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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glycolysis is not of importance for the process of carcinogenesis. It is very likely, however, that certain molecular-biological and genetic changes are produced which enable the malignant cell to develop an intensive glycolysis, for instance, to form specialized glycolytic isoenzymes already during oncogenesis, and may possible become effective in the primary tumour. As soon as the capacity of the cancer cell to intensive aerobic and anaerobic glycolysis has become manifest, this process is an irreversible one. The extent of glycolysis of a malignoma is greatly dependent on the degree of its dedifferentiation and vascularization (glucose supply), although a direct correlation between growth and the amount of lactic acid formed does not seem to exist. However, a certain utilization of glucose is essential for cell proliferation (supply of basic substances). In many cases there is a correlation between the extent of glycolysis measurable under optimal conditions in vitro (glycolytic power) in a malignant tumour and its growth rate recognizable in vivo. The formation of a strong capacity for glucose degradation via the Embden-Meyerhof pathway that cannot be fully utilized by the whole tumour in vivo is first of all designed to ensure survival and proliferation of cells even at extremely low levels of glucose supply. This process can be regarded as an adaptation of cancer cells to a situation of unsufficient supply. This circumstance endows the cancer cell with an essential advantage over the normal cell which enables or even promotes its invasive and destructive growth and metastatic dissemination. In this respect they differ, for instance, from benignant neoplasms. The possibility is discussed to control neoplastic growth by adjusting an optimal pH difference between normal and tumour tissue by combined administration of detoxicated drugs which are converted to their toxic forms only in the tumour by means of strongly pH-dependent exogenous enzymes.
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PMID:[Origination and importance of glycolysis for malignomas and utilization of this property in the chemotherapy of cancer (author's transl)]. 0 18

The first case of germinal cell tumor of the testis in a patient with congenital total hemihypertrophy is reported. The literature is discussed with emphasis placed on the frequent association of hemihypertrophy with oncogenesis and teratogenesis. We conclude that because of the high incidence of malignancy in the undescended testis prophylactic orchiectomy should be considered in a patient with hemihypertrophy and cryptorchidism.
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PMID:Congenital total hemihypertrophy and carcinoma of undescended testicle: a case report. 1 34

Five cases of hepatocellular carcinoma in whom diagnosis was made when the tumor was relatively small, are described. In 2 cases, serum alpha-fetoprotein (AFP) strted to rise sharply, which enabled early detection and surgical removal of the tumor. Serum AFP was below 100 ng per ml, but above the upper normal limit by radioimmunoassay, and was unfluctuating for a considerable period of time before it began to rise in 2 cases. It was negative throughout in 1 case, who lived more than 4 years after the tumor had reached a detectable size. In 4 of 5 cases, the tumor seemed to have evolved during a stage of chronic hepatitis or its transition to cirrhosis. In 1 case with chronic schistosomiasis and advanced mixed macro- and micronodular cirrhosis, a 1.5-cm tumor was detected by celiac angiography. These observations on time relationship of oncogenesis may be generalized to modify the cirrhotic liver. Necessity is emphasized for the early detection of this type of carcinoma to monitor serum AFP in chronic hepatitis patients, particularly in those with unfluctuating, mildly abnormal levels of AFP.
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PMID:Clinical observations during a relatively early stage of hepatocellular carcinoma, with special reference to serum alpha-fetoprotein levels. 5 Feb 51

Specific cell-mediated immunity to SV40 tumor-specific transplantation antigen (TSTA) in BALB/c mice undergoing progressive tumorigenesis by syngeneic SV40-transformed cells (VLM) was investigated in vivo using a tumor-cell neutralization test. Specific cellular reactivity to SV40 TSTA was not detected in BALB/c mice bearing large tumors (10-15 mm mean diameter) but was demonstrable after tumor excision. Specific cytotoxic reactivity against syngeneic SV40-transformed cells in vivo could be restored to lymphoid cells from VLM tumor-bearing mice either by culturing the lymphoid cells in vitro or by treating them with papain or trypsin. Enzyme-treated lymphoid cells from MCA tumor-bearing BALB/c mice had no cytotoxic reactivity against VLM cells. These studies suggest that tumor-bearing hosts possess lymphocytes which are sensitized to the TSTA of the tumor but that the reactivity of these lymphocytes is blocked.
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PMID:Restoration of specific immunity against SV40 tumor-specific transplantation antigen to lymphoid cells from tumor-bearing mice. 5 Oct 12

Blood group ABH determinants in human erythrocytes are carried by four kinds of glycolipid carbohydrate chains, differing in their structural complexity. They are Aa, Ab, Ac, and Ad for A variants, and H1, H2, H3, and H4 for H variants (Table I and Fig 1). Based on the surface labeling of A variants and on the reactivity of erythrocytes to antibodies directed against H3 and against its degradation products, it is concluded that complex variants of A or H determinants (Ac and Ad/or H3 and H4) are absent or significantly low in fetal erythrocytes (80-150 days after gestation) and in new born erythrocytes, whereas these complex structures are fully developed in adult erythrocytes. In contrast, A determinants linked to simpler carbohydrate chains (Aa, Ab variants) are fully developed before birth and do not show significant change after birth. The precursor of blood group carbohydrate chains seems to be abundant in fetal or newborn erythrocytes. This assumption is based on the higher reactivity of fetal or newborn erythrocytes to an antibody, which is directed against the precursor N-acetylglucosaminly beta1 leads to 3 galactosyl beta1 leads to 4 glucosylceramide than in adult erythorocytes. Reactions of glycolipids of gastrointestinal mucosa, with antibodies directed against H3 glycolipid and its degradation products, were compared to that of gastrointestinal tumors. The reaction to bela Glc NAc1 leads to 3 beta Gall leads to 4 Glc leads to ceramide (structure 4), which is the precursor of all blood group glycolipids, was consistently high in many cases of tumor glycolipid than that of normal glycolipid. This as well as other evidence supports a general concept that the process of ontogenesis of a blood group carbohydrate chain occurs as step-by-step elongation and arborization, and that blocking of such a development of a carbohydrate chain occurs in the process of oncogenesis.
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PMID:Status of blood group carbohydrate chains in ontogenesis and in oncogenesis. 6 Apr 62

"Fingerprints" of 0.9% NaCl solution extracts obtained from fetal guts and individual adenocarcinoma of the colon show a randomized pattern of expression of carcinoembryonic antigen (CEA) determinants by CEA radioimmunoassay and isoelectric focusing. All CEA-containing antigens found in a pool of 20 primary adenomas were found at some stage in fetal development. No single CEA-reacting peak was typical of any one period of fetal development. When fetal gut profiles were grouped according to trimester in utero, however, an expanded gene pool was found in the second trimester which correlates well with maximum gastrointestinal growth and differentiation. Isoelectric focusing-CEA radioimmunoassay profiles of individual primary adenomas were similar to but never identical with individual fetal gut profiles. "Fingerprints" of metastatic adenomas of entodermal origin showed quantitative and qualitative increases in molecules with CEA determinants unlike these latter categories. Such data suggest that both integrator and controller gene activities may be lost in metastatic disease. Rather than "phase-specific gene sets" on different chromosomes being activated by various oncogenic modalities, it is more probable that individual chromosomes are involved in oncogenesis. While more data are needed to confirm this idea, it is safe to say that the expression of molecules with CEA determinants need not be caused by either derepressive or reexpressive gene activation. These data point to the individuality of gene expression of molecules with CEA determinants both in fetal development and in early neoplasia. Since CEA-reacting molecules were not found in tumors of ectodermal or mesodermal origin by these methods, such products should be termed carcino-developmental antigens of entodermal or colonic origin.
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PMID:Gene activation of molecules with carcinoembryonic antigen determinants in fetal development and in adenocarcinoma of the colon. 6 12

Problems relating to immunoselection of neoplastic, in particular leukemic, cell lines are reviewed. Since there is ample evidence that specific immune reactions of the host against malignant neoplastic cells do occur, it becomes important to consider the effectiveness and the relevance of immunity in suppression or elimination of neoplastic growth. Emphasis is placed on experimental results obtained in syngeneic tumor-host combinations, because they more closely resemble the situation of spontaneous tumorigenesis or leukemogenesis than xenogeneic or allogeneic model systems. Studies of types of neoplasia observed in cases of human immunodeficiency syndromes offer an important insight into problems involved in immunoselection of leukemic cell lines: the marked predominance of leukemias and lymphoreticular neoplasias in immunodeficient patients invites speculation on both the mechanisms of leukemogenesis and the relative importance of the immune system in eliminating malignant neoplastic cells.
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PMID:Problems relating to immunoselection of leukemias. 6 43

This article concerns the molecular mechanisms by which RNA tumor viruses, commonly called as oncornaviruses, transfer their genetic information from the genomic RNA (70 s RNA) of the virions to the cellular DNA, leading to neoplastic transformations. The article describes biochemical and serological properties of reverse transcriptase, its role in the life cycle of RNA tumor viruses and broader implications to molecular biology. In this connection, the authors report their own findings on the role of reverse transcriptase in a preleukemic disease, myelofibrosis. This enzyme, discovered in their laboratory, is antigenically closely related to reverse transcriptase of certain primate RNA tumor viruses, and of human leukemic cells. The article also describes the role of reverse transcriptase inhibitors in viral oncogenesis. Of particular interest, is the partially thiolated polycytidylic acid (MPC) which has been developed by the authors, and is known to have a very high binding affinity to the viral reverse transcriptase. The implication of these basic data on the clinical effectivity of MPC in human leukemia, documented in a few cases, has been discussed.
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PMID:[Molecular biological aspects of oncogenesis caused by RNA tumor viruses (author's transl)]. 7 88

A study on the experimentally induced yolk sac tumor in the rat was made in special regard to the characteristics and origin of tumor cells. Pregnant rats which fetuses were removed on the 12th day of gestation, developed tumors derived from the fetal membranes left outside the uterus, which were composed of differentiated teratomas and yolk sac tumors. Serial observation of the oncogenesis revealed that an early lesion of the yolk sac tumor appeared in a nodule found as early as 3 weeks after the fetectomy and production of alpha-phetoprotein (AFP) was observed histochemically in the tumor cells 5 weeks after the fetectomy. A cultured cell line established after cloning from the transplantable yolk sac tumor which had been induced similarly and converted into ascitic form was also investigated. Light and electron microscopic studies on both induced tumors and the cultured cells indicated a similarity of AFP producing tumor cells with parietal yolk sac cells and of PAS-positive hyaline-like substance with the Reichert membrane. It is reasonable to conclude that the yolk sac tumor observed is regarded as a parietal yolk sac carcinoma described by Pierce. Histogenesis of the tumor is also discussed.
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PMID:[Experimental yolk sac tumors in the rat (author's transl)]. 8 66

The abilities of the racemic trans-3,4-, 5,6-, and 8,9-dihydrodiols of 7,12-dimethylbenz(a)anthracene to initiate skin tumors in mice were determined by using a two-stage system of tumorigenesis. The 7,12-dimethylbenz(a)anthracene trans-3,4-dihydrodiol was found to be much more active as a tumor initiator than the parent hydrocarbon. The 7,12-dimethylbenz(a)anthracene trans-5,6- and 8,9-dihydrodiols were essentially inactive as skin tumor initiators. Our results suggest that the 3,4-dihydrodiol of 7,12-dimethylbenz(a)anthracene is a proximal carcinogen and that the "bay region" diol-epoxide may be the ultimate carcinogenic form of DMBA.
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PMID:Potent tumor-initiating activity of the 3,4-dihydrodiol of 7,12-dimethylbenz(a)anthracene in mouse skin. 10 89


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