Seborrheic keratosis is one of the most common benign growths of the skin, arising from keratinocytes within the epidermis. Unlike actinic keratosis, which frequently progresses to squamous cell carcinoma, seborrheic keratosis generally has a low risk of malignancy. The reasons for this low risk are not fully understood, but some studies suggest it may be due to the lack of mutations in tumor suppressor genes. This case report describes a rare instance of squamous cell carcinoma arising from a long-standing seborrheic keratosis located in a sun-protected area. We performed immunohistochemical staining for tumor suppressor proteins p53 and p16, as well as the proliferation marker Ki-67. Based on this case, we speculate that cumulative mutations in tumor suppressor genes might play a role in the progression of seborrheic keratosis to squamous cell carcinoma. Further studies involving a larger sample size and combining immunohistochemical staining with genomic analysis are necessary to elucidate the mechanisms underlying malignant transformation in seborrheic keratosis.

Seborrheic keratosis is one of the most common benign growths of the skin, arising from keratinocytes within the epidermis. Unlike actinic keratosis, which frequently progresses to squamous cell carcinoma, seborrheic keratosis generally has a low risk of malignancy. The reasons for this low risk are not fully understood, but some studies suggest it may be due to the lack of mutations in tumor suppressor genes. This case report describes a rare instance of squamous cell carcinoma arising from a long-standing seborrheic keratosis located in a sun-protected area. We performed immunohistochemical staining for tumor suppressor proteins p53 and p16, as well as the proliferation marker Ki-67. Based on this case, we speculate that cumulative mutations in tumor suppressor genes might play a role in the progression of seborrheic keratosis to squamous cell carcinoma. Further studies involving a larger sample size and combining immunohistochemical staining with genomic analysis are necessary to elucidate the mechanisms underlying malignant transformation in seborrheic keratosis.

Seborrheic keratosis is one of the most common benign growths of the skin, arising from keratinocytes within the epidermis. Unlike actinic keratosis, which frequently progresses to squamous cell carcinoma, seborrheic keratosis generally has a low risk of malignancy. The reasons for this low risk are not fully understood, but some studies suggest it may be due to the lack of mutations in tumor suppressor genes. This case report describes a rare instance of squamous cell carcinoma arising from a long-standing seborrheic keratosis located in a sun-protected area. We performed immunohistochemical staining for tumor suppressor proteins p53 and p16, as well as the proliferation marker Ki-67. Based on this case, we speculate that cumulative mutations in tumor suppressor genes might play a role in the progression of seborrheic keratosis to squamous cell carcinoma. Further studies involving a larger sample size and combining immunohistochemical staining with genomic analysis are necessary to elucidate the mechanisms underlying malignant transformation in seborrheic keratosis.

Seborrheic keratosis is one of the most common benign growths of the skin, arising from keratinocytes within the epidermis. Unlike actinic keratosis, which frequently progresses to squamous cell carcinoma, seborrheic keratosis generally has a low risk of malignancy. The reasons for this low risk are not fully understood, but some studies suggest it may be due to the lack of mutations in tumor suppressor genes. This case report describes a rare instance of squamous cell carcinoma arising from a long-standing seborrheic keratosis located in a sun-protected area. We performed immunohistochemical staining for tumor suppressor proteins p53 and p16, as well as the proliferation marker Ki-67. Based on this case, we speculate that cumulative mutations in tumor suppressor genes might play a role in the progression of seborrheic keratosis to squamous cell carcinoma. Further studies involving a larger sample size and combining immunohistochemical staining with genomic analysis are necessary to elucidate the mechanisms underlying malignant transformation in seborrheic keratosis.

BACKGROUND: Yes-associated protein (YAP) in the Hippo signaling pathway is a growth control pathway that regulates cell proliferation and stem cell functions. Abnormal regulation of YAP was reported in human cancers including liver, lung, breast, skin, colon, and ovarian cancer. However, the function of YAP is not known in prostate adenocarcinoma. The purpose of this study was to investigate the role of YAP in tumorigenesis, differentiation, and prognosis of prostate adenocarcinoma. METHODS: The nuclear and cytoplasmic expression of YAP was examined in 188 cases of prostate adenocarcinoma using immunohistochemistry. YAP expression levels were evaluated in the nucleus and cytoplasm of the prostate adenocarcinoma and the adjacent normal prostate tissue. The presence of immunopositive tumor cells was evaluated and interpreted in comparison with the patients’ clinicopathologic data. RESULTS: YAP expression levels were not significantly different between normal epithelial cells and prostate adenocarcinoma. However, YAP expression level was significantly higher in carcinomas with a high Gleason grades (8–10) than in carcinomas with a low Gleason grades (6–7) (p < .01). There was no statistical correlation between YAP expression and stage, age, prostate-specific antigen level, and tumor volume. Biochemical recurrence (BCR)–free survival was significantly lower in patients with high YAP expressing cancers (p = .02). However high YAP expression was not an independent prognostic factor for BCR in the Cox proportional hazards model. CONCLUSIONS: The results suggested that YAP is not associated with prostate adenocarcinoma development, but it may be associated with the differentiation of the adenocarcinoma. YAP was not associated with BCR.
Adenocarcinoma* ; Breast ; Carcinogenesis ; Cell Proliferation ; Colon ; Cytoplasm ; Epithelial Cells ; Humans ; Immunohistochemistry ; Liver ; Lung ; Ovarian Neoplasms ; Prognosis ; Proportional Hazards Models ; Prostate* ; Prostate-Specific Antigen ; Recurrence ; Skin ; Stem Cells ; Tumor Burden

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been associated with the overproduction of serum amyloid A protein, resulting in systemic AA amyloidosis. In this report, we describe a case of gastrointestinal (GI) AA amyloidosis following SARS-CoV-2 infection. A 75-year-old male presented to the emergency department with upper abdominal pain 6 weeks post kidney transplantation. He had a history of SARS-CoV-2 infection 4 weeks prior. On day 7 of hospitalization, while receiving conservative management, the patient developed symptoms of cough and fever, leading to a diagnosis of SARS-CoV-2 reinfection. The patient’s abdominal pain persisted, and hematochezia developed on day 30 of hospitalization. Esophagogastroduodenoscopy and colonoscopy revealed multiple ulcers in the stomach and colon, with histologic findings revealing the presence of amyloid A. The patient was managed conservatively and was also given remdesivir for the SARS-CoV-2 infection. His clinical symptoms subsequently improved, and endoscopic findings demonstrated improvement in multiple gastric ulcers. GI amyloidosis may be a subacute complication following SARS-CoV-2 infection in immunocompromised patients.

Neuroendocrine carcinoma (NEC) arising from the extrahepatic bile duct is extremely rare and commonly mistaken for cholangiocarcinoma. Therefore, NEC of the bile duct is difficult to diagnose preoperatively. Previously reported cases were resected with a diagnosis of cholangiocarcinoma and diagnosed with NEC after surgery. This paper reports an 84-year-old female with small-cell NEC of the extrahepatic bile duct, confirmed by a biopsy from an ERCP, with a review of the relevant literature. Contrast-enhanced abdomen computed tomography and magnetic resonance cholangiopancreatography revealed an approximately 1.7 cm enhancing intraductal mass in the proximal common bile duct with dilatation of the upstream bile duct. ERCP showed a long strictured segment in the proximal common bile duct with bile duct dilatation. A biopsy was performed at the site of the stricture. Histological examinations and hematoxylin–eosin staining showed the solid proliferation of small tumor cells with irregularly shaped hyperchromatic nuclei.Immunohistochemical examinations showed that the tumor cells were positive for CD56 and synaptophysin. Small-cell NEC of the extrahepatic bile duct was confirmed based on the histology and immunohistochemistry findings. The patient and their family denied treatment because of the patient’s old age.

BACKGROUND: Stroke involving the cerebral white matter (WM) has increased in prevalence, but most experimental studies have focused on ischemic injury of the gray matter. This study was performed to investigate the WM in a unique rat model of photothrombotic infarct targeting the posterior limb of internal capsule (PLIC), focusing on the identification of the most vulnerable structure in WM by ischemic injury, subsequent glial reaction to the injury, and the fundamental histopathologic feature causing different neurologic outcomes. METHODS: Light microscopy with immunohistochemical stains and electron microscopic examinations of the lesion were performed between 3 hours and 21 days post-ischemic injury. RESULTS: Initial pathological change develops in myelinated axon, concomitantly with reactive change of astrocytes. The first pathology to present is nodular loosening to separate the myelin sheath with axonal wrinkling. Subsequent pathologies include rupture of the myelin sheath with extrusion of axonal organelles, progressive necrosis, oligodendrocyte degeneration and death, and reactive gliosis. Increase of glial fibrillary acidic protein (GFAP) immunoreactivity is an early event in the ischemic lesion. WM pathologies result in motor dysfunction. Motor function recovery after the infarct was correlated to the extent of PLIC injury proper rather than the infarct volume. CONCLUSIONS: Pathologic changes indicate that the cerebral WM, independent of cortical neurons, is highly vulnerable to the effects of focal ischemia, among which myelin sheath is first damaged. Early increase of GFAP immunoreactivity indicates that astrocyte response initially begins with myelinated axonal injury, and supports the biologic role related to WM injury or plasticity. The reaction of astrocytes in the experimental model might be important for the study of pathogenesis and treatment of the WM stroke.
Astrocytes ; Axons ; Coloring Agents ; Extremities ; Glial Fibrillary Acidic Protein ; Gliosis ; Gray Matter ; Internal Capsule* ; Ischemia ; Microscopy ; Models, Animal ; Models, Theoretical ; Myelin Sheath ; Necrosis ; Neurons ; Oligodendroglia ; Organelles ; Pathology ; Plastics ; Prevalence ; Recovery of Function ; Rupture ; Stroke ; White Matter