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PubMedDate not supplied

[Histological variants of parasympathetic paragangliomas (chemodectomas) of the neck and morphological variants of their malignancy].

Histotopograms of 28 chemodectomas have been studied. Principal microscopic features of malignancy are as follows: structural atypia (complete in solid or fibrous variants) or partial (alveolar chemodectoma) loss of alveolarity as the most important sign of organotypia; another sign of malignancy is cell cataplasia (cell and nuclear polymorphism, change in nuclear-cytoplasmic relationship in the direction of its increase, nuclear hyperchromatism, appearance of large ungly hyperploid nuclei, mitotic activity of tumour cells in one case. Incomplete angiogenesis characteristic for malignant tumours was also detected. Invasive growth in the majority of chemodectomas in the form of partial growth through the walls of great vessels and ubiquitous growth through the walls of small vessels were present in most chemodectomas. Thus, there is a basis to claim that the chemodectomas studied are malignant tumours although they are characterized by a slow (years) growth and slow progression.

Cell Nucleus↗
PubMed1991

Structure of laminin variants. The 300-kDa chains of murine and bovine heart laminin are related to the human placenta merosin heavy chain and replace the a chain in some laminin variants.

A variant of laminin has previously been isolated from murine heart and shown to be distinct from laminin purified from a traditional source, the murine Engelbreth-Holm-Swarm (EHS) tumor (Paulsson, M., and Saladin, K. (1989) J. Biol. Chem. 264, 18726-18732). It contains a novel polypeptide chain designated as 300 kDa, which is not found in laminin from the EHS tumor. In the present study, heart laminin was purified from bovine tissue and shown to be structurally and immunochemically closely related to the murine protein. Further, heart laminins were compared with merosin, a laminin-like protein isolated from human placenta (Ehrig, K., Leivo, I., Argraves, W. S., Ruoslahti, E., and Engvall, E. (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 3264-3268). The 300-kDa chain of bovine heart laminin cross-reacted with the heavy chain of merosin, showing that these polypeptides are closely related, albeit from different species. Heart laminin is more resistant to proteolysis than laminin derived from the EHS tumor. A large fragment could be prepared by digestion with thermolysin, which consisted of an almost intact long arm structure and variably long, residual short arm structures. Analysis of its structure shows that the 300-kDa heavy chain is disulfide-bonded to the B1 and B2 chains in the center of the laminin cross and forms the long arm together with these chains. It thereby replaces the A chain, well known from tumor sources, in the laminin structure.

Amino Acid Sequence↗
PubMed1990

Association of a functional prostaglandin E2-protein kinase A coupling with responsiveness of metastatic Lewis lung carcinoma variants to prostaglandin E2 and to prostaglandin E2-producing nonmetastatic Lewis lung carcinoma variants.

Cloned Lewis lung carcinoma (LLC) variants were used in an in vitro migration model for dissemination, to determine if prostaglandin E2 (PGE2) produced by nonmetastatic LLC cells could directly stimulate dissemination of metastatic LLC cells and to identify an intracellular mechanism for such an effect. The migration of metastatic LLC clones was stimulated not only by exogenous PGE2 but also by nonmetastatic LLC cells, by their production of a migration-stimulatory factor which was sensitive to indomethacin and anti-PGE2 antibodies. Nonmetastatic LLC clones were unresponsive to migration stimulation by PGE2. The results of in vivo metastasis studies were consistent with those of in vitro migration studies. In vivo lung metastasis was increased by PGE2, as well as by nonmetastatic cells when they were either admixed with the metastatic LLC inoculum, irradiated and injected adjacent to the metastatic LLC tumor, or localized in chambers and implanted s.c. into mice given injections of metastatic LLC cells. Indomethacin blocked metastasis stimulation by nonmetastatic cells. The in vitro PGE2 stimulation of metastatic LLC cells appeared to be linked to a cyclic AMP (cAMP) response, since migration could also be stimulated by dibutyryl-cyclic AMP and blockage of a cAMP response with nicotinic acid ablated the PGE2 stimulation of migration. In vivo metastasis could be stimulated by elevation of cAMP with aminophylline. The differential responsiveness of metastatic versus nonmetastatic LLC cells to PGE2 could not be due to PGE2-adenylate cyclase coupling, since PGE2 increased the cAMP levels in cultures of both metastatic and nonmetastatic LLC cells. There was, however, a difference in the cyclic AMP-dependent protein kinase (PKA) response to PGE2, with PKA activity of metastatic LLC being stimulated by PGE2 and by the adenylate cyclase-stimulator forskolin, whereas PKA of nonmetastatic LLC was not stimulated by these cAMP elevators, suggesting a dysfunction in the cAMP-PKA coupling.

Animals↗
PubMed1989

Characterization of hemoglobin variants. Prenatal diagnosis on a fetus at risk of having the hemoglobin variants S and/or C in combination with beta-thalassemia.

The determination of hemoglobin types in a fetus whose father and mother were heterozygous for Hb S and Hb C, respectively, is used as an example for demonstrating different techniques. The parents were furthermore suspected of being heterozygous for beta-thalassemia. Several of the possible combinations give rise to such serious conditions that abortus provocatus would be considered. The conclusion from the analyses was that the fetus was normal, having no variants nor thalassemia.

Anemia, Sickle Cell↗
PubMed1985

Hydropic cell variant (clear cell variant) of Wilms' tumor.

We report an unusual clear cell tumor of the kidney in infancy. The presence in our patient of a discrete mass with foci of primitive nephroblastic cells indicates the neoplastic nature of the clear cells. We discuss its distinction from clear cell sarcomas and carcinomas, and we suggest that this lesion may be inadequately separated from pediatric renal carcinomas in the literature. We recommend the term hydropic cell variant as a less confusing and more accurate descriptive designation.

Adenocarcinoma↗
PubMed2025

A Comprehensive Bioinformatics Approach to Analysis of Variants: Variant Calling, Annotation, and Prioritization.

Next-Generation Sequencing (NGS), also known as high-throughput sequencing technologies, has enabled rapid and efficient sequencing of large amounts of DNA and RNA. These technologies have revolutionized the field of genomics, transcriptomics, and proteomics and have been widely used in cancer research, leading to advances in clinical diagnosis and treatment. Improvements in the NGS technologies enabled millions of fragments to be sequenced simultaneously in a time- and cost-effective manner and resulted in large amount of genomic data which require efficient analysis methods. Analysis of the genomic data requires both efficient computer resources and bioinformatics approaches. This chapter details a comprehensive computational approach and analysis steps for genomic data analysis.

Computational Biology↗
PubMed1997

Isolation of a measles virus variant: protection of newborn mice from measles encephalitis by 24 h prior intracerebral inoculation with the variant.

A small plaque mutant with reduced neurovirulence in newborn mice was obtained from Edmonston strain measles virus after propagation for 5 months in NIH3T3 cells. It retained the antigenicity of the parental virus and tended to induce higher neutralizing antibody titers in the adult BALB/c mice. The intracerebral (but not intraperitoneal) inoculation of the live mutant virus one day before prevented the newborn BALB/c mice from encephalitis caused by the intracerebral challenge with the parental strain at a dose of 10-20 LD50. The intracerebral inoculation with the mutant virus whose replication capacity was inactivated by UV-irradiation was ineffective. The protection was not attributed to interferons nor to viral interference. The mechanism remains unknown.

3T3 Cells↗