Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0278488 (metastatic breast cancer)
 7,812 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

50 patients with advanced metastatic breast cancer were matched into 25 "twin" pairs. In each pair, one "twin" received chemotherapy (FAC) and the other received chemoimmunotherapy (FAC + intratumorally Propionibacterium granulosum KP-45 (PG)). The therapeutic effects of this 2-year follow-up study were carefully documented and analysed. The mean survival time of FAC + PG-treated patients was about 17 months as compared to 8.5 months in FAC controls. PG-therapy responders showed increasing values of T-lymphocytes in peripheral blood, as well as higher blast transformation indices than nonresponders and controls. The skin reactivity to PHA, Distreptase, and Tuberculin was markedly enhanced in the FAC + PG-group. The incidence rate of hematological and/or infectious complications was significantly lower in PG-treated patients than in the controls. Local PG-immunotherapy was proven beneficial in advanced breast cancer when combined with FAC-chemotherapy, providing better toleration of chemotherapy and lower risk of myelosuppression and infections.
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PMID:Local immunotherapy with propionibacterium granulosum KP-45 in advanced breast cancer. 384 Jun 65

Comprehensive immune function by integrated score was assessed in 158 operable, 55 inoperable, and 52 metastatic breast cancer patients relative to 107 healthy controls. The score was derived from in vivo response to PPD and DNCB and in vitro lymphocyte stimulation by PPD and PHA. Proportion of E-RFC was significantly lower in patients than in controls but was not found to correlate directly with the above functional criteria. Fifty-one percent of the patients with early, operable tumors were shown to be at least partially immunosuppressed by integrated score achievement vs. 11% of controls. This proportion rises to 68% of inoperable and 89% of metastatic patients. Quantitative analysis by graded response revealed an additional, significant degree of immune impairment in the respective patient groups by all testing parameters. Depression of immune function in operable patients was not related to age nor influenced by surgery. Immunocompetence of patients with mammary dysplasia did not differ from controls. Increasing size of primary tumor (T) was not found to be matched by progressive degree of immunosuppression, excepting that associated with large T4 tumors. Patients with lymph node involvement (N+) were not significantly immunologically inferior to those without (N0) where the larger operable T2-3) tumors are concerned. In the smallest, T1 tumors, nodal involvement (N+) is accompanied by remarkable immunosuppression relative to T1N0 cases. This finding suggests a pre-existing immune defect inherent in T1N+ patients. It supports the hypothesis that the immunosuppression associated with early breast cancer is primary, patient related. Secondary tumor-induced depression of immune response characterizes advanced and metastatic human breast cancer.
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PMID:Immunocompetence, immunosuppression, and human breast cancer. II. Further evidence of initial immune impairment by integrated assessment effect of nodal involvement (N) and of primary tumor size (T). 737 Sep 52

The purpose of the present study was to investigate the impact of the use of peripheral blood progenitor cells (PBPCs) on the induction of autologous graft-versus-host disease (GVHD) in patients with advanced breast cancer. 14 women with stage IIIB and 36 women with stage IV breast cancer received cyclosporine (CsA) 2.5 mg kg-1 i.v. daily, d 0-28, and interferon-gamma (IFNg) 0.025 mg/m2 s.c. qod, d7-28, following PBPC-T +/- bone marrow transplantation (BMT). Preceding high-dose chemotherapy consisted of cyclophosphamide 6 g/m2 and thiotepa 800 mg/m2. Histologically proven > or = grade II cutaneous GVHD was induced in18/50 (36%) of patients and was independent of the source of haematopoietic support. In vitro studies showed that post-transplant, 76% of patients had developed auto-cytotoxicity against their own pre-transplant PHA-lymphoblasts. A significant correlation between the occurrence of GVHD > or = grade II and cytolysis was observed in the NK cell-line K562 and the T47D breast cancer cell-line. With a median follow-up of 2(1/2) years, the overall survival (OS) is 58%, the disease-free survival (DFS) 26%, both independent of the development of GVHD and similar to what has been observed in other studies on high-dose chemotherapy in advanced breast cancer. It therefore remains unclear whether the induction of autologous GVHD with the occurrence of auto-cytotoxic lymphocytes can result in an anti-tumour effect in this group of patients.
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PMID:Autologous graft-versus-host disease induction in advanced breast cancer: role of peripheral blood progenitor cells. 1107 45

Chitosan oligosaccharides (COS) have been shown to regulate various cellular and biological functions. The aim of this study was to investigate the antimetastatic potency of COS and the underlying mechanism. Here, we established a stably N-acetylglucosaminyltransferase V (GnT-V)-overexpressed MCF10A cell line. As expected, GnT-V overexpression greatly promoted cell migration in the transfectants by using wound healing assay. However, the induction in the cell migration was significantly suppressed by an addition of COS. Curiously, COS inhibited the protein expression of GnT-V in a dose dependent manner. Consistent with that, the reactivities with datura stramonium (DSA) and leuko-agglutinating phytohemagglutinin (L4-PHA) lectins, which specifically recognize branched N-acetylglucosamine (GlcNAc) structure, were also suppressed by COS. Taken together, these results demonstrated COS inhibited breast epithelial cell migration through down-regulation of GnT-V and its products, branched N-glycans, indicating that COS may serve as a potential novel therapeutic candidate for the treatment of metastatic breast cancer.
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PMID:Chitosan oligosaccharides inhibit epithelial cell migration through blockade of N-acetylglucosaminyltransferase V and branched GlcNAc structure. 2852 93