Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bcl-2 is one of the many proteins that regulate programmed cell death and is overexpressed in B-cell lymphomas. The expression of bcl-2 in mesenchymal cells and soft tissue tumours was the subject of this study. Normal mesenchymal tissue and representative cases of soft tissue tumours of different types (n>200) were investigated immunohistochemically for bcl-2 expression. Although bcl-2 expression was normally relatively restricted to some smooth muscle cells and neural cells, bcl-2 immunoreactivity was widespread in different types of soft tissue neoplasms, both benign and malignant. Consistently positive tumours included solitary fibrous tumour, haemangiopericytoma, schwannoma and synovial sarcoma. The few soft tissue tumours that were consistently negative for bcl-2 included nodular fasciitis and desmoid tumour. Leiomyomas and leiomyosarcomas were heterogeneous; all uterine leiomyomas were bcl-2 positive, but all oesophageal leiomyomas were negative, paralleling the reactivity observed in the smooth muscle at those sites. Gastrointestinal stromal tumours showed bcl-2 reactivity; this was less consistent in malignant tumours. Along the malignancy gradient, there was no consistent trend in the bcl-2 reactivity. Dermatofibrosarcomas showed increase of bcl-2 expression with fibrosarcomatous transformation, whereas smooth muscle sarcomas and malignant peripheral nerve sheath sarcomas were less consistently positive than the corresponding benign neoplasms. We conclude that bcl-2 expression is widespread in soft tissue tumours, but shows constitutional expression patterns that are often parallel to the normal tissue counterparts. Compared with benign soft tissue tumours, bcl-2 expression is often reduced in sarcomas, but it cannot be used as a prognostic marker without correlation of the data to its phenotypic expression patterns.
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PMID:Cell-type- and tumour-type-related patterns of bcl-2 reactivity in mesenchymal cells and soft tissue tumours. 976 29

Desmoid tumors and fibrosarcomas (FS) are part of a wide spectrum of disordered fibroblastic growth that display striking clinical and phenotypic differences. This study was designed to characterize molecular abnormalities that are associated with these differences and to determine their clinical relevance. A cohort of 24 desmoid tumors and 25 low-grade (LG) and 14 high-grade (HG) FS that were clinically and pathologically well characterized was analyzed for alterations in expression of Ki-67, Bcl-2, retinoblastoma gene product (pRB), and p53 by immunohistochemistry. LG-FS and HG-FS showed abnormal expression of Ki-67 (32 versus 86%), Bcl-2 (48 versus 57%), and pRB (56 versus 93%). In contrast, desmoid tumors showed a normal phenotype with these markers. p53 overexpression was identified in 20% of LG-FS and in 29% of HG-FS cases but only in 4% of desmoid tumors. There was an increasing trend in the proportion of abnormal expression of Ki-67, Bcl-2, pRB, and p53 with the increase of tumor aggressiveness from desmoid tumors to LG-FS to HG-FS. The molecular differences between tumor entities were highly statistically significant (P < 0.01). Significant associations between abnormal expression of pRB and recurrence-free survival of LG-FS patients (P = 0.05) and between Ki-67 overexpression and recurrence-free survival for tumors of >5 cm were observed (P = 0.02). The demonstrated differences of molecular alterations in HG-FS, LG-FS, and desmoids appear to be related to biological aggressiveness of such tumors, and they might be useful to differentiate between histologically similar cases of desmoid tumors and LG-FS. pRB and Ki-67 status may be useful to predict recurrence in certain subsets of patients.
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PMID:Characterization of molecular abnormalities in human fibroblastic neoplasms: a model for genotype-phenotype association in soft tissue tumors. 1130 4

Desmoid tumors are uncommon benign tumors composed of fibrous tissue, which originate from aponeuroses. Little is known about their molecular pathogenesis and the reason that they recur. We report the case of a 20-year-old man with a recurrent desmoid tumor of the chest wall, focusing on our analysis of the apoptosis and its related molecular events. Immunohistochemical examination showed higher expression of antiapoptotic Bcl-2, Bcl-XL, survivin, and the transcription factor, NF-kappaB, in the recurrent tumor than in the adjoining normal tissue. Proapoptotic Bax was not detected in the tumor. Similar findings were obtained in the original primary tumor. Both tumors had a low apoptotic index according to the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay. These changes occurred in the absence of cell proliferation, shown by the absence of both Ki-67 staining and increased telomerase activity. This derangement of apoptosis gives the aggressive desmoid tumor cells a proliferative advantage, and presumably, forms the basis of its high recurrence rate. Therefore, inhibitors of apoptosis proteins (IAPs) may be useful for predicting recurrence. The regulation of apoptosis by antisense therapy against these inhibitors could prove beneficial for overcoming repeated recurrence, even after surgery.
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PMID:Characterization of apoptosis-related molecular changes in a desmoid tumor of the chest wall: report of a case. 1273 31