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 R3327-H model of prostatic adenocarcinoma was employed for the study of the cellular changes that occur during induction, regression, and recurrence of prostate cancer after endocrine therapy. The present study was designed to compare the glandular and stromal elements of the relapse phase with the histologically distinct early and intermediate phases of tumor progression. Morphometric analysis revealed significant differences between all three groups in the percentages of total tumor occupied by the epithelial component. At all three time periods, high-power inspection of autoradiograms prepared after incubation of the tissues with radioactive dihydrotestosterone revealed large cells in the stroma, especially in the intermediate phase. Immunohistochemistry further revealed evidence of invasion across the prostatic acinar basement membranes by similar cells. These studies lead the authors to postulate a mechanism by which hormone-independent cells in the epithelium repopulate the stroma, causing a recapitulation of the original morphology of the tumor in the postremission period. They propose that prostate tumor response to estrogen therapy can be operationally defined in three phases: involution, rebound, and relapse. They infer that further knowledge of the timing of these phases may permit early selective use of specific therapeutic strategies which will be able to balance the clinical risk with the known behavior of the neoplasm during progression of the disease.
Am J Pathol 1987 Sep
PMID:Analysis of changes in rat prostate carcinoma following hormone deprivation. 330 45

Two novel monoclonal antibodies, KL-3 (IgM) and KL-6 (IgG1), which can detect soluble antigens in sera and effusions (molecular weights greater than 1,000 K) were produced against human pulmonary adenocarcinoma VMRC-LCR cells. KL-3 and KL-6 antibodies reacted with asialo- and sialo-carbohydrate antigenic determinants, respectively. Both carbohydrate epitopes appear, from competitive inhibition studies, to be different from Lex, Ley, sialyl Lea and sialyl Lexi which were recognized with FH2, AH6, NS19-9 and FH6 antibodies, respectively. Using an enzyme linked immunosorbent assay, elevated KL-6 antigen levels were frequently observed in the sera of patients with lung adenocarcinoma [52% (17/33)], pancreatic cancer [44% (4/9)] and breast cancer [40% (8/20)], but infrequently in the sera of patients with lung squamous cell carcinoma [18% (4/22)], lung small cell carcinoma [8% (1/13)], gastric cancer [0% (0/19)], colorectal cancer [0% (0/8)] and hepatocellular cancer [13% (1/8)]. The levels and positive rates of serum KL-6 antigen increased with the progression of clinical stage of lung adenocarcinoma. In pleural effusions, the prevalences of lung adenocarcinoma cases with elevated levels of KL-3 and KL-6 antigens were 76% (13/17) and 82% (14/17), respectively. These monoclonal antibodies can define novel soluble antigens in sera and effusions which could be useful in tumor diagnoses and for monitoring tumor progression.
Jpn J Clin Oncol 1988 Sep
PMID:Detection of soluble tumor-associated antigens in sera and effusions using novel monoclonal antibodies, KL-3 and KL-6, against lung adenocarcinoma. 341 86

Oncogene amplification has been observed in various primary tumors and tumor-derived cell lines. In several types of cancer, amplification of specific oncogenes is correlated with the stage of tumor progression. To estimate the frequency of gene amplification in other tumor types and to determine whether the ability to grow in vivo is associated with gene amplification in tumor cell lines, we have developed a modified version of the in-gel renaturation assay that detects human DNA sequences of unknown nature amplified as little as 7- to 8-fold. This assay was used to screen 16 cell lines derived from various solid tumors and leukemias. Amplified DNA sequences were detected in only one cell line, Calu-3 lung adenocarcinoma. This cell line was found to contain coamplified NGL (formerly termed neu) and ERBA1 oncogenes. However, when one of the amplification-negative cell lines, PC-3 prostatic carcinoma, was selected for in vivo growth in nude mice, amplified DNA sequences became detectable in these cells. The amplified sequences included the MYC oncogene, which showed no amplification in the parental cell line but was amplified 10- to 12-fold in the in vivo-selected cells. MYC amplification may, therefore, provide tumor cells with a selective advantage specific for in vivo growth.
Proc Natl Acad Sci U S A 1988 Sep
PMID:Analysis of gene amplification in human tumor cell lines. 341 26

In Columbus, OH, 46 patients with measurable metastatic colorectal cancer were treated with leucovorin (LV) 80 mg/m2/20 h intravenous (IV) infusion followed by 5-fluorouracil (5-FU) 400 mg/m2 IV bolus daily for three days and then once weekly. Many patients had liver (62%) and/or multisite metastases (53%), carcinoembryonic antigen (CEA) greater than 10 (76%), documented tumor progression before entry (51%), and tumor-related symptoms (36%), but also good performance status (84%). Prior therapy consisted of radiotherapy (RT) in 18%, chemotherapy in 22%, both in 4%, and none in 56%. There were 36% objective responses and 31% stabilization, which we believe is a significant change in the natural history of these patients. Median survival was 8 months. Improved survival was seen in patients with single- rather than multiple-site involvement. Decreasing CEA levels were seen in 59% (always in responders or patients with stable disease), and correlated with longer survival time (11.0 v 5.5 months, P = 0.01). Palliation of tumor related symptoms occurred in 75%, with or without antitumor effect. One patient with prior RT died of neutropenic sepsis after only the three-day load, so we now recommend only weekly therapy in previously radiated patients. Otherwise, toxicity was mild, manifest as weakness in 62%, nausea in 53%, or diarrhea in 47%, which was the most common dose-limiting side effect. The occurrence or absence of toxicity did not predict outcome. Because of equivalent efficacy, mild toxicity, and less expense, this regimen should be considered for patients who desire therapy.
J Clin Oncol 1987 Sep
PMID:Leucovorin plus 5-fluorouracil: an effective treatment for metastatic colon cancer. 349 15

Radioimmunoscintigraphy is presented as a new imaging modality in nuclear medicine, using specific antigen-antibody interactions. Monoclonal antibodies to tumor-associated antigens facilitate the characterization of molecular differences between tumors and normal cells. Labelled with gamma-emitting radioisotopes like I-131, I-123, In-111, and Tc99M, these antibodies can be used for in-vivo imaging. Radioimmunoscintigraphy does not compete with morphological modalities like CT and ultrasound, but provides additional information based on its functional principle. Hidden lesions may be detected. Target-to-background ratios, however, are still rather low hampering scintigraphic imaging. The use of Single Photon Emissions Computed Tomography (SPECT) in addition to planar scintigraphy resolves background activities thus providing better visualization and localization of tumors, and increasing sensitivity. The high cost of these time-consuming studies is still a limiting factor to its wider use. Its preliminary indication is founded on the suspicion of tumor progression, based on clinical findings and/or increasing serum tumor markers (CEA, CA 19-9, CA 12-5). This paper provides an overview over possible applications of radioimmunoscintigraphy. Its clinical use is demonstrated by studies of malignant melanoma, colorectal cancer and ovarian cancer.
Digitale Bilddiagn 1987 Sep
PMID:[Radioimmunoscintigraphy with monoclonal antibodies]. 350 11

We tested the hypothesis that highly malignant cell lines are genomically more unstable than their less malignant counterparts, and that this instability is more pronounced in clones than in cell lines. We compared MDAY-D2 to its non-metastatic variant, D36W25, with regard to (1) the rate of development of ouabain resistance within parallel clones and (2) the prevalence of G-banded karyotypic abnormalities. We detected no significant difference between the spontaneous mutation rates for ouabain resistance. However, the MDAY-D2 cell line possessed both a higher prevalence and greater diversity of chromosomal abnormalities. One possible explanation for these seemingly inconsistent results is that genomic instability may remain essentially constant throughout tumor progression, whereas an accumulation of genetic changes may be responsible for the observed increased prevalence of abnormalities and the development of selective survival advantages during progression.
Int J Cancer 1987 Sep 15
PMID:Spontaneous mutation rates in cloned murine tumors do not correlate with metastatic potential, whereas the prevalence of karyotypic abnormalities in the parental tumors does. 362 19

From the third year after its clinical diagnosis and onward the cancer hazard rate continuously declines. This phenomenon is common to all cancers irrespective of stage, and far less pronounced in other chronic diseases. It is so typical of cancer as to be regarded as a "law of the improving chances of the cancer patient". Although the cancer hazard rate itself is higher than in most other chronic diseases, it always declines while in other chronic diseases it rises. Two kinds of processes operate in cancer: a noxa and host resistance. Throughout cancer progression the organism maintains a delicate equilibrium with the noxa, only its reserves are continuously depleted and when exhausted the noxa overpowers the host's resistance and the patient dies. The hazard rate is inversely proportional to the patient's reserve. Its decline indicates that the host resists the noxa better and better, since however his reserves are limited, he ultimatelly succumbs to it. This phenomenon also shapes cancer age specific incidence and mortality rates. From the age of 15 years and onward the curves ascend in an exponential fashion, gradually tapering off, which is viewed here as a token of a mounting resistance of the organism to the carcinogenic noxa. Host resistance operates also during tumor growth, accounting for the Gompertzian shape of its growth curve. The growth rate of most human tumors progressively decreases and is therefore best described by the Gompertz function which initially rises in an exponential fashion and gradually tapers off. Tumor size and growth rate indirectly reflect the host's condition or reserve. The two tumor attributes are related to the hazard rate in the following manner: Tumor size is proportional to the hazard rate, indicating host reserve. Tumor growth rate is proportional to the hazard rate change, indicating host resistance. Both indicators may be estimated independently and applied to the assessment of the host's reserve and resistance during cancer progression.
Med Hypotheses 1985 Sep
PMID:The estimation of host-resistance in cancer. 406 38

There were 122 deaths among 803 children registered, randomized, and followed in the second National Wilms' Tumor Study; 17 occurred in children apparently free of disease and were attributable to causes other than tumor progression. Seven deaths were attributed to infection during periods of drug-induced leukopenia; four were due to liver failure; and one each was attributable to radiation pneumonopathy, intestinal obstruction, renal failure, myocardial disease, and encephalopathy. The cause of one death was unexplained. Of particular concern were four (of 47) infants under one year of age with group I or II disease who had toxic deaths. Subsequent to these experiences the doses of all chemotherapeutic agents were reduced by 50% for infants under one year of age. No deaths from toxicity were observed thereafter in infants. An analysis of the therapeutic effect of this dose reduction showed three of 47 relapsed on full dose and five of 54 on half dose. The difference is not statistically significant. This report is a further demonstration of the potentially serious vulnerability of infants to standard doses of anticancer drugs even when they are calculated on a per kilogram basis.
J Clin Oncol 1984 Sep
PMID:Toxic deaths in the Second National Wilms' Tumor Study. 608 9

Multiple daily fractionated radiation therapy (MDF) may be more effective than conventionally fractionated radiation therapy (CF) in the treatment of malignant glioma. The hypoxic cell sensitizer misonidazole (MISO) could be more effective when employed with small fractions of radiation every 4 hours to take advantage of the long half-life of the drug. To evaluate MDF and MDF in combination with MISO, a randomized prospective trial was initiated. Between January 1981, and December 1982, patients with histologically verified astrocytoma with anaplastic foci or glioblastoma multiforme were randomized to CF (5800 cGy, 30 fractions, 6 weeks), MDF (6141 cGy, 69 fractions, 4 1/2 weeks, at 89 cGy every 4 hours 3 times daily) and MDF in combination with MISO (1.25 gm/M2 three times weekly for the first 3 weeks). In January 1983, the CF arm was dropped and a high dose MDF arm added (7120 cGy, 80 fractions, 5 1/2 weeks, at 89 cGy per fraction every 4 hours 3 times daily). CCNU chemotherapy was given at the time of tumor progression. One hundred and twenty-eight patients were evaluated (38 CF, 42 MDF, 37 MDF plus MISO, and 11 high dose MDF). Median survival was 29 weeks for CF, 45 weeks for MDF and 50 weeks for MDF plus MISO. Survival was significantly improved for patients treated with MDF compared to patients treated with CF (p less than .002). The addition of MISO to MDF did not result in further improvement in survival. Acute toxicity was acceptable. No clinically apparent delayed toxicity was observed.
Int J Radiat Oncol Biol Phys 1984 Sep
PMID:Misonidazole combined with hyperfractionation in the management of malignant glioma. 609 Mar 67

Cultures of skin fibroblasts (SF) from individuals with hereditary adenomatosis of the colon and rectum (ACR) and from normal individuals were exposed to 12-O-tetradecanoyl phorbol-13-acetate (TPA) (0.5-100 ng/ml), and epidermal growth factor (EGF) (0.01-10.0 ng/ml) at both low and high cell densities. Cell proliferation of low density cultures (4.75 x 10(3) cells/cm2) was inhibited by TPA, while cell proliferation of high density cultures (6 x 10(4) cells/cm2) was stimulated by TPA. EGF was mitogenic at both cell densities of normal and ACR-SF cultures. TPA and EGF each produced characteristic changes in the morphology of ACR-SF colonies. These results suggest that EGF and TPA may share only 1 class of receptors, and that TPA may be used to monitor cancer progression.
Cancer Lett 1981 Sep
PMID:Effects of 12-O-tetradecanoyl phorbol-13-acetate and epidermal growth factor on the proliferation of human mutant fibroblasts in vitro. 611 6


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