclusion: Early identification of immune related adverse events is very important. In immune mediated pericardial effusion, pericardial fluid should be drained, and corticosteroids should be started promptly. Permanent discontinuation of immunotherapy is recommended for grade 3 and 4 cardiotoxicity. Re-challenge of immunotherapy after treating the adverse event is a subject that needs further research.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.

Background: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.

Background: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.