Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The measurement of tumor markers is currently one of the most rapidly growing areas in laboratory medicine. Lack of sensitivity and specificity preclude the use of most existing markers for the early detection of malignancy. For patients with diagnosed malignancy, however, markers are potentially useful in determining prognosis, predicting therapeutic response, maintaining surveillance following curative surgery and monitoring therapy in advanced disease. Clinically useful markers include CEA in the surveillance of patients with diagnosed colorectal cancer, AFP and HCG in the management of patients with non-seminomatous germ cell tumors, HCG in the management of patients with trophoblastic disease, CA 125 for monitoring therapy in patients with ovarian cancer, estrogen receptors for predicting response to hormone therapy in breast cancer and HER-2 for the identification of women with breast cancer likely to respond to trastuzumab (Herceptin). Although widely used, the impact of PSA screening in reducing mortality from prostate cancer remains to be shown.
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PMID:Role of tumor markers in patients with solid cancers: A critical review. 1744 88

Androgen ablation therapy is the most common strategy for suppressing prostate cancer progression; however, tumor cells eventually escape androgen dependence and progress to an androgen-independent phase. The androgen receptor (AR) plays a pivotal role in this transition. To address this transition mystery in prostate cancer, we established an androgen-independent prostate cancer cell line (LNCaPdcc), by long-term screening of LNCaP cells in androgen-deprived conditions, to investigate changes of molecular mechanisms before and after androgen withdrawal. We found that LNCaPdcc cells displayed a neuroendocrine morphology, less aggressive growth, and lower expression levels of cell cycle-related factors, although the cell cycle distribution was similar to parental LNCaP cells. Notably, higher protein expression of AR, phospho-Ser(81)-AR, and PSA in LNCaPdcc cells were observed. The nuclear distribution and protein stability of AR increased in LNCaPdcc cells. In addition, cell proliferation results exhibited the biphasic nature of the androgen (R1881) effect in two cell lines. On the other hand, LNCaPdcc cells expressed higher levels of Her2, phospho-Tyr(1221/1222)-Her2, ErbB3, and ErbB4 proteins than parental LNCaP cells. These two cell lines exhibited distinct responses to Her2 activation (by heregulin treatment) on Her2 phosphorylation and Her2 inhibition (by AG825 or Herceptin treatments) on proliferation. In addition, the Her2 inhibitor more effectively caused AR degradation and diminished AR Ser(81) phosphorylation in LNCaPdcc cells. Taken together, our data demonstrate that Her2 plays an important role in the support of AR protein stability in the transition of androgen requirement in prostate cancer cells. We hope these findings will provide novel insight into the treatment of hormone-refractory prostate cancer.
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PMID:The significance of Her2 on androgen receptor protein stability in the transition of androgen requirement in prostate cancer cells. 2136 23