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)

60,000 women in France have received RU 486 and a prostaglandin to induce abortion. In the late 1980's, clinical researchers assessed the safety and effectiveness of 600 mg of oral RU 486 in 2040 French women. 2 days later, health workers either injected 0.25-0.5mg of sulprostone or inserted a 1mg vaginal suppository of gemeprost in 1964 women who had not yet aborted. 96% experienced complete abortions. Physicians needed to conduct either a vacuum aspiration of dilation and curettage on the other 4%. RU 486 was most successful with 0.5mg of sulprostone, but these women also experienced considerable vaginal bleeding and pain. Overall uterine bleeding occurred for 8.9 days. The researchers recommended that adequate medical facilities be accessible to women using this method. Mild side effects were nausea, vomiting, and diarrhea. Efficacy and safety matched those of other early abortion methods. In April 1991, a grand multiparous women who smoked heavily and received RU 486 and a prostaglandin died--the 1st reported RU 486 related death. RU 486 may be able to treat fibroids, endometriosis, premenstrual syndrome, meningioma, hypertension, adrenal cancer, glaucoma, some forms of Cushing's syndrome, and breast cancer. The US Food and Drug Administration forbade the commercial import of RU 486 in 1989, even though it deemed RU 486 safe and effective. FDA considered the antiabortion view of the Bush Administration when making this decision. It made this decision despite the fact that abortion was still legal. RU 486 should be available soon for use as an abortifacient in the UK, the Netherlands, Sweden, Norway, Denmark, and Finland. These countries do not intent providing it to US women, however. Further the manufacturer is not willing to provide it to US researchers because it is afraid of antiabortion repercussions which may jeopardize WHO's approval of RU 486.
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PMID:The RU 486 story: the French experience. 173 8

Plasma lipid-bound sialic acid (LSA) was assayed in normal volunteers, patients with non-malignant diseases, and a variety of cancer patients. Mean plasma LSA in 50 normal volunteers, 16 patients with non-malignant diseases, 54 breast cancer, 17 lung cancer, 15 colon cancer, 7 ovarian cancer, 5 prostate cancer, 4 leukemia, 4 gastrointestinal, 3 thyroid cancer, 3 pancreas cancer and 2 adrenal cancer patients were 17.7, 23.2, 58, 85, 56.7, 46.2, 56.7, 53.3, 31.1, 33.2 and 119.5 mg/dl, respectively. None of the normal volunteers had elevated plasma LSA values. Plasma LSA level was not significantly different in male and female volunteers. Two out of 114 different cancer patients had plasma LSA levels within normal range exhibiting 98.2% sensitivity of the assay. Plasma LSA, which is relatively simple to assay, may be used as a tumor marker in wide variety of neoplastic diseases.
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PMID:Plasma lipid-bound sialic acid alterations in neoplastic diseases. 229 88

The cytotoxic effects of ketoconazole, an antifungal agent known to have some activity against human prostate cancer, adrenal cancer, and male metastatic breast cancer, were evaluated using colony-growth and clonogenic assays in eight malignant cell lines. The cytotoxicity of ketoconazole showed a dose- and time-dependent pattern, with the following concentrations inhibiting 90% of the growing colonies (IC90): MCF 7 (human breast cancer) 7.25 micrograms/ml, T 47 D (human breast cancer) 9.0 micrograms/ml, MiaPaCa (human pancreatic carcinoma) 10.0 micrograms/ml, COLO 357 (human pancreatic carcinoma), 9.5 micrograms/ml, HCT 8 (human colonic adenocarcinoma) 27.1 micrograms/ml, DU 145 (human prostatic cancer) 40.0 micrograms/ml, AR 42 J (rat pancreatic carcinoma) 9.0 micrograms/ml, and L1210 (murine leukemia) 8.6 micrograms/ml. Since a concentration of 10 micrograms/ml can be achieved in humans, the use of ketoconazole in human malignancies might be worthy of clinical evaluation.
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PMID:Cytotoxicity of ketoconazole in malignant cell lines. 337 Jul 40

We have utilized a recently developed human tumor cloning system to screen for antitumor effects in vitro of a new anthracene derivative, CL216,942. The object was to determine whether the system is useful for pinpointing the types of tumors in patients which should be studied in early phase II clinical trials. Tumors from 684 patients were placed in culture (27 different histologic tumor types). Two hundred seventy-three tumors both grew and formed enough colonies for drug sensitivity assays. In vitro antitumor activity was noted for CL216,942 against human breast cancer, ovarian cancer, renal cancer, squamous cell, small cell and large cell lung cancer, lymphoma, acute myelogenous leukemia, melanoma, adenocarcinoma of unknown origin, adrenal cancer, gastric cancer, pancreatic cancer, and head and neck cancer. The drug definitely showed no in vitro activity against colon cancer. These data indicate that CL216,942 has a wide spectrum of in vitro antitumor activity. A comparison of these in vitro results with the results of phase II clinical trials with the drug should allow an evaluation of the utility of the human cloning system for predicting clinical activity of a new compound.
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PMID:Activity of 9-10 anthracenedicarboxaldehyde bis[(4,5-dihydro-1 H-imidazol-2-yl)hydrazone]dihydrochloride (CL216,942) in a human tumor cloning system. Leads for phase II trials in man. 730 32

Over a period of 11 years a total of 140 liver resections for non-colorectal, non-neuroendocrine hepatic metastases were performed in 127 patients (73 women, 54 men; median age 53 years). There were 120 first, 14 second and 6 third liver resections. Primary tumors were: breast cancer (n = 34), leiomyosarcoma (n = 20), pancreatic cancer (n = 16), renal cell carcinoma (n = 13), melanoma (n = 9), gastric cancer (n = 9), lung cancer (n = 6) and adrenal cancer (n = 6) and miscellaneous tumors (n = 14). Extrahepatic tumor manifestation (including synchronous primary tumors) was found in 69/140 cases (49%); 61 of 120 patients with a first liver resection had extrahepatic tumor (51%). In the 120 first liver resections, 82 (68%) R0, 13 (11%) R1 and 25 (21%) R2 excisions were possible. Median survival after first liver resection was 20 months; after R0 resection a median survival of 28 months and after R1/2 resection of 8 months was achieved. The 5-year survival rate was 16% for the total group, 24% in patients with R0 resection and 0% for R1/2 resections. After a second liver resection (n = 14) there was a median survival of 28 months (5-year-survival-rate of 21%) for all patients and of 41 months (5-year survival rate 38%) after R0 resection. Morbidity and mortality after the first liver resection were 32.5% and 5.8%, respectively. In patients without extrahepatic tumor at the time of the first liver resection a median survival of 32 months (5-year survival rate 25%) and 7 months was achieved after R0 resection and R1/2 resection, respectively. In case of extrahepatic tumor the median survival was 24 months (5-year survival rate 23%) for R0 resection compared to 8 months after R1/2 resection. These data suggest that not the presence of extrahepatic tumor but rather the possibility of a R0 resection is most decisive for the prognosis after liver resection. We conclude that patients with liver metastases of non-colorectal, non-neuroendocrine tumors may benefit from liver resection. Similar to colorectal metastases, a second or third liver resection can be worthwhile in selected cases. Even in more unfavorable tumor entities, several cases of long-term survival were observed after surgical therapy. Therefore, the indication for liver resection should be considered carefully in every single case.
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PMID:[Liver resection for non-colorectal, non-neuroendocrine hepatic metastases]. 1035 43

KRAS- and BRAF-mutant tumors are often dependent on MAPK signaling for proliferation and survival and thus sensitive to MAPK pathway inhibitors. However, clinical studies have shown that MEK inhibitors are not uniformly effective in these cancers indicating that mutational status of these oncogenes does not accurately capture MAPK pathway activity. A number of transcripts are regulated by this pathway and are recurrently identified in genome-based MAPK transcriptional signatures. To test whether the transcriptional output of only 10 of these targets could quantify MAPK pathway activity with potential predictive or prognostic clinical utility, we created a MAPK Pathway Activity Score (MPAS) derived from aggregated gene expression. In vitro, MPAS predicted sensitivity to MAPK inhibitors in multiple cell lines, comparable to or better than larger genome-based statistical models. Bridging in vitro studies and clinical samples, median MPAS from a given tumor type correlated with cobimetinib (MEK inhibitor) sensitivity of cancer cell lines originating from the same tissue type. Retrospective analyses of clinical datasets showed that MPAS was associated with the sensitivity of melanomas to vemurafenib (HR: 0.596) and negatively prognostic of overall or progression-free survival in both adjuvant and metastatic CRC (HR: 1.5 and 1.4), adrenal cancer (HR: 1.7), and HER2+ breast cancer (HR: 1.6). MPAS thus demonstrates potential clinical utility that warrants further exploration.
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PMID:A transcriptional MAPK Pathway Activity Score (MPAS) is a clinically relevant biomarker in multiple cancer types. 2987 25

In various cancers, high-grade tumor and poor survival rate in patients with upregulated lncRNAs UCA1 have been confirmed. Urothelial carcinoma associated 1 (UCA1) is an oncogenic non-coding RNA with a length of more than 200 nucleotides. The UCA1 regulate critical biological processes that are involved in cancer progression, including cancer cell growth, invasion, migration, metastasis, and angiogenesis. So It should not surprise that UCA1 overexpresses in variety of cancers type, including pancreatic cancer, ovarian cancer, gastric cancer, colorectal cancer, breast cancer, prostate cancer, endometrial cancer, cervical cancer, bladder cancer, adrenal cancer, hypopharyngeal cancer, oral cancer, gallbladder cancer, nasopharyngeal cancer, laryngeal cancer, osteosarcoma, esophageal squamous cell carcinoma, renal cell carcinoma, cholangiocarcinoma, leukemia, glioma, thyroid cancer, medulloblastoma, hepatocellular carcinoma and multiple myeloma. In this article, we review biological function and regulatory mechanism of UCA1in several cancers and also, we will discuss the potential of its as cancer biomarker and cancer treatment.
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PMID:The Functional Role of Long Non-coding RNA UCA1 in Human Multiple Cancers: a Review Study. 3256 Jun 5