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)

To investigate whether autoimmunity against thyroid antigens is induced or exacerbated by granulocyte-macrophage colony-stimulating factor, thyroid function and thyroid autoantibodies were studied in 14 patients with advanced breast cancer and 11 with soft-tissue sarcoma who received several cycles of doxorubicin and cyclophosphamide plus GM-CSF 250 micrograms/m2 intravenously daily for 10 days in every 21 day cycle. All patients had normal thyroid function before treatment. In 2 patients with pre-existing thyroid antibodies, thyroid dysfunction developed but disappeared after cessation of GM-CSF. No other autoimmune abnormalities appeared. Stimulation of antigen-presenting cells by GM-CSF may bring about this phenomenon.
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PMID:Reversible thyroid dysfunction during treatment with GM-CSF. 168 46

Tumor-infiltrating lymphocytes from 120 samples of human cancers, including melanoma, renal cell carcinoma, breast cancer, sarcoma, and colon cancer, were examined. The percentage of lymphocytes recovered from the cancer varied widely; that of renal cell carcinoma was higher than that of breast or colon cancer (65% vs 45%), which was higher than that of melanomas or sarcomas (30% to 35%). The types of lymphocytes before and after interleukin 2 activation showed specific patterns. CD4+ helper T cells predominated in all tumors except melanomas, which had more CD8+ cytotoxic T cells. CD16+ natural killer cells were recovered in renal cell carcinoma and sarcomas. Three different cytotoxic lymphocytes were identified among interleukin 2-activated tumor-infiltrating lymphocytes: (1) CD3+ CD16- cytotoxic T lymphocytes with cytotoxicity restricted to autologous tumor cells in melanomas, (2) CD3-CD16+ natural killer cells with vigorous major histocompatibility complex-nonrestricted cytotoxicity in renal cell carcinoma, and (3) CD3+ CD16- T cells with modest levels of major histocompatibility complex-nonstricted cytotoxicity in all cancers except melanomas. Thus, there was considerable diversity of tumor-infiltrating lymphocytes among these histologically distinct tumors with respect to magnitude of lymphocyte infiltration, phenotypic expression, and functional capacity.
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PMID:Patterns of human tumor-infiltrating lymphocytes in 120 human cancers. 168 43

An association exists in primary human breast tumors between high epidermal growth factor receptor (EGFR) expression and a reduced number or even absence of estrogen receptors (ER). To determine whether an increase in EGFR expression might alter the estrogen responsiveness of an ER-positive human breast cancer cell line, ZR 75-1 cells were cotransfected with a plasmid containing the full-length cDNA for the human EGFR under the transcriptional control of the Harvey murine sarcoma virus (HaMSV) long terminal repeat (LTR) and with a pSV2neo plasmid. Two of the isolated G418-resistant clones were found to constitutively express EGFR levels 15- to 60-fold higher than those found on nontransfected ZR 75-1 cells. The EGFR in these clones were functionally normal since EGF could increase their autophosphorylation and since EGF could enhance the transphosphorylation of p185erbB-2. No change was seen in either the number or affinity of ER in these clones. In addition, the ability of estrogen to stimulate the anchorage-dependent and anchorage-independent growth of these clones was not significantly modified. These results suggest that an increase in EGFR expression alone is not sufficient to induce a hormone-independent phenotype in vitro in human breast cancer cells.
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PMID:Over-expression of the epidermal growth factor receptor in human breast cancer cells fails to induce an estrogen-independent phenotype. 169 33

There have been described three cases of the breast phyllodes tumour, i.e., fibroepithelial tumour, histologically both benign and on borderline, or expressively malignant (sarcoma). The mean age of patients concerned is of about 50 years old at the time of neoplasm diagnosis. If the surgical removal is incomplete, therein a large number of recurrences occurs. Diagnostic procedures are based on clinical examination (it is remarked the abnormal wideness of the tumour) as well as mammography, echography, needle biopsy. Surgical treatment is always based on large tumorectomy which results are sufficient in benign tumours. In malignant phylloides a total mastectomy is required without axillary lymphadenectomy owing to the hematic dissemination. Usually, after surgical treatment, survival rate seems better as compared to that of breast cancer.
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PMID:[Phyllodes tumor of the breast (cystosarcoma phyllodes) (apropos 3 cases)]. 196 18

Restriction fragment length polymorphisms (RFLPs) of 2 oncogenes, c-Ha-ras and L-myc, have been analyzed in 101 patients with bone and soft-tissue sarcoma and in 98 normal individuals. The c-Ha-ras gene was highly polymorphic both in sarcoma patients and in normal individuals. In contrast to our previous observation in breast cancer patients (Honda et al., 1988), no significant difference in allele frequencies between normal and sarcoma populations was observed. The L-myc locus revealed 2-allele polymorphism, allele L (10-kb) and S (6.6-kb), after digestion with Eco RI. The allele frequencies of L and S in sarcoma patients were 0.381 and 0.619, respectively, and those in normal individuals were 0.485 and 0.515, respectively. While the distributions of alleles in both populations fitted well with the Hardy-Weinberg equilibrium, the frequency of the S allele was significantly higher in sarcoma patients than in normal individuals (p less than 0.05). When sarcoma patients were divided into male and female subpopulations, this difference was highly significant only in males (p less than 0.01) but not in females. Our results suggest that males carrying the S allele may be prone to develop sarcoma.
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PMID:Elevated frequency of a specific allele of the L-myc gene in male patients with bone and soft-tissue sarcomas. 196 96

Relatives of 88 long-term survivors of childhood sarcoma were examined for the familial cancer syndrome of sarcoma, breast cancer, and other neoplasms (Li-Fraumeni syndrome). Twenty-six of 402 close relatives developed cancer (expected, 23.8), including breast cancer in four mothers (expected, 3.1). Two sarcoma probands who developed second malignant tumors have multiple relatives with cancer and might have an inherited predisposition. An increased cancer risk and exceptional requirement for disease screening appear to be confined to first-degree relatives of a small fraction of children with sarcoma, notably probands with second cancers.
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PMID:Cancer in relatives of survivors of childhood sarcoma. 199 15

Mothers of a population-based series of young adults with bone and soft tissue sarcoma were traced and their cancer risks estimated. No overall excess of cancers compared with expected numbers calculated from population rates was seen but mothers of patients with synovial sarcoma had significantly more cancers than expected and this was accounted for mainly by an excess of breast cancer. In addition there were strong indications that a proportion of cases were members of families with inherited cancer-prone syndromes, in particular with neurofibromatosis or with the Li Fraumeni cancer family syndrome.
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PMID:Malignant disease in the mothers of a population-based series of young adults with bone and soft tissue sarcomas. 200 83

Although doxorubicin is one of the most commonly used antineoplastics, no studies to date have clearly related the area under the concentration-time curve (AUC) to toxicity or response. The limited sampling model has recently been shown to be a feasible method for estimating the AUC to facilitate pharmacodynamic studies. Data from two previous studies of doxorubicin pharmacokinetics were used, including 26 patients with sarcoma and five patients with breast cancer or unknown primary. The former were divided into a training data set of 15 patients and a test datum set of 11 patients, and the latter patients formed a second test data set. The model was developed by stepwise multiple regression on the training data set: AUC (nanogram hour per milliliter) = 17.39 C2 + 163 C48-111.0 [dose/(50 mg/m2)], where C2 and C48 are the concentrations at 2 and 48 hours after bolus dose. The model was subsequently validated on both test data sets: first test data set--mean predictive error (MPE), 4.7%; root mean square error (RMSE), 12.4%; second test data set--MPE, 4.5%, RMSE, 9.2%. An additional model was also generated using a simulated time point to estimate the total AUC for a daily x 3-day schedule: AUC (nanogram hour per milliliter) = 44.79 C2 + 175.65 C48 + 47.25 [dose/(25 mg/m2/d)], where the C48 is obtained just prior to the third dose. We conclude that the AUC of doxorubicin after bolus administration can be adequately estimated from two timed plasma concentrations.
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PMID:Limited sampling models for doxorubicin pharmacokinetics. 201 31

1. A complete perusal of the literature revealed twenty cases of primary liposarcoma of bone acceptable as such to the authors. These were tabulated as to location and age. 2. Eight cases of osteo-liposarcoma, primary in bone, were encountered in the literature and an additional case was reported by the authors. 3. The authors described for the first time in the literature a new primary tumor of bone of mixed origin: osteo-rhabdomyosarcoma. After careful perusal of the literature they added three additional cases: two cases, previously reported as primary rhabdomyosarcoma of bone, which on careful evaluation of the radiographs in said publications and the paucity of microphotographs they considered to be osteo-rhabdomyosarcomas, and the other case, previously reported as malignant mesenchymoma of the sternum following radiotherapy for breast cancer. 4. The authors prefer to classify these tumors (osteo-liposarcoma and osteo-rhabdomyosarcoma) as "Tumors of Mixed Origin" and not as "Malignant Mesenchymomas". 5. A complete review of the literature revealed 219 reported "dedifferentiated" chondrosarcomas, or chondrosarcomas "with additional mesenchymal component", among which only nine (9) contained a bona fide rhabdomyosarcomatous component. The rest exhibited other mesenchymal tumors as osteogenic sarcoma, fibrosarcoma, malignant fibrous histiocytoma, angiosarcoma, and undifferentiated sarcoma. The authors recommend to continue classifying these tumors as chondrosarcomas with additional mesenchymal component or even as "dedifferentiated" chondrosarcomas but not as malignant mesenchymomas.
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PMID:Bone tumors of mixed origin: osteo-liposarcoma and osteo-rhabdomyosarcoma. 207 43

Familial aggregations of defined malignancies are of great importance for determining the genetic factors involved, as has been demonstrated for familial and sporadic retinoblastoma. In nearly all organs, neoplasms occur that are inherited similar to familial retinoblastoma (Rb). For example, more than 5% of all women suffering from breast cancer belong to breast cancer families in which the occurrence of the malignancy suggests an autosomal dominant pattern of inheritance. Familial colon cancer is associated with several well-known autosomal dominantly inherited polyposis syndromes, and also other susceptibilities without obvious clinical features. Site-specific cancers are often accompanied by other malignancies. In addition, there seem to be predispositions to a wider range of different, but well-defined neoplasms: e.g., adenocarcinomatosis of the colon and the endometrium, or the Li-Fraumeni/SBLA syndrome. The latter shows a spectrum of sarcoma, brain tumours, breast cancer, leukaemias, lung and adenocortical cancer. The genes leading to these types of dominantly inherited predispositions appear to be the tentatively so-called tumour suppressor genes, for which the Rb gene serves as a model. It manifests itself recessively on the level of the individual cell, which means both alleles must be deleted or inactivated before a retinoblast develops into a neoplastic cell. Clinical, epidemiological and molecular genetic studies have yet to establish whether the Rb model can be extended to all other forms of dominantly inherited human cancers.
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PMID:Dominant inheritance in human cancer. 219 May 28


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