Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical course of 77 surgical cases of cancer of the large bowel was evaluated versus levels of estrogen, androgen, progesterone and glucocorticoid hormone receptors. Within the follow-up period (range 6-41 months), 7 (9%) patients died of tumor progression, 16 (21%) developed recurrence or metastases, while the rest 54 (70%) cases continued in remission. Patients with steroid hormone receptor-positive tumors revealed more favorable clinical course as well as longer disease-free and overall survival than cases of receptor-negative cancer. Estrogen receptor status was found to be of the highest prognostic value in terms of clinical course and survival, as compared to all other hormone receptors studied.
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PMID:[Prognostic value of the level of steroid hormone receptors in cancer of the large intestine]. 366 Jul 56

The retinoid N-(hydroxyphenyl) retinamide (4-HPR) appears to be a promising tool for chemoprevention of breast carcinoma, and clinical trials to evaluate its effect are in progress. However, its action on tumor cells has remained largely undefined. We report here that 4-HPR induced apoptosis and/or differentiation in breast cancer cell lines, independent of hormone receptor status and retinoic acid receptor expression, although it was slightly more efficient in inhibiting proliferation of estrogen receptor-positive cells. 4-HPR up-modulated expression of several differentiation markers (class 1 HLA, laminin, and beta 1 integrin chain) and down-regulated expression of molecules associated with tumor progression, including the p185/HER2 oncoprotein, the epidermal growth factor receptor, and the M(r) 67,000 laminin receptor. These data suggest that 4-HPR could exert a beneficial effect by inhibiting cell proliferation and modulating breast tumor aggressiveness.
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PMID:Modulation of markers associated with tumor aggressiveness in human breast cancer cell lines by N-(4-hydroxyphenyl) retinamide. 754 8

A total of 409 postmenopausal patients with advanced metastatic breast cancer were randomized to receive either formestane (Lentaron) 250 mg every 2 weeks by intramuscular injection, or tamoxifen 30 mg/day orally. Treatment continued until tumor progression. The groups were well matched for pretreatment characteristics including age, performance status, hormone receptor status (patients with known negative receptor status of their primary tumor were excluded), site and extent of metastases, disease-free interval, and previous primary and adjuvant therapy. Patients were assessed for antitumor efficacy at 3-monthly intervals using UICC criteria. Of the 348 patients evaluable for response, 33% had an objective response to formestane (14 complete and 43 partial responses), while 37% had an objective response to tamoxifen (10 complete and 54 partial responses). Median duration of response was 15 months for formestane and 20 months for tamoxifen; survival was 35 and 38 months respectively. There were no statistically significant differences between the treatments for all these variables, but time to disease progression and time to treatment failure significantly favoured tamoxifen. Systemic tolerability was excellent for both treatments. Local side effects due to intramuscular injection of formestane were mild and transient. In this comparative trial of first-line therapy for advanced breast cancer, formestane gave results comparable to tamoxifen for both efficacy and tolerability. We conclude that formestane is an effective and well tolerated addition to the therapeutic options available for the treatment of postmenopausal women with advanced breast cancer.
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PMID:Comparison of the selective aromatase inhibitor formestane with tamoxifen as first-line hormonal therapy in postmenopausal women with advanced breast cancer. 787 57

The whey acid protein (WAP) is a major mouse milk protein and its gene expression is induced by various lactotrophic hormones (eg, estrogen, progesterone). Transgenic animals harboring the early SV40 coding region (T/t-antigen) under the transcriptional control of the WAP promoter develop breast cancer after the first lactation period. The tumor cells synthesize the SV40 T-antigen with a high efficiency indicating that WAP-SV-T expression escapes down-regulation after the lactation period. However about 5-10% of the tumors became T-antigen negative during tumor progression and WAP-SV-T expression was only demonstrable by PCR analysis. Both T-antigen positive and negative tumor cells expressed the estrogen and progesterone receptor at a comparable rate, indicating that hormone receptor levels do not determine expression of the WAP-SV-T transgene. Furthermore, WAP and WAP-SV-T gene expression are not restricted to the pregnancy-lactation period. Virgin animals also express both genes with a low efficiency and about 70% of these animals also developed T-antigen positive breast tumors. The tumor rate however was strongly reduced in ovariectomized animals, indicating that the ovary hormones play a critical role in breast cancer formation.
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PMID:SV40 T-antigen induces breast cancer formation with a high efficiency in lactating and virgin WAP-SV-T transgenic animals but with a low efficiency in ovariectomized animals. 863 5

Breast cancer is the second leading cause of cancer death in North American women. There is considerable need for reliable prognostic markers to assist clinicians in making management decisions. Although a variety of factors have been tested, only tumor stage, grade, size, hormone receptor status, and S-phase fraction are used on a routine basis. The cell cycle is governed by a family of cyclin-dependent kinases (cdks), which are regulated by associated cyclins and by phosphorylation. p27Kip1, a cyclin-dependent kinase inhibitor, regulates progression from G1 into S phase by binding and inhibiting cyclin/cdks. p27Kip1 protein levels and/or activity are upregulated by growth inhibitory cytokines including transforming growth factor-beta (TGF-beta) and, thus, provide an important link between extracellular regulators and the cell cycle. Loss of p27Kip1, a negative cell-cycle regulator, may contribute to oncogenesis and tumor progression. However, p27Kip1 mutations in human tumors are extremely rare. We have demonstrated by immunohistochemistry that p27Kip1 protein levels are reduced in primary breast cancers and that this is associated with tumor progression in both in situ and invasive lesions. This was confirmed by western analysis, reflected in increased G1/S-phase cyclin-dependent kinase activities and shown to be regulated posttranscriptionally by in situ hybridization. Furthermore, on multivariate analysis, low p27Kip1 is a predictor of reduced disease-free survival. This simple and reliable immunohistochemical assay may become a routine part of breast cancer evaluation and may influence patient management.
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PMID:Decreased levels of the cell-cycle inhibitor p27Kip1 protein: prognostic implications in primary breast cancer. 901 30

The global DNA methylation status was investigated on a series of 59 breast cancers by Southern blotting, using methylation sensitive restriction enzymes. By comparison to control DNA, almost all tumor DNAs were found globally hypomethylated. However, the demethylation was variable from tumor to tumor. Compared to other biological parameters, the methylation did not correlate with chromosome alterations, steroid hormone receptor status, or histopathological grading. Tumors which appeared to be the most evolved for other parameters were only mildly hypomethylated, whereas tumors with strongly hypomethylated DNA corresponded to those with slight alterations of the other parameters. Thus, DNA hypomethylation is a consistent characteristic of breast cancer, but its variations may not correlate with tumor progression of most breast cancers.
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PMID:DNA hypomethylation in breast cancer: an independent parameter of tumor progression? 928 86

Several studies have suggested that endothelial cells participate in tumor development. Soluble E-selectin (sE-selectin) is specifically released by activated endothelial cells, and its serum concentration can be considered a marker of endothelial activation. In this study, we assessed the prognostic value of sE-selectin concentrations in node-negative breast cancer patients. Serum sE-selectin concentrations were measured by an ELISA method prior to surgery in 456 node-negative breast cancer patients. We analyzed also tumor size (TS), histoprognostic grading, and steroid hormone receptor status. The mean sE-selectin concentration was 24.9 +/- 15.0 ng/ml. The sE-selectin concentrations were mildly correlated with the TS but not with the other factors. For prognostic analyses, the median follow-up duration was 7.5 years. The cutoff sE-selectin concentration used was 40 ng/ml. In overall survival studies, univariate analyses demonstrated a prognostic value of sE-selectin, TS, and histoprognostic grading, and multivariate analyses demonstrated a prognostic value of sE-selectin and TS. For disease-free survival, univariate and multivariate analyses demonstrated a prognostic value of sE-selectin and TS. sE-selectin concentration is an easily measurable and strong prognostic factor in node-negative breast cancer patients. These results provide further evidence for the role of adhesion molecules expression by endothelial cells in tumor progression.
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PMID:Prognostic value of circulating soluble E-selectin concentrations in node-negative breast cancer patients. 1038 28

CD44 is an adhesion molecule involved in many biological functions and has been described to play a role in tumor progression as well as in promotion of metastasis. It has also been suggested that expression of certain CD44 isoforms could be useful for breast and ovarian cancer screening, detection or staging. However, many other reports document no correlation between CD44 isoform expression and tumor malignancy. In light of such contradictory findings, we evaluated by exon-specific RT-PCR whether the expression of CD44 isoforms in breast and ovarian tumors correlated with any of the diagnostic criteria used to assess these diseases. We found a deregulation in the CD44 expression pattern in malignant tumors of both type of cancer compared with the one in benign tumors or normal tissue. However, we could not find a clear correlation between this deregulation or a given CD44 isoform and any diagnostic criteria evaluated, such as age, clinical data, tumor size, hormone receptor status, histological grade or aggressiveness.
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PMID:Splice variant expression of CD44 in patients with breast and ovarian cancer. 1111 87

To date, poor standardization in HER2 status evaluation has precluded reliable comparison of overexpression rates in different tumors. However, standardized methodologies have been introduced recently for these analyses, and have identified frequencies of 51%, 44%, 26% and 25% in Wilm's tumor, bladder, pancreatic and breast carcinoma, respectively. Other tumors tested had frequencies below 20%. The frequency was greater than that predicted by gene amplification data in some tumor types, which may indicate overexpression due to gene deregulation, rather than gene amplification. Analysis of a large retrospective series of breast carcinomas demonstrated an association between HER2 positivity and a number of other prognostic markers. Together, these variables identify a subset of tumors with poor prognosis and early relapse post-surgery. HER2 expression is relatively stable, with 95% concordance between the HER2 status of primary and metastatic lesions. However, contralateral tumors are unrestricted with regard to HER2 status. Preliminary data indicate that the HER2 status of a hormone receptor-positive tumor may fluctuate according to the menstrual cycle. It is anticipated that the emerging wealth of standardized data for HER2 status will help to elucidate the role of HER2 in tumor progression.
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PMID:HER2 overexpression in various tumor types, focussing on its relationship to the development of invasive breast cancer. 1152 15

Kallikreins are a subgroup of serine proteases with diverse physiological functions. The human kallikrein gene family has now been fully characterized and includes 15 members tandemly located on chromosome 19q13.4. Strong experimental evidence supports a link between kallikreins and endocrine malignancies and especially, ovarian cancer. Three new kallikreins have been shown to be potential diagnostic and prognostic markers for ovarian cancer. Many other kallikreins are also differentially expressed in ovarian cancer, and preliminary reports underline their possible prognostic value. The mechanism by which kallikreins could be involved in ovarian cancer pathology is not known. A likely link could be their regulation through the steroid hormone receptor pathway. Most kallikreins are under sex steroid hormonal regulation in cancer cell lines. Given the co-expression of many kallikreins in ovarian cancer, it is reasonable to postulate that kallikreins are involved in a cascade enzymatic pathway that plays a role in cancer progression. A multiparametric kallikrein expression profile may be a useful tool for ovarian cancer diagnosis/prognosis when used either alone or in conjunction with existing markers.
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PMID:Kallikreins, steroid hormones and ovarian cancer: is there a link? 1209 91


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