Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spermatic Cord Liposarcoma are uncommon soft tissue neoplasm. Association with others tumors is so exceptional. We describe and relation between liposarcoma and prostate cancer in a 66 years old patient who had a left paratesticular tumor with low speed growth and 12 cm of length; nodule in prostate gland was detected. Ecography demostrate an hipoecoic tumor in the spermatic cord; Prostate Specific Antigen (PSA) was 1276 ng./ml. and bone gammagraphy reported metastatic lesions. We made an radical orquiectomy and pathological diagnosis including inmunohistoquimical process was sclerosing dedifferenciated liposarcoma. We discuss clinical and pathologic behaviour of this lesions and diagnosis and treatment options.
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PMID:[Spermatic cord liposarcoma. Association with prostate cancer. Report of a case and review of literature]. 1618 Mar 22

Progression of prostate cancer is highly dependent upon the androgen receptor pathway, such that knowledge of androgen-regulated proteins is vital to understand and combat this disease. Using a proteomic screen, we found the RNA-binding protein FUS/TLS (Fused in Ewing's Sarcoma/Translocated in Liposarcoma) to be downregulated in response to androgen. FUS has recently been shown to be recruited by noncoding RNAs to the regulatory regions of target genes such as cyclin D1, in which it represses transcription by disrupting complex formation. Here we show that FUS has some characteristics of a putative tumor suppressor, as its overexpression promoted growth inhibition and apoptosis of prostate cancer cells, whereas its knockdown increased cell proliferation. This effect was reproducible in vivo, such that increasing FUS levels in tumor xenografts led to dramatic tumor regression. Furthermore, FUS promoted conditions that favored cell-cycle arrest by reducing the levels of proliferative factors such as cyclin D1 and Cdk6 and by increasing levels of the antiproliferative Cdk inhibitor p27. Immunohistochemical analysis revealed that FUS expression is inversely correlated with Gleason grade, demonstrating that patients with high levels of FUS survived longer and were less likely to have bone metastases, suggesting that loss of FUS expression may contribute to cancer progression. Taken together, our results address the question of how androgens regulate cell-cycle progression, by demonstrating that FUS is a key link between androgen receptor signaling and cell-cycle progression in prostate cancer.
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PMID:FUS/TLS is a novel mediator of androgen-dependent cell-cycle progression and prostate cancer growth. 2116 11