Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here a case of esophageal cancer patient who developed tumor lysis syndrome after chemotherapy. A 57- year-old man received esophagectomy for advanced esophageal cancer. CT study revealed multiple lymphnode metastases, multiple bone metastases and multiple lung metastases after 15 months from the operation. So, chemotherapy was performed for the patient. Eleven days following the administration of docetaxel: 30 mg/m2 and nedaplatin: 30 mg/m2, the patient developed TLS (serum creatinine: 8.57 mg/dL, uric acid: 11.0 mg/dL, serum potassium: 6.3 mEq/L, serum phosphorus: 7.18 mg/dL). The patient responded well to an appropriate treatment with a combination of vigorous intravenous hydration, carperitide, allpurinol and potassium citrate sodium citrate. This case report describes the first patient to develop TLS following chemotherapy for esophageal cancer.
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PMID:[A case of esophageal cancer patient who developed tumor lysis syndrome after chemotherapy]. 1910 13

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