Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Green tea is an aqueous infusion of dried unfermented leaves of Camellia sinensis (family Theaceae) from which numerous biological activities have been reported including antimutagenic, antibacterial, hypocholesterolemic, antioxidant, antitumor and cancer preventive activities. From the aqueous-alcoholic extract of green tea leaves, six compounds (+)-gallocatechin (GC), (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin gallate (EGCG) and caffeine, were isolated and purified. Together with (+)-catechin, these compounds were tested against each of four human tumor cells lines (MCF-7 breast carcinoma, HT-29 colon carcinoma, A-427 lung carcinoma and UACC-375 melanoma). The three most potent green tea components against all four tumor cell lines were EGCG, GC and EGC. EGCG was the most potent of the seven green tea components against three out of the four cell lines (i.e. MCF-7 breast cancer, HT-29 colon cancer and UACC-375 melanoma). On the basis of these extensive in vitro studies, it would be of considerable interest to evaluate all three of these components in comparative preclinical in vivo animal tumor model systems before final decisions are made concerning which of these potential chemopreventive drugs should be taken into broad clinical trials.
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PMID:Inhibitory effect of six green tea catechins and caffeine on the growth of four selected human tumor cell lines. 882 14

The mucin-like carcinoma-associated antigen (MCA) enzyme immunoassay was tested in 962 healthy controls. MCA levels were compared with CA 125 in 70 patients with benign and 76 with malignant ovarian tumors. In addition MCA was compared with CA 15.3 in 58 patients with breast cancer and with CEA in 50 patients with colon carcinoma. In healthy controls the 95th percentile cutoff of 19.2 U/ml appeared to be higher than generally used. With the common cutoff value of 14 U/ml, a 38% sensitivity and 100% specificity was reached in malignant versus benign ovarian tumors. In colorectal cancer only 4% of patients had elevated MCA serum levels (CEA: 50%). In breast cancer patients the MCA assay performed better than CA 15.3 although only 17.2% showed elevated levels (CA 15.3: 7.4%). Thus MCA seems to be of limited value in the diagnosis and follow-up of adenocarcinomas of breast, ovary or colon.
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PMID:Mucin-like carcinoma-associated antigen serum levels in patients with adenocarcinomas originating from ovary, breast and colon. 884 Jan 80

37 cases of extragenital tumours metastatic to the ovaries are analysed from a clinicopathological viewpoint. In 25 out of 334 patients who were operated on between 1978 and 1990 because of a palpable malignant ovarian tumour, ovarian involvement from extragenital cancer was diagnosed. The most frequent primary sites were the stomach (n = 7), colon (n = 6) and breast (n = 6). 4 of the 6 patients with metastatic colon carcinoma had previously documented diagnosis of colon cancer with a time interval between diagnosis of primary tumours and secondary ovarian tumour ranging up to 11 years. Only one patient had a previously known stomach cancer, operated on 32 months earlier. All our patients with gastrointestinal primary tumour died within 1 year (gastric origin) of detection of metastases and 2 years (colon carcinoma) except for one patient with metastasis of colon carcinoma, who is still living after more than 4 years and one patient with gastric carcinoma who survived 34 months after oophorectomy. Surprisingly, ovarian metastases of breast cancer were detected before the primary tumour in 2 out of 6 cases. The other 4 patients were operated on because of an ovarian tumour but had a known and previously operated breast cancer. 27 patients had therapeutic ovarian ablation in metastatic breast cancer without a palpable pelvic mass. None of these patients had symptoms related to the ovaries. In 12 (40%) patients we found microscopic metastases which were bilateral in 9 cases. Metastases to the ovary may not infrequently mimic primary ovarian tumour and are difficult to diagnose preoperatively. We hope that some clinical features described by us (nationality, patient's history, bilateral ovarian tumours in young women) will alert the clinician to investigate further in order to achieve the best possible therapeutic management, because some patients may benefit from adequate treatment and survive for a long time.
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PMID:[Ovarian metastasis of extragenital tumors at the Zurich University Gynecologic Clinic 1978-1990]. 896 49

Interstitial laser photocoagulation (ILP) causes tumor necrosis with local hyperthermia produced by laser light energy. We treated with US-guided ILP 14 patients (7 men and 7 women; mean age: 67 years) and 20 metastases: 9 of them were < 3 cm in max. diameter and 11 were > 3 cm (mean diameter: 2.9 cm); 14 metastases were from colon carcinoma, 5 from breast cancer and 1 from lung cancer. ILP was performed with 300 and 600 microns quartz fiberoptic guides advanced in 21-18G Chiba needles and a continuous-wave Nd: YAG laser with 1064 nm wavelength. We used single expositions of 5-6 minutes with an irradiation power of 5 watts and scheduled 3 treatment sessions, performing CT scans and biopsies at the end of each session. The extent of induced necrosis was classified as follows on the basis of CT findings: grade 1 = 100% necrosis; grade 2 = necrosis > 50%; grade 3 = necrosis < 50%. The average follow-up was 6 months. After the 3 scheduled treatment sessions, CT showed grade 1 necrosis in all the lesions < 3 cm in diameter and in 4/9 (44%) lesions > 3 cm and grade 2 and 3 necrosis in the remaining cases (necrosis > 50% in 95% of the lesions and 92% of the patients). The cytologic findings were in agreement with CT results in all grade 2 and 3 cases, but in one grade 1 necrosis cytology showed residual viable tumor. To conclude, ILP is a safe and well-tolerated procedure. Maximum efficacy was observed in the lesions < 3 cm, while lesion volume was markedly reduced in the lesions > 3 cm. US is a useful tool in the real-time monitoring of this procedure and CT is the most accurate imaging technique to assess treatment efficacy.
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PMID:[Interstitial photocoagulation with laser in the treatment of liver metastasis]. 904 47

The metabolism of 25-hydroxycholesterol in different cell types was studied and the role of 7 alpha-hydroxylation for the effect of 25-hydroxycholesterol on the activity of HMG-CoA reductase was determined. Human diploid fibroblasts (HDF) and the human melanoma cell line SK-MEL-2 converted 25-hydroxycholesterol into 7 alpha,25-dihydroxycholesterol and 7 alpha,25-dihydroxy-4-cholesten-3-one while the virus-transformed fibroblast line 90VA-VI, the colon carcinoma cell line WiDr and the breast cancer cell line MDA-231 did not express 7 alpha-hydroxylase activity. The 7 alpha-hydroxylation of 25-hydroxycholesterol in HDF could be stimulated by dexamethasone and cortisol and inhibited by metyrapone. An unidentified, possibly 4-hydroxylated, metabolite was formed by 90VA-VI cells and a polar, probably conjugated, metabolite was formed by WiDr cells. The 7 alpha-hydroxylated metabolites of 25-hydroxycholesterol suppressed the activity of HMG-CoA reductase to a similar extent as 25-hydroxycholesterol in HDF but not in 90VA-VI cells, while the 7 alpha-hydroxylated metabolites of 27-hydroxycholesterol suppressed the activity of HMG-CoA reductase also in 90VA-VI cells. The suppression of HMG-CoA reductase activity by 25- and 27-hydroxycholesterol was decreased or abolished by dehydroepiandrosterone or pregnenolone which have little or no effect on the 7 alpha-hydroxylation. The results indicate that 7 alpha-hydroxylation is not directly involved, positively or negatively, in the action of 25- or 27-hydroxycholesterol as suppressors of HMG-CoA reductase activity.
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PMID:Studies on the relationships between 7 alpha-hydroxylation and the ability of 25- and 27-hydroxycholesterol to suppress the activity of HMG-CoA reductase. 905 14

p53 is a pivotal regulator of apoptosis but its mechanism of action is obscure. We report that the polyproline (PP) region located between p53's transactivation and DNA binding domains is necessary to induce apoptosis but not cell growth arrest. The PP region was dispensable for DNA binding, inhibition of SAOS-2 tumor cell growth, suppression of E1A + RAS cell transformation, and cell cycle inhibition. A temperature-sensitive dominant inhibitory p53 mutant lacking PP (p53ts deltaPP) retained its ability to cooperate with adenovirus E1A in transformation of primary BRK cells. However, while activation of wt p53 induced apoptosis in E1A + p53ts-transformed cells, activation of p53 deltaPP induced cell cycle arrest but not apoptosis in E1A + p53ts deltaPP-transformed cells. Similarly, PP deletion abolished apoptosis in LoVo colon carcinoma cells, which are killed by wt p53 overexpression. Transactivation was largely unaffected by PP deletion. Significantly, BAX induction was intact, indicating that additional events are required for p53 to induce apoptosis. As a recently described site for familial mutation in at least one breast cancer family, the PP region represents a domain that may be altered in human tumors. We concluded that p53's ability to induce apoptosis is dispensable for inhibiting cell growth and transformation and that the PP region plays a crucial role in apoptotic signaling.
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PMID:The polyproline region of p53 is required to activate apoptosis but not growth arrest. 928 84

Cryosurgical ablation of hepatic metastases from colon carcinoma has become a useful adjunct in the management of patients whose tumors are not amenable to surgical resection. We evaluated cryoablation of hepatoma and noncolorectal hepatic metastases by examining its effect on serum levels of tumor markers in 20 patients with primary liver cancer (N = 5) or liver metastases (N = 15) from breast cancer, neuroendocrine tumors, ovarian cancer, and thyroid cancer. All patients had failed conventional therapy and had no evidence of extrahepatic spread. After cryosurgery, 17 patients had a significant decrease in tumor marker levels (median 77%) and a significant improvement in symptoms. One patient died of nontumor causes, and five patients died of recurrent disease. Median interval to death or last follow-up was 28.3 months overall (range, 2-45 months), 17.9 months for nonsurvivors (range, 2-44 months), and 35.2 months for survivors (range, 26-45 months). Median survival was 32 months following curative surgery (range, 16-45 months) and 25 months following palliative surgery (range, 2-42 months). Cryosurgical ablation of noncolorectal hepatic metastases and primary hepatomas produces a profound reduction in serum levels of tumor markers. It is safe, provides excellent palliation of symptoms, and in selected patients can be performed with curative intent.
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PMID:Cryosurgery causes a profound reduction in tumor markers in hepatoma and noncolorectal hepatic metastases. 929 May 24

The human genome contains at least 50 copies of the human endogenous retrovirus K (HERV-K) family which is related to the mouse mammary tumor virus (MMTV). Some members have been shown to be transcriptionally active and to have large open reading frames. Using the RT-PCR method we have investigated the HERV-K env transcription pattern in several malignant tissues and in peripheral blood mononuclear cells PBMCs). Samples were derived from chronic myelogenous leukemia (CML), breast cancer, colon cancer, high and low grade non-Hodgkin's lymphomas, Hodgkin's disease, myelodysplastic syndrome, thyroid adenoma (TA) and from PBMCs of patients with breast cancer, gastric cancer, and of healthy individuals. We found abundant HERV-K env transcripts in all tissues under investigation. Using HERV-K 10 specific primers for amplification we detected in addition to transcripts with high homology to HERV-K 10 (ca. 96% homology on the amino acid level) also transcripts of low homology to HERV-K10 (ca. 71%). Interestingly, all solid tissues containing high percentages of malignant cells such as breast cancer, colon carcinoma, low and high grade non-Hodgkin's lymphomas showed exclusively HERV-K env related transcripts with low homology to HERV-K 10. In contrast, in samples containing only a low proportion of malignant cells or no malignant cells at all we observed both types of transcripts. Thus, our data suggest that the expression pattern of HERV-K elements in human cells is very heterogenous and subjected to a complex transcriptional regulation.
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PMID:Two groups of endogenous MMTV related retroviral env transcripts expressed in human tissues. 942 77

The Her-2/neu oncogene encodes a Mr 185,000 transmembrane protein with homology to the epidermal growth factor receptor. It is overexpressed in 30-40% of breast and ovarian cancers, and this overexpression was shown to correlate with aggressiveness of malignancy and poor prognosis. Using tumor-associated lymphocytes isolated from patients with ovarian or breast cancer, several HLA-A2-restricted, Her-2/neu-derived peptides were identified. Further studies revealed that these tumor-associated CTLs can also lyse other tumors, including non-small cell lung and pancreatic cancer cells, suggesting that Her-2/neu epitopes are shared between several distinct types of epithelial tumors. To analyze whether Her-2/neu epitopes are tumor-associated antigens for renal cell carcinoma (RCC) and colon carcinoma, we induced Her-2/neu peptide-specific CTL responses by primary in vitro immunization and used these CTLs to determine the presentation of Her-2/neu epitopes on human tumor lines. Autologous dendritic cells (DCs) generated from peripheral blood monocytes were pulsed with Her-2/neu-derived peptides E75 and GP2 and used as antigen-presenting cells for CTL priming. High CTL activity toward peptide-pulsed targets was obtained after two weekly restimulations. CTLs induced with DCs generated in the presence of TNF-alpha elicited a higher cytotoxic activity when they were stimulated with the cognate peptide than did CTLs induced with DCs grown in granulocyte macrophage colony-stimulating factor and interleukin 4 alone. The cytotoxicity of induced CTLs was antigen specific and HLA-A2 restricted. Furthermore, these CTLs lysed, in a MHC- and antigen-restricted fashion, not only breast cancer cells but also colon carcinoma and RCC cell lines expressing Her-2/neu. The cytotoxic activity against tumor cells was blocked by cold HLA-A2-positive targets pulsed with the cognate peptide in cold target inhibition assay and by anti-HLA-A2 monoclonal Ab. These results suggest that epitopes derived from Her-2/neu protein might be attractive candidates for broadly applicable vaccines and may prove useful for adoptive immunotherapies designed for colon carcinoma or RCC.
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PMID:Her-2/neu-derived peptides are tumor-associated antigens expressed by human renal cell and colon carcinoma lines and are recognized by in vitro induced specific cytotoxic T lymphocytes. 948 28

(+)-Discodermolide, a sponge-derived natural product, stabilizes microtubules more potently than paclitaxel despite the lack of any obvious structural similarities between the drugs. It competitively inhibits the binding of paclitaxel to tubulin polymers, hypernucleates microtubule assembly more potently than paclitaxel, and inhibits the growth of paclitaxel-resistant ovarian and colon carcinoma cells. Because paclitaxel shows clinical promise for breast cancer treatment, its effects in a series of human breast cancer cells were compared to those of (+)-discodermolide. Growth inhibition, cell and nuclear morphological, and electrophoretic and flow cytometric analyses were performed on (+)-discodermolide-treated MCF-7 and MDA-MB231 cells. (+)-Discodermolide potently inhibited the growth of both cell types (IC50 < 2.5 nM) at concentrations similar to those observed with paclitaxel. Complete inhibition of growth occurred with 10 nM or greater of each drug and was not reversed by removal. (+)-Discodermolide-treated cells exhibited condensed and highly fragmented nuclei. Flow cytometric comparison of cells treated with either drug at 10 nM, a concentration well below that achieved clinically with paclitaxel, showed both caused cell cycle perturbation and induction of a hypodiploid cell population. (+)-Discodermolide caused these effects more extensively and at earlier time points. The timing and type of high molecular weight DNA fragmentation induced by the two agents was consistent with induction of apoptosis. The results suggest that (+)-discodermolide has promise as a new chemotherapeutic agent against breast and other cancers.
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PMID:The potent microtubule-stabilizing agent (+)-discodermolide induces apoptosis in human breast carcinoma cells--preliminary comparisons to paclitaxel. 949 94


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