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Biomedical subjects

D Birnbaum

Publications and source records attributed to D Birnbaum.

At least 253 records · Page 14Linked to original sources
PubMed1990

Biology of the fibroblast growth factor gene family.

The biology of the fibroblast growth factor (FGF) gene family is reviewed. The structure, expression and known and putative functions of the seven members of this family characterized to date are discussed. These genes include: acidic and basic FGF, the INT.2 and HST proto-oncogenes and the recently characterized FGF.5, FGF.6 and KGF genes. These genes play a role in various processes such as cell proliferation, angiogenesis and embryogenesis, and possibly carcinogenesis.

Animals↗
PubMed1990

[Extracorporeal circulation as a risk factor in heart surgery].

Extracorporeal circulation has a complex influence on the biology of the various organ systems. Knowledge of interactions with biomaterials and the resultant pathophysiological reactions is still very limited. The safety of the heart-lung machine lies, to a great extent, in the hands of the operator; precautions against breakdowns and accidents are necessary. The effects of the extracorporeal circulation process manifest themselves clinically as organ malfunctions. The risk is clearly associated with the age of the patient and the duration of the procedure. The fact that the extracorporeal circulation--and with it the heart operation--affects not just a single organ, but rather the entire organism, requires detailed knowledge of the general state of health of the patient to be operated upon. Only on this basis can the necessary individual operational strategies be developed.

Aged↗
PubMed1990

BCL-1 participates in the 11q13 amplification found in breast cancer.

In an attempt to probe the significance of HST and INT-2 gene amplification in human breast carcinomas, we have surveyed the amplification status of five molecular markers located on the long arm of chromosome 11 (BCL-1, HST, INT-2 & SEA on 11q13, and ETS-1 on 11q23) in a population of 297 mammary tumors. ETS-1 was rarely amplified and always independently from the other proto-oncogenes. Concerning band q13: (i) 50 tumors (approximately 17%) were co-amplified for BCL-1, HST & INT-2; (ii) in 3 cases, amplification extended to the SEA gene; (iii) in 6 carcinomas, BCL-1 was the only amplified marker. The fact that we never observed amplification of HST & INT-2 independently of BCL-1, which in turn can be amplified solely, suggests the presence, between HST/INT-2 and BCL-1, of a genetic element which could be important in the development of a subset of mammary tumors.

Breast Neoplasms↗
PubMed1990

[Proto-oncogenes activation in human solid tumors].

Genetic alterations in solid human tumors occur in several groups of genes, one of which contains the proto-oncogenes. These genes are involved in the control of cell proliferation and become activated in oncogenes by various mechanisms. These activations are reviewed herein.

Gene Expression Regulation↗
PubMed1989

Regulation of the lysine biosynthesis in Pichia guilliermondii.

The regulatory properties of four enzymes (homocitrate synthase, alpha-aminoadipate reductase, saccharopine reductase, saccharopine dehydrogenase) involved in the lysine biosynthesis of Pichia guilliermondii were investigated and compared with the regulatory patterns found in other yeast species. The first enzyme of the pathway, homocitrate synthase, is feedback-inhibited by L-lysine. Some other amino acids (alpha-aminoadipate, glutamate, tryptophan, leucine) and lysine analogues are also inhibitors of one or more enzymes. It is shown that only the synthesis of homocitrate synthase is weakly repressed by L-lysine.

Aldehyde Oxidoreductases↗
PubMed1989

Influence of mood on health-relevant cognitions.

Three experiments assessed the effects of mood on symptom appraisal, health behavior self-efficacy, outcome expectations, and perceptions of vulnerability. Ss in Experiments 1 and 2 were acutely ill, whereas Ss in Experiment 3 were healthy. In each experiment, happy, sad, and neutral moods were induced. In Experiment 1, Ss who experienced sadness reported more aches and pains and greater discomfort than happy Ss. Sad Ss were less confident that they could carry out illness-alleviating behaviors. Experiments 2 and 3 demonstrated that mood's influence on vulnerability perceptions is moderated by health status. Although mood had little impact on perceptions of vulnerability among ill Ss, probability estimates of future negative health-relevant events among healthy Ss were mood sensitive. Seeing oneself as invulnerable to future negative events was accentuated among happy Ss and attenuated among sad Ss. Mood may be an important determinant of care seeking, adherence, and recovery from illness.

Adult↗
PubMed1989

Amplification of FGF-related genes in human tumors: possible involvement of HST in breast carcinomas.

In order to document a possible involvement of structural alterations of FGF (Fibroblast Growth Factor)-like genes in human oncogenesis, we have screened a large series of human tumors for amplification of five FGF-related genes (Basic-FGF, INT2, HST, FGF5 and FGF6). None of 37 hematopoietic neoplasms, one out of 13 melanomas (8%), three out of 43 bladder tumors (7%) and 41 out of 238 breast carcinomas (17%) contained amplified FGF-related sequences, namely HST and INT2. Only these two genes, both located on band q13 of chromosome 11 have been found amplified. In all cases they were co-amplified and in only one instance did amplification extend to the ETS1 locus at position 11q23. INT2 and HST RNA could be evidenced by RNA/RNA in situ hybridization in breast carcinomas. Our results indicate a correlation between RNA expression and gene amplification in the case of HST but not of INT2. Although evaluation of the clinical significance of HST amplification and expression must await long-term follow-up of the patients, we suggest that HST gene product could play a role in development and/or progression of human breast cancer.

Breast Neoplasms↗
PubMed1989

[Oncogenes and anti-oncogenes in breast cancer].

Recent developments in molecular oncology have permitted the definition of alterations in proto-oncogenes (ras, myc, neu and hst/int.2) and anti-oncogenes (Rb.1) in human breast carcinomas. Detection of these abnormalities could be of prognostic interest. However, this remains controversial.

Breast Neoplasms↗
PubMed1989

Characterization of the HST-related FGF.6 gene, a new member of the fibroblast growth factor gene family.

By screening a mouse cosmid library with a human HST probe under reduced conditions of stringency, we isolated several positive clones. One of them was identified as a new member of the fibroblast growth factor gene family, and called FGF.6. The human FGF.6 gene was subsequently isolated and sequenced. The deduced amino-acid sequence exhibited 70% identity with the HST gene product over the C-terminal two-thirds of the putative protein. FGF.6 was mapped to chromosome 12 at band p13 by in situ hybridization. The cloned normal human gene was able to transform mouse NIH3T3 fibroblasts using both focus- and tumorigenicity-assays.

Amino Acid Sequence↗
PubMed1989

[Research on the molecular basis of neoplasms: malignant melanoma as an example].

Knowledge about genetic alterations occurring in human tumors has dramatically increased following the development of cytogenetic and molecular techniques. Various alterations have been characterized: chromosomal damages, oncogene activations, loss of genetic material. Some of those alterations, such as c-abl rearrangements in certain leukemias, are characteristic of a certain type of malignancy. However, in most tumors, no such correlation has been demonstrated. We review here the genetic alterations discovered in human malignant melanomas.

Cell Transformation, Neoplastic↗
PubMed1988

Detection of a low frequency of activated ras genes in human melanomas using a tumorigenicity assay.

We have used an assay combining DNA-mediated gene transfer and tumorigenicity in Swiss athymic mice to look for activated ras genes in solid human sporadic melanomas. This assay can detect ras oncogenes mutated at codons 12, 13, or 61. We examined a panel of 13 independent surgical specimens of primary tumors and metastases. No H- or K-ras oncogenes were detected; an N-ras oncogene, mutated at codon 61, was identified in one of the 13 samples. No N-ras genes mutated at codon 13 were detected. Thus, the tumorigenicity assay detects a low frequency of ras gene activation in melanomas.

Amino Acid Sequence↗