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At least 703 records · Page 39Linked to original sources
PubMed1991

Variations in centromeric heterochromatin among patients with pre-malignant and malignant oral diseases.

Polymorphism of heterochromatic regions of chromosomes 1, 9 and 16 was studied in 60 oral cancer patients, in 40 patients with oral submucous fibrosis (OSMF) and in 60 normal healthy subjects. The size heteromorphism was significantly greater (p less than 0.001) in chromosome I of the patients. Localization variants were also significantly more frequent among the patients (p less than 0.05 for OSMF and less than 0.001 for oral cancer patients). The C-band heteromorphism patterns remained comparable in OSMF and in oral cancer patients, with chromosome I being the most frequently involved. On correlating the tobacco/areca-nut chewing habit with the presence of C-band heteromorphism, we observed that C-band heteromorphism was present in 89% of the habit-free oral cancer patients and 80% of the OSMF patients with relatively shorter exposure to this habit, i.e. less than 5 years. This signifies that genetic factors are important in the causation of oral precancerous and cancerous conditions and that polymorphism of the heterochromatic regions does appear to play a role in these conditions.

Adult↗
PubMed1979

Expression of malignancy in hybrids between normal and malignant cells.

Somatic cell hybrids between either normal human fibroblasts, phenotypically normal mouse fibroblasts or mouse peritoneal macrophages and HT1080 human diploid fibrosarcoma cells were studied for their ability to form tumors in nude mice. The results of this study indicate that tumorigenic behavior is expressed as a dominant trait in both human-human and mouse-human hybrid cells.

Animals↗
PubMedDate not supplied

Immunomagnetic separation and analysis of non-malignant variants and parental malignant mouse lymphoma cells.

We have devised conditions whereby non-tumorigenic, immunogenic cell variants of S49 mouse lymphoma were analyzed and separated from parental tumorigenic lymphoma cells. This was carried out using polyclonal antibodies (raised against the immunogenic variants) and immunomagnetic beads. The efficacy of the procedure depended on the amount of polyclonal antiserum, the immunobead to cell ratio, incubation time and the number of repetitions of the procedure. Experiments with mixed tumorigenic and non-tumorigenic cells have resulted in an enrichment of up to 200-fold of the non-tumorigenic, immunogenic cells in the population. These findings indicate the potential use of this procedure (in conjunction with other approaches) to isolate from a population of tumorigenic cells those variant cells that might be used to immunize against the parental tumor.

Animals↗
PubMed2004

Expression of PTEN in malignant and non-malignant human prostate tissues: comparison with p27 protein expression.

The role of the putative tumour suppressor PTEN in prostate carcinogenesis is controversial. There are conflicting data regarding the rate of its gene inactivation, the role of transcriptional and post-transcriptional factors, as well as its relationship to tumour progression and to the potential downstream regulator, the cell-cycle inhibitor p27. The present study has assessed the in situ expression of PTEN mRNA and protein in 26 prostate intraepithelial neoplasias (PINs), 58 primary prostate carcinomas, and 15 metastases. Although there was a correlation between PTEN mRNA and protein expression, mRNA detection exceeded detection of protein in 19% of PINs and 30% of all invasive tumours. Using RT-PCR and western blotting on microdissected tissue, this discrepancy was attributed, at least in part, to transcription of the PTEN pseudo-gene, which lacks introns. Total or partial loss of PTEN protein occurred with tumour progression but this association was not statistically significant. Analysing the relationship between PTEN and p27 protein expression on consecutive sections by immunohistochemistry, the results do not support a direct link between the two oncosuppressors, other than an associated loss of expression in advanced tumour stages. However, in the basal cells of prostate glands and in most PINs, an inverse relationship was observed between PTEN and p27. This may reflect the existence of a functional balance that controls the cell cycle in prostatic epithelium and that is probably disturbed in invasive tumour cells.

Adenocarcinoma↗
PubMed1987

Expression of c-myc in non-malignant and pre-malignant gastrointestinal disorders.

A monoclonal antibody 1-6E10 against the protein product p62c-myc of the c-myc oncogene was used to assess, by immunohistology, a variety of non-neoplastic and preneoplastic disorders of gastric and colonic mucosa. There were low levels of expression of the c-myc oncogenic product in normal gastric and colonic tissue. In gastric mucosa, increased expression was observed with inflammatory, metaplastic and dysplastic histological appearances. In the normal colon low levels of expression were observed, but there was increased expression in inflammatory disorders including Crohn's disease and ulcerative colitis. There was also increased expression in colonic dysplasia associated with ulcerative colitis. The oncogene product was localized in the cytoplasm, nuclei and Golgi apparatus. C-myc 1-6E10 may therefore be used as a marker to identify the cellular proliferative response in gastric and colonic mucosa that is associated with inflammation as well as potentially neoplastic hyperproliferative states.

Antibodies, Monoclonal↗
PubMed1995

Malignant progression of B16 melanoma cells induced in vitro by growth factors produced by highly malignant cells.

Four mouse B16 melanoma subclones (G3.15, G3.5, G3.12 and G3.26) exhibit progressively greater growth capacity in vitro and in vivo. Previously, non-metastatic G3.15 cells were sequentially converted, in monolayer cultures, to the moderately-metastatic G3.5 cells, and then to a highly-metastatic G3.5* phenotype. Both conversions were induced by hypoxia followed by confluence, and also occurred in tumors. G3.5* cells were comparable with, yet distinguishable from, G3.12 cells in being growth-autonomous in culture. In this study, the presumption that rapidly-growing G3.26 cells represented the ultimate progression step in this clonal system was examined. Both G3.12 and G3.5* cells converted in vitro to the G3.26 phenotype during growth in serum-free medium conditioned by G3.26 cell growth. By selective filtration of conditioned medium and characterization of the stability of growth- and conversion-promoting activities, three distinct activities were found to promote a two-step G3.12 to G3.26 phenotype conversion: (1) a < 10 kDa filtrate stimulated slight attachment and proliferation of G3.12 cells, effects that were reversible, partly attributable to accumulated lactate, and fully mimicked by medium acidification to pH 6.5; (2) medium acidification, together with a heat- and acid-stable but partially trypsin-sensitive > 10 kDa activity, induced G3.12-->G3.5* conversion that resulted in acquisition of growth autonomy; and (3) a heat-, acid- and trypsin-sensitive > 10 kDa activity induced G3.5*-->G3.26 conversion, characterized by anchorage-independent growth in soft agar, and potent lung colonization following intravenous injection. Phenotype analysis of G3.12 tumors and lung metastases revealed that G3.5*-like cells were regularly present in tumors and metastases, whereas G3.26-like cells occurred almost exclusively in large lung metastases. While G3.12 cells might convert to G3.5* cells in order to disseminate, G3.26 cells are apparently not involved in metastatic spread but probably account for the rapid growth of established metastases.

Animals↗
PubMed1987

Human non-malignant and malignant brain tumor derived cell cultures: proliferation and sensitivity to natural human fibroblast (beta) interferon.

Twenty-one human brain tumor biopsies were processed by mechanical and enzymatic methods to produce mixed cell suspensions. Cultures were prepared in small plastic flasks, and primary outgrowth occurred in 16/21 cultures. The period required for primary outgrowth ranged from 3 days to 14 days. We established serial propagation with 15/16 of the primary cultures. Sensitivity to HuIFN-beta was determined between passages 3 to 12, using a microassay based on cell viability (uptake of a supravital stain, neutral red). Extracted dye was quantified in acidic-methanol using the MR580 Microelisa Autoreader (Dynatech). We observed a broad range of responsiveness to the drug among the 12 cell-strains tested. Thus, 4 cell strains were relatively sensitive; 4 were resistant to 10(4) IRU/ml of purified HuIFN-beta. Four cell strains exhibited a level of responsiveness that was intermediate to that of these two groups. During propagation of these biopsies, cytopathology suggestive of paramyxovirus-infection appeared in 4 of the cell-strains. This characteristic was not uniformly associated with high sensitivity to human beta interferon which is a very potent, naturally occurring antiviral substance. Our results support the concept that information concerning sensitivity to HuIFN-beta and other cytostatic agents may be rapidly obtained using microcultures of brain tumor cultures in conjunction with supravital stain uptake studies. Additionally, these results suggest that further clinical studies with beta interferon should be undertaken to define the parameters which determine successful in vivo application.

Astrocytoma↗