Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stimulation of tumor growth and induced hypercalcemia both may occur during the initiation of estrogen therapy in breast cancer. This study was conducted to determine whether cyclophosphamide (CTX) as an adjuvant to estrogen therapy might (1) prevent induced hypercalcemia or (2) achieve a higher tumoricidal effect during the phase of tumor stimulation. Fifty postmenopausal women with inoperable or recurrent disseminated breast carcinoma were divided into two random groups. Results could be evaluated in 44 patients; 21 received diethylstilbestrol (DES), and 23 received DES plus a 4-week course of cyclophosphamide (DES + CTX). The response rate was 5/21 (24%) in the DES group and 8/23 (35%) in the DES + CTX group (p greater than 0.05). The median duration of response for both groups was 9 months. The survival rate at 24 months was 52% in the DES group and 25% in the DES + CTX group (p = 0.05). Induced hypercalcemia occurred in 3 patients treated with DES + CTX. Short-term cyclophosphamide adjuvant to estrogen therapy did not prevent induced hypercalcemia nor prolong the duration of response or survival.
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PMID:The effect of short-term cyclophosphamide on estrogen therapy in metastatic breast cancer. 123 33

MRMT-1 is a mammary carcinoma induced in immunologically impaired female Sprague-Dawley rats fed 3-methylcholanthrene. Its biological characteristics include transplantability to syngeneic normal rats and spontaneous metastases to various organs. Hypophysectomy performed 48 hr after tumor inoculation resulted in tumor regression accompanied by the disappearance of the metastasis in lungs of all the animals. The hypophysectomized animals were given replacement treatments, such as transplantation of pituitary homogenates, pituitary homograft underneath the renal capsule, or prolactin administration, and the inhibited tumor growth was markedly reactivated, with the reappearance of lung metastasis. These results indicate that MRMT-1 mammary carcinoma is prolactin dependent.
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PMID:Pituitary role in the growth of metastasizing MRMT-1 mammary carcinoma in rats. 124 97

Epstein-Barr virus, the apparent cause of infectious mononucleosis, may also be an etiological agent in nasopharyngeal carcinoma and Burkitt's lymphoma. Lymphocytes from normal individuals with anti-Epstein-Barr virus antibody activity may be sensitized to Epstein-Barr virus and contain transfer factor with the potential to program and/or recruit other lymphocytes to react against the virus and/or viral antigens. A patient with nasopharyngeal carcinoma refractory to conventional therapy was treated with transfer factor obtained from normal, young adults with previous history of infectious mononucleosis. Following immunotherapy, apparent slowing of tumor growth was observed, which was associated with intense lymphocytic infiltration of the tumor and reconstitution of delayed cutaneous hypersensitivity reactions to microbial recall antigens. A double-blind randomized clinical trial has been initiated to determine whether transfer factor immunotherapy is a useful adjunct to radiotherapy in the primary treatment of patients with nasopharyngeal carcinoma. If successful, a similar trial might be considered for African patients with Burkitt's lymphoma.
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PMID:In vivo and in vitro studies of immunotherapy of nasopharyngeal carcinoma with transfer factor. 125 57

Tumor growth was measured in inbred (C3H and C3Hf) and hybrid (C3H X C57BL/6F1 and BALB/c X C3HF1) mice after partial hepatectomy, sham hepatectomy, and hind limb amputation. Epithelial tumors (mammary carcinoma) and mesenchymal tumors (methylcholanthrene-induced and spontaneous tissue culture) were used in order to determine the tissue specificity of the tumor growth stimulation. Immunological parameters were defined by: (a) utilization of tumors that were either antigenic or nonantigenic, and (b) measurement of the host versus graft response in partially hepatectomized mice. Partial hepatectomy and the control operations were done on the same day as the tumor cell inoculation. All tumors, regardless of their tissue type or antigenicity, grew significantly better in partially hepatectomized mice as compared with the control mice. There was a significant positive correlation between the magnitude of tumor growth stimulation and the degree of antigenicity of the tumor. Last, skin allograft survival was significantly prolonged in the hepatectomized mice. The results suggest that : (a) the stimulation of tumor growth in hepatectomized mice is not tissue specific as previously reported; and (b) the antigenicity of a tumor is not necessary for growth stimulation after partial hepatectomy.
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PMID:Depression of host versus graft immunity and stimulation of tumor growth following partial hepatectomy. 126 27

This experimental study was undertaken to evaluate the effectiveness of a large-dose intratumoral administration of OK-432, which has already been found to be effective when combined with Mitomycin-C, 5-fluorouracil, and cytosine arabinoside, and/or small-dose of OK-432 in clinical use. Large-dose of OK-432 was administered intratumorally 15 days after the subcutaneous inoculation of 2.5 X 10(6) Ehrlich carcinoma cells. At the same time, 2.5 X 10(6) tumor cells were re-challenged intraperitoneally. A combined treatment with a small-dose of OK-432 and Mitomycin-C, cyclophosphamide, or 5-fluorouracil was also made. As a large-dose of OK-432, three-dose regimen of 1,000, 500, and 100 KE/kg was tested. As a small-dose of OK-432, 4 consecutive daily intramuscular injection of 50 KE/kg was examined. From the results obtained the initial intratumoral administration of a large-dose of OK=432 was found to be beneficial for the following combined treatment with a small-dose of OK-432 and Mitomycin-C or cyclophosphamide. The change of phytohemagglutinin (PHA) responsiveness of spleen cells after intratumoral injection of a large-dose of OK-432 was investigated in mice. These results indicated a decrease of PHA responsiveness of spleen cells according to the tumor growth. The intratumoral large-dose administration of OK-432 suggested inhibition of the decrease in PHA responsiveness. The most effective and suitable dose in this experiment was found to be 500 KE/kg in the three-dose regimen.
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PMID:Experimental study on the effect of large-dose intratumoral OK-432 administration in mice. 126 51

The study was performed to investigate the effect of ascitic fluid globulins of tumor on tumor growth and life span of mice. The globulins are shown to shorten the life span of Ehrlich tumor mice from 86.8 to 61.8 days, to increase 3-5-fold the growth rate of Ehrlich carcinoma and P388/DOX tumor. It was found that globulins of ascitic fluids and serum globulins of tumor have equal effects of tumor growth. It is proposed to use globulins of ascitic fluid to study the globulin role in tumor growth.
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PMID:[The effect of ascitic fluid globulins on the growth of leukemia P388/DOX and Ehrlich's carcinoma in mice]. 129 Aug 28

Silver-stained nucleolar organizer regions (AgNORs) in human breast carcinoma were studied using a computer-assisted system of image analysis. Standardized, automatic measurements of 7 morphometric parameters (area, perimeter, shape factor, bend energy, angle, and small and large diameters) performed on paraffin sections and cell imprint were compared and correlated with nuclear morphometry, histopathological grading, tumor growth fraction, (monoclonal Ki67-immunostaining), DNA nuclear content (stoechiometric Feulgen staining) and axillary lymph node invasion. The major findings were as follows: (i) variations in AgNORs and nuclear parameters were correlated, (ii) the ratio of AgNOR area/nuclear area was significantly different in low and high grade tumors, (iii) mean AgNOR parameter values increased significantly with the tumor growth fraction and tumor hyperploidy and were significantly higher in patients with axillary lymph node metastases and (iv) AgNOR evaluation was more accurate for cell preparations than for tissue sections.
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PMID:Correlation of nucleolar organizer regions and nuclear morphometry assessed by automatic image analysis in breast cancer with aneuploidy, K167 immunostaining, histopathologic grade and lymph node involvement. 130 May 97

Endocrine-paracrine (APUD, neuroendocrine) cells are located in the prostatic ductal and acinar epithelium. These cells are of the open and closed type and have dendritic processes. There is a wide range of secretory granule morphology presumably indicating a variety of different cell "types." Secretory immunoreactive peptides include serotonin, calcitonin (and related peptides), somatostatin, bombesin-like, thyroid-stimulating hormone-like (beta chain), and alpha-glycoprotein chain-like. These cells may function by endocrine, paracrine, neurocrine, and lumencrine mechanisms and play an important regulatory role both during growth and differentiation of the prostate as well as in the secretory process of the mature gland. Neuroendocrine differentiation in prostatic carcinoma is a frequent occurrence and manifests itself in several forms, including (1) small cell carcinoma, (2) carcinoid and carcinoid-like tumors, and (3) conventional adenocarcinoma with focal neuroendocrine differentiation. This latter pattern is the most common, and there is evidence that all or nearly all prostatic adenocarcinomas show at least some focal neuroendocrine differentiation. A review of the world's literature on this topic is included. Neuroendocrine differentiation generally portends a poorer prognosis but may also correlate directly with the grade. There is some evidence to suggest that neoplastic cells with neuroendocrine differentiation are resistant to hormonal therapy. Eutopic and ectopic hormone production may allow screening for prostatic carcinoma and/or monitoring for recurrence of prostatic carcinomas. Finally, the more basic implications of endocrine-paracrine cells and neuroendocrine differentiation are speculated on in reference to prostatic carcinogenesis and autocrine/paracrine tumor growth factor activity.
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PMID:Neuroendocrine differentiation in human prostatic carcinoma. 131 90

Previously we have shown that a murine mammary carcinoma cell line, designated SPI, grows and metastasizes more efficiently in the mammary gland than in the subcutis. In this report, we examine the tissue specificity of this phenomenon. Our results show that SPI cells grow best in the mesenteric and ovarian fat pads and well in the mammary gland, but very poorly in the subcutis or peritoneal cavity. Massive dissemination of tumors from the ovarian and mesenteric sites occurs to the liver, spleen and diaphragm. In contrast, metastases from the mammary site occur primarily in the lung. Co-transplantation of a threshold number of SPI cells with mammary or ovarian fat fragments into the subcutis results in increased tumor growth, whereas very few tumors form in sham controls receiving no fat fragments. Removal of the ovaries of donor and recipient mice abrogates tumor growth in adipose tissue transplants. Estrogen can stimulate growth of SPI in adipose tissue sites, whereas progesterone inhibits growth. In contrast, in vivo growth of a stable metastatic variant selected from SPI cells was not inhibited by progesterone. SPI cells growing in ovarian and mesenteric fat pads showed increased expression of estrogen receptors and progesterone receptors, as well as detectable levels of epidermal-growth-factor receptors, whereas receptor levels decreased to baseline on tumors in the subcutis. The levels of estrogen-receptor mRNA reflect the corresponding functional expression of receptors; this finding suggests that the regulation of estrogen-receptor expression in this system is, at least in part, at the mRNA level. Our results are consistent with the model that adipose tissue exerts an estrogen-dependent positive regulatory effect on primary SPI tumor growth, and promotes the formation of metastases.
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PMID:Capacity of adipose tissue to promote growth and metastasis of a murine mammary carcinoma: effect of estrogen and progesterone. 131 63

Carmethizole hydrochloride [1-methyl-2-methylthio-4,5-bis(hydroxymethyl)imidazole-4', 5'-bis(N-methylcarbamate)hydrochloride, NSC 602,668; hereafter called carmethizole] is a new antitumor drug that has shown relatively broad activity in initial evaluations against several murine tumors and human tumor xenografts in vivo. The present studies were designed to address questions about carmethizole's activity against established disease, its activity on different treatment schedules, and the extent of its cross-resistance with established drugs. Human MX-1 mammary carcinoma, human NCI-H82 small-cell lung carcinoma, and human LOX amelanotic melanoma xenografts in athymic mice were used to determine the drug's activity against established disease; the NCI-H82 lung-tumor xenograft in athymic mice was used to explore its schedule dependence; and a series of drug-resistant murine leukemias provided an in vivo cross-resistance profile. When injected i.p., carmethizole exhibited antitumor activity against advanced-stage s.c. MX-1 mammary, s.c. NCI-H82 lung, and i.p. LOX melanoma xenografts and was as effective against established disease (MX-1 and LOX) as it was against early-stage disease (no data are available for early-stage NCI-H82). The therapeutic effect of carmethizole was not route-dependent, as was evidenced by the similar delays observed in tumor growth following i.p. and i.v. administration. The use of a split-dose schedule on a single day instead of one bolus injection yielded an increase in the total dose delivered, resulting in an increased delay in tumor growth. Murine leukemias resistant to vincristine (VCR), amsacrine (AMSA), or methotrexate (MTX) were not cross-resistant to carmethizole. However, murine leukemias resistant to doxorubicin (ADR), melphalan (L-PAM), cisplatin (DDPt), 1-beta-D-ara-binofuranosylcytosine (ara-C), and 5-fluorouracil (5-FU) were cross-resistant to carmethizole, suggesting that patients who have previously been treated with any of these agents might be less likely to respond to carmethizole than those who have had no opportunity to develop resistance to any of these compounds. We anticipate that the information derived from these studies may be useful in the design of clinical trials of carmethizole and may stimulate additional basic research on the mechanism of action of this new agent.
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PMID:Antitumor activity and cross-resistance of carmethizole hydrochloride in preclinical models in mice. 132 3


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