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Biomedical subjects

B Jandrig

Publications and source records attributed to B Jandrig.

30 records · Page 2Linked to original sources
PubMed1996

A defined chromosome 6q fragment (at D6S310) harbors a putative tumor suppressor gene for breast cancer.

Recent evidence obtained by cytogenetic and molecular studies indicates that in breast cancer chromosome 6q is often affected by genetic changes suggesting the existence of putative tumor suppressor genes (TSGs). However the function of gene(s) on this chromosome in breast cancer suppression is not understood. To substantiate further the presence of breast cancer related TSGs at 6q and to define their location, we first performed microcell-mediated transfer of chromosome 6 to CAL51 breast cancer cells for studying possible suppression of malignant phenotype and secondly, we analysed DNAs from 46 primary breast cancers for loss of constitutive heterozygosity (LOH) using 24 poly-morphic microsatellite markers. The chromosome transfer resulted in loss of tumorigenicity and reversion of other neoplastic properties of the microcell hybrids. Polymorphism analysis of single hybrids revealed that they harbored only a small donor chromosome fragment defined by the marker D6S310 (6q23.3-q25) and flanked by D6S292 and D6S311. The LOH data suggest that four tumor suppressor gene loci mapped to the central and distal portion of 6q may be independently deleted in breast cancer. One of these regions corresponds to the region identified by chromosome transfer.

Breast Neoplasms↗
PubMed1996

Genomic structure and chromosomal localization of the human interleukin 15 gene (IL-15).

Interleukin 15 (IL-15) is a novel cytokine whose biological activities are similar to those of interleukin 2 (IL-2). The genomic sequence of human IL-15 has been isolated based on its sequence homology with a cDNA clone encoding human IL-15. The human sequence is 14968 bp in length and includes all six protein-coding exons and five introns. The location of the introns in the human sequence is identical to their positions in the murine IL-15 gene. The same is true for the overall size of the gene, which was estimated to be at least 32 kb. Using Polymerase Chain Reaction (PCR) with gene-specific primers on a panel of human/rodent hybrid cell DNAs, as well as by fluorescence in situ hybridization the human IL-15 gene was mapped to chromosome 4 region q25-35.

Amino Acid Sequence↗
PubMed1996

BRCA1 mutation update and analysis.

The discovery of the BRCA1 gene involved in the development of human hereditary breast cancer led to extensive international efforts to identify the mutations leading to the disease. The new listing covers 127 mutations published in the indicated papers before 30 April 1996; 55% of the mutations are localized in exon 11, followed by exons 2 (5.5%), 5 and 16 (4.7% each).

Exons↗
PubMed1996

Estradiol receptors and metastasis in human breast cancer.

The localization and extent of metastasis determined the prognosis of breast cancer in a decisive manner. Thereby axillary lymph node involvement represents one of the most important prognostic indicators. The estradiol receptor status is also attributed some prognostic importance. There might therefore be relations between these prognostic factors. However, the majority of investigators could not find a correlation between the extent and timing of regional lymph node involvement and estradiol receptor status. In contrast, there are numerous findings which confirm correlations between estradiol receptors and the localization, extent, and timing of distant metastasis. The findings obtained in more recent years have been collected and discussed in relation to events included in the process of metastasis such as release of proteases and existence of receptor variants.

Breast Neoplasms↗
PubMed1992

Membrane transport in multidrug resistance, development, and disease. AACR special conference in cancer research.

The main goal of this meeting was to provide the scientists and clinicians active in this field with a comprehensive overview of the progress that has been made. The meeting was a forum in which new advances in membrane transport were discussed in depth and which gave new impulses for clinical applied research. Again, the importance of intensive cooperation between basic research and clinical use became evident during this symposium.

Animals↗
PubMed1990

Amplification of oncogenes and disease prognosis.

Amplification is one mechanism for activation of oncogenes and results in an excess of DNA template, which can lead to overproduction of oncogene-specific RNA and protein. Amplification of oncogenes has been observed in different tumor tissues. In certain cases amplification and overexpression of particular oncogenes have been correlated with tumor progression and clinical behavior. The best example is neuroblastoma in which the N-myc oncogene frequently is found to be amplified. Over 1,000 patients with breast cancer have been studied for amplification of the c-erbB-2 oncogene until now. The evidence from the studies that amplification of c-erbB-2 is correlated with poor prognosis is in our opinion not convincing. More and more investigations about oncogenes and disease prognosis will take place rather at the protein level than at the DNA level.

Gene Amplification↗
PubMed1988

In vitro transformation of rat cells by 3-methylcholanthrene: activation of the ras oncogene.

Rat cells of the established, immortalized line rat-2 were treated with the polycyclic aromatic hydrocarbon 3-methylcholanthrene. No characteristic morphological transformation occurred during three weeks after treatment. However, the carcinogen-treated cells formed colonies in soft agar. Cell lines established from single soft agar colonies were characterized by an increased proliferation rate, an enhanced colony formation in soft agar and an increased expression of the Ha-ras oncogene.

Animals↗
PubMed1988

Activated fos oncogene in rat embryo fibroblasts transformed by ras and myc oncogenes.

Rat embryo fibroblasts (REF) were transformed by simultaneous gene transfer of the complementary oncogenes ras and myc using the calcium phosphate coprecipitation method. Cell lines derived from transformation foci expressed in addition to ras and myc cellular oncogene fos while normal REF did not express ras, myc and fos according to the hybridization methods used. The transformed cell lines produced colonies in soft agar and tumors in newborn syngeneic rats. From one tumor a cell line was established which was characterized by a high level of fos gene expression.

Animals↗
PubMed1987

Transformation of rodent immortalized and embryo cells by oncogenes. I. Mouse (NIH 3T3) and rat (FR 3T3) immortalized fibroblasts.

Immortalized mouse NIH 3T3 cells were transformed by gene transfer of DNA isolated from a human bladder tumor cell line and plasmids containing an activated human Ha-ras oncogene insert. For gene transfer the calcium-phosphate co-precipitation method was used. Transformation was evaluated by morphological focus formation, growth in soft agar and tumor development in nude mice. In addition, immortalized rat FR 3T3 cells were transformed by Ha-ras, too. The co-transfer of ras and myc oncogenes did not enhance focus formation in FR 3T3 cells.

Animals↗
PubMed1987

Transformation of rodent immortalized and embryo cells by oncogenes. II. Rat embryo fibroblasts (REF).

Rat embryo fibroblasts were transformed by co-transfer of two plasmids carrying the oncogenes ras and myc, respectively. In contrast to immortalized cells gene transfer of ras alone was not sufficient for transformation of rat embryo cells. Embryo cells transformed by both oncogenes showed an altered morphology and produced colonies in soft agar. Cell lines were established from transformation foci. These cells are characterized by a high proliferation capacity, they expressed the oncogenes ras and myc and produced regressing tumors in syngeneic newborn rats. Oncogene expression was demonstrated by in situ and blot hybridization. A cell line was established from a rat tumor induced by oncogene transformed cells. This cell line, designated FTD5, showed in addition to an increased expression of the transferred oncogenes ras and myc an elevated expression of the cellular oncogene fos.

Animals↗
PubMedDate not supplied

Steroid hormone receptors related to parameters characterizing the biology of human breast cancer.

Steroid hormone receptors are important parameters to characterize breast tumors. Thus, it is important to evaluate their relationships with factors such as histological type and size of the tumor, axillary lymph node invasion and distant spread, age and menopausal status of the patients, and parameters of tumor differentiation. The receptor levels observed vary within wide ranges. Therefore, statistically significant differences between different groups of parameters are seldom found. A significant dependence on receptor levels has been observed only for patient age and menopausal status. The parameters clinical stage, tumor size, tumor histology, metastatic involvement and histopathologic grading showed no statistically significant relation with receptor levels. Nevertheless, a relationship exists between all parameters mentioned and the frequency of a positive receptor status. Consequently, receptor status can contribute to define the biological behavior of the disease in specific groups of patients. In individual cases other parameters than the biochemical evidence of steroid receptor binding seem to be more important. We found that data derived from DNA flow cytometric measurements allowed a better recognition of tumor aggressiveness than ER status. In axillary lymph node metastases we usually observed higher receptor levels than in primary tumors, but we did not find an age dependency of ER levels in these metastases.

Adult↗