Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High levels of HER2 expression identify those patients who might benefit from treatments that target HER2. Among women with metastatic breast cancer, the predictive markers may be different from the primary tumor. We compared predictive markers: Estrogen Receptor (ER), Progesterone Receptor (PR) and HER2 of primary breast carcinomas with those of lymph node (LN) and blood spread metastases (BM). ER, PR and HER2 status were compared between the primary breast tumor and the LN metastasis and blood spread metastasis. ER, PR and HER2 were performed on primary tumor core biopsies and available FNA cell blocks and on metastatic lesions using FDA approved antibodies and HercepTest (Dako). ER and PR were positive when >/=10%. Her2 was positive (amplified/expressed) when 3+ >30% by immunostain or >2.2 by FISH. Sixty four metastatic breast cancer patients were included in this analysis. Forty-eight patients had LN metastases (35 [73 %] diagnosed by FNA) and twenty seven patients had BM (16 [60 %] diagnosed by FNA). P value was determined comparing primary breast with BM and LN for ER, PR and HER2. ER p values when compared for primary breast with BM and LN were 0.45 and 0.57 respectively, and for PR were 0.31 and 0.06 and for HER2 were 0.45 and 0.07. All three predictive markers are similar in the primary and two metastatic sites (lymph node, bloodspread). Only in primary versus lymph node metastases is there a tendency for PR and HER2 (P values 0.06, 0.07) to be different. For HER2, the majority of lymph node metastases are in cell blocks (FNA), fixed in ethanol rather than formalin, which may have caused false positive HER2 expression.
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PMID:Predictive markers in primary breast cancer compared with lymph node and bloodspread metastases. 2138 78

Brain metastases are uncommon localizations in epithelial ovarian cancer (EOC), their reported incidence is increasing and no predictive biomarkers have been identified yet. Goals of this study were: i) to define a possible association between Estrogen Receptor (ER), Progesterone Receptor (PR), Androgen Receptor (AR),human EGF receptor 2 (HER2) and brain progression in EOC patients, and ii) to identify differences in ER, PR, AR and HER2 protein expression from primary EOC and its matched resected brain metastasis. A retrospective series of 11 EOC with matched brain metastasis surgically removed was collected. For comparison, a "Control dataset" of 22 patients, without evidence of brain involvement after an adequate follow up was matched. ER, PR, AR and HER2 status were analyzed by means of immunohistochemistry forCases (both primary and metastatic lesions) and Controls.Univariate analysis showed that AR status was significantly associated with brain localization, both considered as discrete variable (cut-off: 10%, p=0.013) and as continuous one (p=0.035). Multivariate analysis confirmed this trend (p=0.053). When considered as continuous variables, ER and AR showed greater expression in primary tumors in comparison with brain metastases (p=0.013 and p=0.032, respectively).In our series, AR predicts brain involvement, with a 9.5 times higher propensity for AR-negative EOC. Moreover, brain dissemination is probably the result of progressive dedifferentiation of primary tumor, shown by reduction of ER and AR expression in metastases. Further studies are required, in order to anticipate and improve multimodal treatment of brain metastases.
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PMID:Androgen receptor status predicts development of brain metastases in ovarian cancers. 2846 4

Previously, a consolidated mathematical model of primary tumor (PT) growth and secondary distant metastasis (sdMTS) growth in breast cancer (BC) (CoMPaS) was presented. The aim was to detect the diagnostic periods for visible sdMTS via CoMPaS in patients with different subtypes ER/PR/HER2/Ki-67 (Estrogen Receptor/Progesterone Receptor/Human Epidermal growth factor Receptor 2/Ki-67 marker) of breast cancer. CoMPaS is based on an exponential growth model and complementing formulas, and the model corresponds to the tumor-node-metastasis (TNM) staging system and BC subtypes (ER/PR/HER2/Ki-67). The CoMPaS model reflects (1) the subtypes of BC, such as ER/PR/HER2/Ki-67, and (2) the growth processes of the PT and sdMTSs in BC patients without or with lymph node metastases (MTSs) in accordance with the eighth edition American Joint Committee on Cancer prognostic staging system for breast cancer. CoMPaS correctly describes the growth of the PT in the ER/PR/HER2/Ki-67 subtypes of BC patients and helps to calculate the different diagnostic periods, depending on the tumor volume doubling time of sdMTS, when sdMTSs might appear. CoMPaS and the corresponding software tool can help (1) to start the early treatment of small sdMTSs in BC patients with different tumor subtypes (ER/PR/HER2/Ki-67), and (2) to consider the patient almost healthy if sdMTSs do not appear during the different diagnostic periods.
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PMID:A Mathematical Model to Predict Diagnostic Periods for Secondary Distant Metastases in Patients with ER/PR/HER2/Ki-67 Subtypes of Breast Cancer. 3282 78


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