Hepatosplenic gammadelta T-cell lymphoma.

AIM: To investigate the clinicopathologic characteristics, immunophenotype and TCR gene rearrangements of hepatosplenic T-cell lymphoma in eight Chinese patients. METHODS: Eight Chinese patients with hepatosplenic gammadelta T-cell lymphomas were studied. Hematoxylin-eosin-stained slides and clinical histories were reviewed. We also carried out immunohistochemical staining for CD3, CD4, CD8, CD20, CD43, CD56, CD79a, UCHL-1, and TCR gammadelta. Rearrangements of TCR gamma and delta chain genes were also studied. RESULTS: The spleens were enlarged and the cut surfaces were homogeneous and red-purple in color without identifiable gross lesions or enlarged hilar lymph nodes. Histologically, lymphoma cells infiltrated the cords of Billroth and often packed the sinuses. Liver biopsy showed lymphoma cell infiltrations in the sinusoids, and three cases showed involvements of the portal tracts. Immunohistochemically lymphoma cells were positive for CD3, CD43, and CD56 in all cases. Four of eight cases were positive for CD8, and all cases were negative for CD4 (6/6). Monoclonal rearrangements of TCR gamma gene were demonstrated by PCR analysis in five out of the eight cases. TCR delta gene rearrangements were detected in six out of the eight cases, which demonstrated single bands on PAGE gel, and the amplification products in two cases were confirmed by sequencing. CONCLUSION: The clinicopathology of hepatosplenic gammadelta T-cell lymphoma in Chinese patients is similar to what was previously reported except that the splenomegaly is not so massive, and CD8 is positive.

[Expression of survivin gene in pancreatic carcinoma].

OBJECTIVE: To determine the expression status of survivin gene in pancreatic carcinoma. METHODS: Expression of survivin gene was evaluated by immunohistochemistry, Western Blot and RT-PCR in 59 cases of pancreatic carcinoma along with their corresponding adjacent benign tissues, 11 cases of chronic pancreatitis, and 7 pancreatic carcinoma cell lines. RESULTS: The positive expression rate of survivin in pancreatic carcinoma was 72.8% (43/59). There was no relationship between the expression of survivin and tumor stage and differentiation. No expression of survivin was detected in benign tissue adjacent to the tumors as well as in samples of chronic pancreatitis. All 7 pancreatic carcinoma cell lines showed a positive expression of survivin mRNA and protein. CONCLUSIONS: The expression of survivin appears to be tumor specific to some extent in our pancreatic carcinoma samples. Survivin may be an ideal target for therapy against pancreatic carcinoma.

[Distinction between benign and malignant pheochromocytomas].

OBJECTIVES: To investigate the differences in morphology, immunohistochemistry, DNA ploidy status, LOH and MSI of 11q13 and 1p between benign and malignant pheochromocytomas, and to find the marker or markers useful in distinction between benign and malignant pheochromocytoma or for predicting the malignant potential of this tumor. METHODS: Twenty-two cases of clinically documented benign and malignant pheochromocytomas from the files of Peking Union Medical College Hospital were analyzed. Aside from histological study, Ki-67, p53, CgA, S-100, PCNA and survivin immunohistochemistry studies were performed. DNA ploidy status was assessed by flow cytometry on cell suspensions prepared from formalin-fixed, paraffin-embedded sections. Twelve tumors (7 benign and 5 malignant) with paired normal tissues were microdissected. Tumor and normal tissue DNA were extracted. The obtained DNAs and 8 microsatellite markers related to 11q13 and 1q were subjected to PCR amplification for analysis of LOH and MSI. RESULTS: None of the tumors showed atypical mitosis, only 1 malignant tumor had a mitotic count > 1/10 HPF (2.3/10 HPF). Two malignant tumors exhibited confluent necrosis. Ki-67 index was low in benign tumors (average 0.73%), and high in malignant tumors (average 2.4%). The difference of Ki-67 index between benign and malignant tumors was statistically significant. DNA ploidy status did not correlate with malignancy. Although LOH and/or MSI of 11q13 and 1p were observed in several tumors, a statistically significant difference could not be reached due to the small number of tumors analyzed. CONCLUSION: Only Ki-67 index (> 3%) is an useful marker for distinguishing benign from malignant or for predicting the malignant potential of pheochromocytoma.

[Thyrotropin-secreting pituitary adenoma:a clinicopathological analysis of seven cases].

OBJECTIVE: To study the clinicopathological features of thyrotropin-secreting pituitary adenoma (TSH adenoma). METHODS: Clinical and pathological features of 7 TSH adenoma cases were studied by review of patients' medical records, light and electronic microscopy, and immunohistochemistry. RESULTS: All seven patients presented with clinical hyperthyroidism and high levels of plasma free T3, free T4, total T3 and total T4. The levels of TSH failed to be suppressed by thyroxin administration. MRI showed macro or giant pituitary adenomas in all seven patients with tumor diameters ranging from 2.0 to 5.0 cm. Under light microscope, there were 5 cases of chromophobe cell adenoma, 1 case of acidophil cell adenoma, and 1 case of mixed acidophil and chromophobe cell adenoma. Immunohistochemical stains showed a strong positivity of TSH in all the tumors, PRL positive cells in 1 tumor, GH positive cells in 2 tumors and scattered GH and PRL double positive cells in 3 tumors. Ki-67 proliferation index ranged from 0 approximately 0.4%. P53 immunostain was negative in all tumors. After initial surgery, 2 cases had recurrences. However, the Ki-67 proliferation index was not elevated in these two tumors. CONCLUSIONS: The histological features of TSH pituitary adenomas are heterogeneous with chromophobe as the most common subtype. Secretion of TSH was detected by immunohistochemistry in all cases. P53 mutation is not a feature of TSH adenoma and the proliferation marker, such as Ki-67, may not predict clinical behavior of the tumor. Recurrence is likely due to incomplete resection.