Tehreem Qamar Nawaz Warrich, MBBS

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Kidney and renal pelvis cancers (KC) represent 4% of new cancer cases in the US. Although it is a common cancer, there is no data to compare the effect of laterality on survival in veteran population. In this abstract, we attempt to bridge this gap and compare the effect of laterality on survival.

Methods

We obtained data from Albany VA (VAMC) for patients diagnosed with KC between 2010-2020. Data were analyzed for age, stage at diagnosis, histopathological type, laterality of tumor, and 6,12 and 60-months survival after the diagnosis and performed a comparison of overall survival of left versus rightsided cancer by calculating odds ratio using logistic regression, significance level was established at p< 0.05.

Results

We reviewed 130 patients diagnosed with KC at VAMC. 62 had right-sided, 62 had left-sided, and 6 had bilateral cancer. Clear cell (40.8%) was predominant type. Other less common histopathological types include Papillary RCC, mixed, papillary urothelial and transitional types. 58 patients had stage 1 (28 right versus 30 left), 8 had stage 2 (5 versus 3), 29 had stage 3 (13 versus 16), 16 with stage 4 (12 versus 4), and 14 had stage 0 (papillary-urothelial). 59.2% patients underwent surgical treatment after diagnosis (R=35, L=39). At 6-months, 60 patients (96.8%) with left-sided and 53 (85.5%) with right-sided cancer survived. The odds of surviving 6-months were 12% higher (95% CI: 1.014, 1.236; p=0.03) in left versus right-sided cancer. For 1-year survival, the results were similar. 111 patients completed a 5-year follow-up and there was no evidence to support a difference in survival between cohorts at 5-years: OR (95% CI: 0.88, 1.47; p=0.32).

Conclusions

In this study, we discovered that leftsided cancer showed better survival at 6-months and 1-year compared to right-sided cancer, but 5-year survival rates appeared similar irrespective of laterality of cancer. Both subgroups had similar distribution for baseline characteristics with majority of patients being males, older than 60 years, with stage 1 disease. Further studies in larger populations with wider distribution of baseline characteristics are needed to establish clear role of laterality as a prognostic factor.

Background

Kidney and renal pelvis cancers (KC) represent 4% of new cancer cases in the US. Although it is a common cancer, there is no data to compare the effect of laterality on survival in veteran population. In this abstract, we attempt to bridge this gap and compare the effect of laterality on survival.

Methods

We obtained data from Albany VA (VAMC) for patients diagnosed with KC between 2010-2020. Data were analyzed for age, stage at diagnosis, histopathological type, laterality of tumor, and 6,12 and 60-months survival after the diagnosis and performed a comparison of overall survival of left versus rightsided cancer by calculating odds ratio using logistic regression, significance level was established at p< 0.05.

Results

We reviewed 130 patients diagnosed with KC at VAMC. 62 had right-sided, 62 had left-sided, and 6 had bilateral cancer. Clear cell (40.8%) was predominant type. Other less common histopathological types include Papillary RCC, mixed, papillary urothelial and transitional types. 58 patients had stage 1 (28 right versus 30 left), 8 had stage 2 (5 versus 3), 29 had stage 3 (13 versus 16), 16 with stage 4 (12 versus 4), and 14 had stage 0 (papillary-urothelial). 59.2% patients underwent surgical treatment after diagnosis (R=35, L=39). At 6-months, 60 patients (96.8%) with left-sided and 53 (85.5%) with right-sided cancer survived. The odds of surviving 6-months were 12% higher (95% CI: 1.014, 1.236; p=0.03) in left versus right-sided cancer. For 1-year survival, the results were similar. 111 patients completed a 5-year follow-up and there was no evidence to support a difference in survival between cohorts at 5-years: OR (95% CI: 0.88, 1.47; p=0.32).

Conclusions

In this study, we discovered that leftsided cancer showed better survival at 6-months and 1-year compared to right-sided cancer, but 5-year survival rates appeared similar irrespective of laterality of cancer. Both subgroups had similar distribution for baseline characteristics with majority of patients being males, older than 60 years, with stage 1 disease. Further studies in larger populations with wider distribution of baseline characteristics are needed to establish clear role of laterality as a prognostic factor.

Background

Kidney and renal pelvis cancers (KC) represent 4% of new cancer cases in the US. Although it is a common cancer, there is no data to compare the effect of laterality on survival in veteran population. In this abstract, we attempt to bridge this gap and compare the effect of laterality on survival.

Methods

We obtained data from Albany VA (VAMC) for patients diagnosed with KC between 2010-2020. Data were analyzed for age, stage at diagnosis, histopathological type, laterality of tumor, and 6,12 and 60-months survival after the diagnosis and performed a comparison of overall survival of left versus rightsided cancer by calculating odds ratio using logistic regression, significance level was established at p< 0.05.

Results

We reviewed 130 patients diagnosed with KC at VAMC. 62 had right-sided, 62 had left-sided, and 6 had bilateral cancer. Clear cell (40.8%) was predominant type. Other less common histopathological types include Papillary RCC, mixed, papillary urothelial and transitional types. 58 patients had stage 1 (28 right versus 30 left), 8 had stage 2 (5 versus 3), 29 had stage 3 (13 versus 16), 16 with stage 4 (12 versus 4), and 14 had stage 0 (papillary-urothelial). 59.2% patients underwent surgical treatment after diagnosis (R=35, L=39). At 6-months, 60 patients (96.8%) with left-sided and 53 (85.5%) with right-sided cancer survived. The odds of surviving 6-months were 12% higher (95% CI: 1.014, 1.236; p=0.03) in left versus right-sided cancer. For 1-year survival, the results were similar. 111 patients completed a 5-year follow-up and there was no evidence to support a difference in survival between cohorts at 5-years: OR (95% CI: 0.88, 1.47; p=0.32).

Conclusions

In this study, we discovered that leftsided cancer showed better survival at 6-months and 1-year compared to right-sided cancer, but 5-year survival rates appeared similar irrespective of laterality of cancer. Both subgroups had similar distribution for baseline characteristics with majority of patients being males, older than 60 years, with stage 1 disease. Further studies in larger populations with wider distribution of baseline characteristics are needed to establish clear role of laterality as a prognostic factor.