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)

Antiestrogen compounds are relatively new in the treatment of breast cancer. A clinical trial of Nafoxidine therapy is being pursued in our institution. In a selected group of patients with metastatic breast cancer who had, in the past, undergone adrenalectomy, Nafoxidine therapy produced objective tumor regression in six out of ten patients. Of the six patients whose tumors contained demonstrable estrogen receptors, four showed regression (67%), one patient had stable disease, and one showed tumor progression. Of the four patients in whom estrogen receptor estimation was not done, two had, in the past, shown regression after endocrine therapy and they also showed regression of tumor with Nafoxidine therapy. In patients with metastatic breast carcinoma, who have undergone adrenalectomy in the past, a therapeutic trial with Nafoxidine may be worthwhile particularly in patients who have demonstrable estrogen receptor in the tumor of those who have in the past shown regression of tumor after endocrine therapy.
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PMID:Clinical trial of nafoxidine in adrenalectomized patients with advanced breast cancer. 33 79

The preliminary results of a still ongoing phase III study in patients with previously untreated metastatic breast cancer are reported. 210 cases are already evaluable. In this study patients are randomized to hormonotherapy either concurrently with combination chemotherapy or alone, chemotherapy being delayed until the occurrence of tumor progression. In both groups patients are further randomly allocated to 3 chemotherapy programs. So far there appear to be differences between remission rates, but not with regard to survival course.
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PMID:[Simultaneous hormonal and drug therapy, compared to hormonal therapy, followed by chemotherapy, in the treatment of metastasizing breast neoplasms. Preliminary results of an ongoing study]. 74 93

Breast cancer is the most common cancer among American women. Because metastatic breast cancer is an incurable disease, efforts to decrease breast cancer mortality have focused on early detection and improved treatment. Identification and analysis of a specific genetic susceptibility could permit detection of susceptible women and greatly increase the understanding of the initial step that eventually leads to cancer. Because susceptibility loci have been recognized as sites that often are altered during tumor progression, the identification and cloning of such loci could be important in developing cancer therapies. In this article, the progress being made in segregation analysis, linkage analysis, and cloning of breast cancer susceptibility loci is reviewed. The evidence for genetic inheritance is most consistent with dominant inheritance for at least three major susceptibility loci. Proliferative breast disease has been hypothesized to be an inherited lesion in breast cancer kindreds with both premenopausal and postmenopausal probands. Currently, there are many genetic markers for mapping the human genome. Technologic advances have progressed from restriction fragment length polymorphisms to highly polymorphic markers. Using this technology, breast cancer susceptibility in some kindreds with an early onset has been shown to be linked to chromosome 17q. Gene isolation eventually will follow with an increased understanding of the percentage of breast cancer cases that are a result of this genetic locus. Li-Fraumeni syndrome, which often is expressed as breast cancer, is due to mutations in the p53 gene. Characterization of the syndrome and its relationship to the altered gene should proceed rapidly. There is also a group of families exhibiting a genetic susceptibility that is not due to either of these loci. Together, these findings indicate that there are at least three separate major loci segregating for breast cancer susceptibility. With the current initiative to map and sequence the entire human genome and the advances that recently have been reported, a detailed molecular understanding of breast cancer predisposition can be envisaged.
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PMID:Genetic predisposition to breast cancer. 151 30

An immunoradiometric assay (IRMA) has been used to determine circulating levels of the breast cancer-associated antigen, CA15-3. Of 1,050 normal control subjects, serum from 99 (9.4%) had CA15-3 antigen levels greater than 22 U/mL, while that from 58 (5.5%) and 14 (1.3%) had levels greater than 25 U/mL and 30 U/mL, respectively. In contrast, 115 of 158 patients (73%) with metastatic breast cancer had CA15-3 levels greater than 22 U/mL. Thirteen of 26 patients (50%) with only local metastases, 27 of 34 (79%) of those with only bone metastases, and 20 of 24 (83%) with hepatic metastases had CA15-3 levels greater than 22 U/mL. Furthermore, nine of 31 patients (29%) with primary breast cancer had CA15-3 levels greater than 22 U/mL. CA15-3 and carcinoembryonic antigen (CEA) levels were compared for the same patient population. Significantly more patients with metastatic breast cancer had elevated CA15-3 levels than had elevated CEA levels (P less than .001). Furthermore, the CA15-3 IRMA was more sensitive than the CEA assay in patients with only bone metastases, as well as those with only local metastases. Significantly more patients with primary carcinoma of the breast also had elevated CA15-3 than had elevated CEA levels (P less than .02). CA15-3 levels were greater than 22 U/mL in patients with nonmalignant conditions, including five of 25 patients (20%) with benign breast diseases, and 23 of 52 patients (44%) with benign liver diseases. Furthermore, CA15-3 levels were also greater than 22 U/mL in 24 of 54 patients (44%) with gastrointestinal (GI) malignancies, 12 of 17 patients (71%) with bronchogenic carcinoma, and 29 of 44 patients (66%) with epithelial ovarian carcinoma. Serial CA15-3 levels correlated with clinical disease course. Nineteen of 21 patients (91%) with tumor progression had at least a 25% increase in CA15-3 levels. Conversely, seven of nine patients (78%) with tumor regression had at least a 50% decrease in CA15-3 levels. Among 27 patients with stable disease, 16 (59%) had levels that did not vary by more than +/- 25% of the original CA15-3 levels. These results indicate that the CA15-3 antigen is a sensitive marker for the evaluation and monitoring of patients with breast cancer.
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PMID:Comparison of circulating CA15-3 and carcinoembryonic antigen levels in patients with breast cancer. 242 49

In this case report the clinical course of a female patient with metastatic breast cancer receiving a mild cytostatic regimen with chlorambucil, methotrexate and prednisone is described. She developed an unusual clinico-pathological syndrome with pancytopenia, fever and bone pain resulting from a bone marrow necrosis. The clinical course illustrates the great diagnostic difficulties and the potential benefit from rapid identification of this prognostically very poor event. Leading symptoms such as fever, bone pain, pancytopenia, an increase in the sedimentation rate, in lactate dehydrogenase and alkaline phosphatase in serum are often misinterpretated as tumor progression with bone or hepatic metastases and bone marrow carcinomatosis. An iliac crest aspirate and biopsy detects the diagnosis of a marrow necrosis. These symptoms should be kept in mind in order to avoid a diagnostic pitfall resulting from a misinterpretation of the morphological picture as necrotic metastasis in bone marrow or as an artefact. It is assumed that, in addition to the underlying malignant disease, cytostatic therapy with chlorambucil, methotrexate and prednisone triggers this event.
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PMID:[Bone marrow necrosis in a patient with metastatic breast cancer in chemotherapy with chlorambucil, methotrexate and prednisone]. 254 86

In this study we report on some lines of ongoing research performed in our laboratory, in relation to the increased expression of FcR on tumor cells, as well as on cells present in the tumor-bearing host, and its possible role in tumor progression. In a previous study we have shown that a Polyoma virus (PyV)-induced anaplastic carcinoma (SEYF-a tumor) contained an FcR-expressing subpopulation of tumorigenic cells. We tested the effect of in vivo passaging of FcR-expressing and of non-FcR-expressing sub-populations of SEYF-a tumor cells on the expression of FcR, as revealed by the ability of these cells to bind the 2.4G2 monoclonal antibody, which is directed against mouse Fc gamma 2b/gamma 1R. It was found that upon in vivo passaging these two sub-populations became practically identical in their ability to bind anti-Fc gamma R antibody. On the other hand, in vitro passaging of FcR-expressing SEYF-a cells resulted in a gradual decrease in the expression of Fc gamma R. These results, indicating that the expression of Fc gamma R on tumor cells, per se, is dependent on a factor present in the in vivo environment were confirmed using 3T3 cells transformed in vitro by PyV (C) and forming tumors at first injection to mice (CTC). C cultures of various clones did not express Fc gamma R, while CTC cultures (cultures from tumors) became positive. We also detected an increase in the level of a soluble form of Fc gamma 2b/gamma 1R in the circulation of mice bearing PyV induced tumors. This increase paralleled the appearance of palpable tumors. A similar pattern of increase was observed in mice inoculated with the c-H-ras transformed tumorigenic clone 8/F/5, but not in mice inoculated with non-tumorigenic 3T3 cells. Data published by us show that metastatic breast cancer patients had significantly elevated Fc gamma R levels on their peripheral blood mononuclear cells (PBMC). Experiments presented here indicate a direct correlation between increased Fc gamma R levels on PBMC and tumor mass in colon, ovary and lung metastatic carcinoma patients. The possibility that malignantly transformed cells have the potential to cause proliferation of Fc gamma R expressing T cells was tested. It was found that extract derived from r-H-ras transformed 3T3 cells triggers the proliferation of a T cell hybridoma expressing Fc gamma R.
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PMID:Increased expression of Fc gamma receptor in cancer patients and tumor bearing mice. 285 35

Seventeen patients with metastatic breast cancer were treated with a high-dose combination chemotherapy regimen and autologous bone marrow support. Thirteen patients had prior combination chemotherapy. Fifteen patients were treated with a phase II regimen of cyclophosphamide (5.625 g/m2), cisplatin (165 mg/m2), and BCNU (600 mg/m2). Bone marrow harvest and reconstitution were uncomplicated. All patients became profoundly myelosuppressed. Fourteen of 16 evaluable patients (88%) responded, including six complete responses (CRs) (38%). The median time to tumor progression was 5 months. The median survival was 8 months. CRs occurred more frequently in patients with no prior chemotherapy for metastatic disease, inflammatory breast cancer; and patients treated within 3 months of first recurrence. The rate of tumor regression was rapid, with a median of 11 days to partial response (PR) and 12 days to CR. Those patients achieving a PR by day 7 had a greater likelihood (P = .03) of attaining a CR than those patients whose PR occurred later. Three deaths (18%) occurred, all in women with inflammatory breast cancer treated with prior chemotherapy. High-dose combined alkylating agent therapy produced high PR and CR rates in metastatic breast cancer patients, most of whom had failed prior chemotherapy. The rate of tumor regression was rapid. Current efforts are directed at developing a regimen using drugs specifically active in breast cancer, with an intent of combining an effective high-dose regimen with additional modalities of therapy in the treatment of breast cancer.
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PMID:High-dose combination alkylating agent chemotherapy with autologous bone marrow support for metastatic breast cancer. 353 55

Nineteen patients with advanced refractory metastatic breast cancer no longer responsive to chemotherapy were treated in the first phase II efficacy trial of recombinant leukocyte A interferon (IFL-rA), a highly purified single molecular species of alpha interferon prepared by recombinant DNA methods. Patients received a previously determined maximum tolerated dose for this agent (50 X 10(6) U/m2 body surface area) by intramuscular injection three times weekly for up to 3 months. The symptoms of toxicity observed in this trial resemble those previously reported for alpha interferons and include fever, chills, fatigue, anorexia, and leukopenia. All patients required dose reductions, most often for reasons of severe fatigue. Of the 17 patients evaluable for tumor response, one patient had stable disease and 16 had evidence of tumor progression. We conclude that IFL-rA is not an active agent in the treatment of advanced, refractory breast cancer when used at a maximum tolerated dose on this treatment schedule.
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PMID:Recombinant leukocyte A interferon in advanced breast cancer. Results of a phase II efficacy trial. 634 90

Seventeen premenopausal women with metastatic breast cancer were treated with the potent Luteinizing Hormone Releasing Hormone (LHRH) agonist Buserelin as a first-line agent. Twelve patients (group A) were treated with Buserelin alone and five patients (group B) with the combination of Buserelin and tamoxifen from the start of treatment. In nine patients of group A tamoxifen was added to Buserelin later on because of tumor progression or recurrent peaks of plasma estradiol (E2). Chronic intranasal therapy with Buserelin alone, preceeded by parenteral administration, caused an objective remission in four patients (2 X C.R., 2 X P.R.) and stable disease in four further patients without causing side effects. The longest duration of response until now is more than 29 months. After addition of tamoxifen a partial response occurred in two more patients of group A. Anovulation with suppressed progesterone secretion was reached in all patients treated with Buserelin alone, but transient peaks of E2 occurred in the majority (60%) of the patients. Addition of tamoxifen to Buserelin treatment caused disappearance of E2 peaks in 2 patients, but also reappearance of progesterone secretion with recurring E2 peaks in 3 other patients; in one case hyperstimulation of the ovaries was observed without progression of tumor growth. In group B only one woman showed a complete castration effect, while in four patients progesterone secretion was not (completely) suppressed. In two of these five patients an objective response occurred. In conclusion, Buserelin appears effective in the treatment of premenopausal women with metastatic breast carcinoma, but with the regimen used close control of endocrine parameters is necessary because of the variation in hormonal response with a risk of (hyper)stimulation of the ovaries, especially during combination therapy with tamoxifen.
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PMID:Anti-tumor and endocrine effects of chronic LHRH agonist treatment (Buserelin) with or without tamoxifen in premenopausal metastatic breast cancer. 643 3

Since in the treatment of advanced breast cancer chemotherapy and the various hormonal manipulations seem recently to have reached a plateau of effectiveness when used alone, it is widely assumed that the combination of both treatment modalities could improve therapeutic results. The outcome is reported of a study encompassing 109 pre- and 297 postmenopausal evaluable cases with previously untreated metastatic breast cancer. The patients were randomized either to a concurrent chemo/hormonotherapy or to the hormonal treatment alone, chemotherapy being delayed until the occurrence of tumor progression. All patients were further randomized to 3 chemotherapy regimens (LMFP, LMP/FVP, LMFP/ADM) representing three different degrees of intensity. Pre-menopausal patients tend to live longer with the concurrent combination of both modalities, whereas postmenopausal patients fare better when chemotherapy is delayed until the occurrence of tumor progression with hormonotherapy alone. However, the differences in survival are statistically significant only in postmenopausal patients with a less aggressive tumor ("low-risk"). The more aggressive cytotoxic combinations elicit higher response rates than "minimal chemotherapy", but the differences translate only marginally into different survivals. These findings are discussed with regard in particular to their importance in establishing widely acceptable therapeutic rules for the treatment of advanced breast cancer.
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PMID:[Simultaneous or sequential hormono/chemotherapy and a comparison of various polychemotherapies in the treatment of metastatic breast cancer]. 704 18


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