Noor Humayun, MD

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

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

Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.

Case Presentation

We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.

Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.

The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.

Conclusions

This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.

Background

Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.

Case Presentation

We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.

Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.

The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.

Conclusions

This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.

Background

Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.

Case Presentation

We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.

Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.

The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.

Conclusions

This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.

Background

GATA3 is a zinc finger transcription factor most commonly used as an immunohistochemical marker in breast and urothelial carcinomas, though it has also been detected—albeit infrequently—in other malignancies. While GATA3 expression is well established in esophageal squamous cell carcinoma, it is rarely documented in esophageal adenocarcinoma. We present a unique case of widely metastatic, strongly GATA3-positive esophageal adenocarcinoma.

Case Presentation

A 59-year-old male smoker with gastroesophageal reflux disease and a history of alcohol use disorder presented with progressive right hip pain following a fall. Imaging revealed multiple lytic bone lesions and a soft tissue mass near the right acetabulum. PET-CT demonstrated widespread osseous metastases and FDG-avid uptake in the distal esophagus and perigastric lymph nodes. Laboratory findings included a PSA of 14. Biopsy of the right pubic ramus revealed adenocarcinoma positive for GATA3, CK7, CK20 (patchy), CK40, and P63, and negative for PSA. Given the unexpected GATA3 positivity, the differential diagnosis included primary urothelial cancer. However, cystoscopy and urine cytology were unremarkable. EGD revealed Barrett’s esophagus without a discrete mass. Biopsy of the distal esophagus confirmed poorly differentiated adenocarcinoma with underlying dysplasia. Molecular profiling showed HER2-negative, microsatellite stable (MSS) disease with PD-L1 expression of 10%. Due to an ECOG performance status ≥3 and extensive metastatic burden, the patient was not a candidate for systemic therapy and was transitioned to hospice care.

Discussion

A large tissue microarray study of over 16,000 tumors found weak GATA3 expression in only 2.4% of esophageal adenocarcinomas, with strong or diffuse positivity virtually undocumented. In this case, the unusual immunoprofile initially raised concern for a primary urothelial tumor, but endoscopic biopsy confirmed an esophageal origin. Aberrant GATA3 expression in poorly differentiated gastrointestinal tumors may complicate diagnosis and has been associated with worse prognosis. Awareness of such atypical patterns is critical for accurate tumor classification and appropriate management in metastatic disease.

Conclusions

This case highlights a rare presentation of GATA3-positive esophageal adenocarcinoma. Further reporting may improve diagnostic accuracy and inform future therapeutic strategies for this unique subset of tumors.

Background

GATA3 is a zinc finger transcription factor most commonly used as an immunohistochemical marker in breast and urothelial carcinomas, though it has also been detected—albeit infrequently—in other malignancies. While GATA3 expression is well established in esophageal squamous cell carcinoma, it is rarely documented in esophageal adenocarcinoma. We present a unique case of widely metastatic, strongly GATA3-positive esophageal adenocarcinoma.

Case Presentation

A 59-year-old male smoker with gastroesophageal reflux disease and a history of alcohol use disorder presented with progressive right hip pain following a fall. Imaging revealed multiple lytic bone lesions and a soft tissue mass near the right acetabulum. PET-CT demonstrated widespread osseous metastases and FDG-avid uptake in the distal esophagus and perigastric lymph nodes. Laboratory findings included a PSA of 14. Biopsy of the right pubic ramus revealed adenocarcinoma positive for GATA3, CK7, CK20 (patchy), CK40, and P63, and negative for PSA. Given the unexpected GATA3 positivity, the differential diagnosis included primary urothelial cancer. However, cystoscopy and urine cytology were unremarkable. EGD revealed Barrett’s esophagus without a discrete mass. Biopsy of the distal esophagus confirmed poorly differentiated adenocarcinoma with underlying dysplasia. Molecular profiling showed HER2-negative, microsatellite stable (MSS) disease with PD-L1 expression of 10%. Due to an ECOG performance status ≥3 and extensive metastatic burden, the patient was not a candidate for systemic therapy and was transitioned to hospice care.

Discussion

A large tissue microarray study of over 16,000 tumors found weak GATA3 expression in only 2.4% of esophageal adenocarcinomas, with strong or diffuse positivity virtually undocumented. In this case, the unusual immunoprofile initially raised concern for a primary urothelial tumor, but endoscopic biopsy confirmed an esophageal origin. Aberrant GATA3 expression in poorly differentiated gastrointestinal tumors may complicate diagnosis and has been associated with worse prognosis. Awareness of such atypical patterns is critical for accurate tumor classification and appropriate management in metastatic disease.

Conclusions

This case highlights a rare presentation of GATA3-positive esophageal adenocarcinoma. Further reporting may improve diagnostic accuracy and inform future therapeutic strategies for this unique subset of tumors.

Background

GATA3 is a zinc finger transcription factor most commonly used as an immunohistochemical marker in breast and urothelial carcinomas, though it has also been detected—albeit infrequently—in other malignancies. While GATA3 expression is well established in esophageal squamous cell carcinoma, it is rarely documented in esophageal adenocarcinoma. We present a unique case of widely metastatic, strongly GATA3-positive esophageal adenocarcinoma.

Case Presentation

A 59-year-old male smoker with gastroesophageal reflux disease and a history of alcohol use disorder presented with progressive right hip pain following a fall. Imaging revealed multiple lytic bone lesions and a soft tissue mass near the right acetabulum. PET-CT demonstrated widespread osseous metastases and FDG-avid uptake in the distal esophagus and perigastric lymph nodes. Laboratory findings included a PSA of 14. Biopsy of the right pubic ramus revealed adenocarcinoma positive for GATA3, CK7, CK20 (patchy), CK40, and P63, and negative for PSA. Given the unexpected GATA3 positivity, the differential diagnosis included primary urothelial cancer. However, cystoscopy and urine cytology were unremarkable. EGD revealed Barrett’s esophagus without a discrete mass. Biopsy of the distal esophagus confirmed poorly differentiated adenocarcinoma with underlying dysplasia. Molecular profiling showed HER2-negative, microsatellite stable (MSS) disease with PD-L1 expression of 10%. Due to an ECOG performance status ≥3 and extensive metastatic burden, the patient was not a candidate for systemic therapy and was transitioned to hospice care.

Discussion

A large tissue microarray study of over 16,000 tumors found weak GATA3 expression in only 2.4% of esophageal adenocarcinomas, with strong or diffuse positivity virtually undocumented. In this case, the unusual immunoprofile initially raised concern for a primary urothelial tumor, but endoscopic biopsy confirmed an esophageal origin. Aberrant GATA3 expression in poorly differentiated gastrointestinal tumors may complicate diagnosis and has been associated with worse prognosis. Awareness of such atypical patterns is critical for accurate tumor classification and appropriate management in metastatic disease.

Conclusions

This case highlights a rare presentation of GATA3-positive esophageal adenocarcinoma. Further reporting may improve diagnostic accuracy and inform future therapeutic strategies for this unique subset of tumors.