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)

The origination and development of cervical cancer occurs in the tumor field, which includes cellular and non-cellular components of the connective tissue and vessels adjacent to the epithelium. During each of these phases of cancer growth alterations in these components may be observed within certain boundaries which widen with the tumor progression. A removal of the neoplasm within the limits of the unchanged, as compared with the normality, components of the stroma and vessels would guarantee against the recurrence and is a reliable criterion of the radicality of surgery being a minimum for preinvasive and microinvasive cancer. The data obtained support the fact of a sufficiently full coincidence of the rate of stromal and vascular changes with the true boundaries of the tumor field.
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PMID:[Morphogenesis of cervical cancer]. 42

Twenty patients previously treated with surgical resection, radiation therapy, and a nitrosourea for malignant gliomas of the brain were given VM-26 as a second chemotherapeutic agent when evidence of tumor progression occurred. Thirty-five percent achieved an arrest or decrease of neurologic symptoms, with a median length of response (arrest and tumor regression) of 22 weeks.
Cancer Treat Rep 1979 Mar
PMID:VM-26 as a second drug in the treatment of brain gliomas. 42 30

The predictive value of serial levels of carcinoembryonic antigen (CEA) in tumor monitoring was examined in 213 patients with ovarian cancer; each patient had been followed-up at monthly intervals for at least 12 months. CEA was not detectable throughout the period of observation in 35% of the patients. In general. patterns showing a disappearance of CEA or persistently low levels were associated with a good prognosis, whereas those showing a reappearance or highly elevated and rising levels were associated with a poor prognosis. A transient reappearance of CEA was observed in 10 patients; this did not appear to be associated with tumor recurrence or progression. "False positive" results were obtained in 6 patients in whom no tumor has been clinically detectable to date. "False negative" results were obtained in 4 patients with obvious tumor progression. In terms of a good or poor prognosis, the use of CEA levels was highly accurate in patients with minimal or no residual disease (97% and 89%, respectively); the rate fell to 62% in patients with extensive disease. As the clinical significance and limitations become better known, serial CEA levels should contribute substantially to the monitoring of patients with ovarian cancer.
Cancer 1979 Jun
PMID:Predictive value of serial carcinoembryonic antigen levels in long-term follow-up of ovarian cancer. 45 31

Antibodies to formalin-fixed, syngeneic melanoma cells were prepared in mice, purified by immunoaffinity chromatography, and tested for binding activity to viable melanoma cells. The radiolabeled antibodies detected congruent to 9 X 10(6) melanoma antigenic sites/cell. The calculated average association constant (Ka) for the antibody population was 7 to 10 X 10(7) M-1. The antibody was shown to block the binding of melanocyte-stimulating hormone in competitive cell surface binding studies. Results are discussed conceptually in terms of the potentially important role that the humoral immune response may play in the phenomenon of tumor progression.
Cancer Res 1979 Aug
PMID:Immunological block to synthetic alpha-melanocyte-stimulating hormone: melanocyte interaction by antibodies isolated from cell-column immunoadsorbents. 45 90

Crown-gall transformation involves the gradual and progressive activation of several biosynthetic capacities of the normal cell. These changes in cellular heredity, although extremely stable, are nonetheless potentially reversible and leave the cell totipotent. There is growing evidence that tumor-inducing principle is a self-replicating entity similar to a plasmid. Thus, it could be argued that tumor progression involves changes in the number or state of these entities in the cell. Studies of CDF habituation bear directly on this problem. Conversion of a cell division factor (CDF)-requiring normal cell to the CDF-autotrophic state is a key event in transformation. The fact that CDF habituation is progressive, occurs in the absence of agents of bacterial origin, and has an epigenetic basis indicates that it is not necessary to invoke either somatic mutation or the addition of foreign genes to account for tumor stability and progression in crown-gall. This conclusion provides further support for the hypothesis that, in the words of Braun,(78) "... the cancer problem is basically a problem of anomolous differentiation... Neoplastic growth, like developmental processes, stems from epigenetic modifications against a constant cellular genome."
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PMID:Reversal of the neoplastic state in plants. 59 24

In 137 patients with different kinds of cancer and different cancer stage, cell-mediated immunity was investigated by DNCB (dinitrochlorobenzene) and tuberculin test. These two skin tests were performed before and after cytostatic drug combination therapy. For a collective of cancer patients we found a positive correlation between skin reactions and prognosis and a negative correlation between skin reactions and cancer stage. After cytostatic drug therapy skin reactions could be significantly stronger. This could be observed in 50% when one test was positive before chemotherapy and in only 20% when both tests were negative before chemotherapy. There existed a significant correlation between an increased reaction after cytostatic drug therapy and objective tumor regression. When skin reactions decreased, tumor progression was seen in all cases. Due to these observations we use skin reactions as a good parameter for therapy results. When delayed cutaneous hypersensitivity impairs 2--3 weeks after chemotherapy, we then change the cytostatic drug combination immediately. We cannot say at this moment, whether an improvement of cytostatic drug therapy can be reached in this way.
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PMID:Tuberculin and dinitrochlorobenzene (DNCB) tests in cancer patients before and after cytostatic drug therapy. 71 20

Cancer is a generic term for a variant manifestation of life caused by genetic mutations of somatic cells. It is not only carcinogenesis which is basically a genetic phenomenon, but also tumor progression which can be influenced by various genetic factors. A group of tumors is known to be inherited in a Mendelian fashion. In addition a great number of single gene disorders is associated with the development of maligne tumors. The further study of these diseases will allow new insights into the fundamental mechanisms leading to clinical cancer. In this respect a series of immunodeficiency diseases is of particular interest. Several organ tumors which seem to occur more frequently in relatives of tumor patients are of practical importance. A more sophisticated classification of these tumors may illuminate their genetic behavior. The geneticist cannot only define groups of individuals with a high cancer risk, but he can identify genetic, e.g. chromosomal, aberrations of cancerous cells which enables him the early detection of neoplasia.
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PMID:[Early diagnosis of neoplasms]. 72 76

In a longitudinal study performed before and after surgical resection of a chemically-induced, transplanted rat tumour we found that a monocytosis- and tumour-induced anti-inflammatory effect directed against macrophages was promptly corrected by tumour excision but recurred with metastasis. These observations indicate that the monocyte abnormalities are acquired and related to cancer progression. The anti-inflammatory effect required relatively large primary or metastatic tumour burdens. Our findings support the clinical impression that monocyte abnormalities are associated with a poor prognosis.
Int J Cancer 1979 Jan 15
PMID:Cancer progression and monocyte inflammatory dysfunction: relationship to tumour excision and metastasis. 75 76

Spontaneous reticulum cell sarcoma in SJL/J mice has been proposed as an animal tumor model for Hodgkin's lymphoma. The relationship of tumor progression and immune function is not clear, however, and has prompted a systematic evaluation of SJL/J immune competence. It was found that the ability to generate cell-mediated immunity and antibody response to allografts was not impaired in 2- to 12-month-old mice, regardless of their tumor status. All animals were capable of generating in vivo cytotoxic effector T-cells and both IgG and IgM classes of cytotoxic antibody to a tumor allograft. In addition to being able to respond, older mice showed an unexpected hyperresponsiveness to alloantigens, which suggested that escape from feedback control might be a characteristic of SJL/J mice. Loss of immune regulation was further indicated by the failure to induce tolerance to human gamma-globulin in mice 4 months and older, while 3-week-old SJL/J mice could be rendered unresponsive. Coincident with this apparent loss of regulation, circulating antibodies to synthetic double-stranded RNA, polyinosinis - polycytidylic acid, were first detected in unimmunized mice at 4 months of age, and titers remained elevated regardless of tumor status. It is suggested that tumor development as well as autoimmunity may result from an effective amplification of the immune response.
Cancer Res 1976 Mar
PMID:Immune functions characteristic of SJL/J mice and their association with age and spontaneous reticulum cell sarcoma. 76 61

Histaminase has been shown to be associated with several types of human cancer. In the present study, we examined the activity of histaminase and its relationship with Regan isoenzyme of alkaline phosphatase in ascitic fluids obtained from patients with ovarian and several other types of cancer. We have found that about 44% of the ovarian cancer patients had elevated levels of histaminase in the ascitic fluid, whereas a less frequent incidence was observed in fluids obtained from other types of cancer. There was concurrence in the elevation of histaminase activity with the appearance of Regan isoenzyme in most of the samples examined. Of the 10 patients who showed elevated histaminase, 9 had high Regan isoenzyme activity; whereas in 9 patients with normal levels of histaminase, all except 1 had low or moderate levels of Regan isoenzyme activity. These results, therefore, confirm the observation of an association of histaminase with human cancer and suggest the possibility for the utilization of histaminase, in conjunction with Regan isoenzyme and cancer-associated proteins, for cancer diagnosis and clinical evaluation of tumor progression and regression during therapy.
Cancer Res 1975 Oct
PMID:Elevation of histaminase and its concurrence with Regan isoenzyme in ovarian cancer. 80 68


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