Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the disordered maturation of mononuclear phagocytes previously found in Hodgkin's disease, integrating microdensitometry was used to quantitate changes in seven cytochemical constituents (NADH dehydrogenase, succinate dehydrogenase, acid phosphatase, alpha-naphthyl butyrate esterase, DNA, RNA and glycogen) of developing macrophages from 19 patients and 19 normal subjects. Individual cells were studied at intervals over six days of suspension culture; the results were subjected to analysis of variance. In both groups, all the constituents studied except DNA showed highly significant increases over the period of culture. Consistently lower levels of alpha-naphthyl butyrate esterase (approximately 65%) and increased levels of glycogen were present in the Hodgkin's group. The results show that (1) maturational changes occur in the cytochemical constituents of developing macrophages of Hodgkin's disease, and (2) there are disturbances affecting the specific enzyme alpha-naphthyl butyrate esterase and glycogen that are likely to have profound implications for host defense mechanisms.
 ...
PMID:Disordered macrophage development in Hodgkin's disease shown by quantitative cytochemistry. 839 46

Infection with SIVmac251 in some rhesus monkeys (Macaca mulatta) leads to B-cell non-Hodgkin's lymphomas (B-NHL) clinically similar to that of HIV-infected AIDS patients. To further characterize the SIV-associated B-NHL we have generated genetic profiles of malignant cells by subtractive hybridization and Northern blot analysis. We have analyzed 21 clones of a subtracted cDNA library corresponding to overexpressed genes in diffuse large B-cell (DLBCL) SIV-associated monkey lymphoma. Eight of these clones represent a sequence homologous to an abundant transcript from KG-1 cells originally established from a human myelogenous leukemia. The protein encoded has a 60% similarity to a hypothetical glycine-rich transmembrane signal protein of Caenorhabditis elegans and 25% similarity to the ret finger protein. The other cDNA clones contained sequences of the serum amyloid A gene (SAA), the alpha1-acid glycoprotein gene (AGP), the ribosomal protein S3a (RPS3a) and L8 (RPL8) genes, the interferon-inducible gene (INF-ind), the metastasin gene (mts1), and the NADH dehydrogenase I gene (ND-I). The remaining cDNA clones consisted of yet unknown sequences. In addition, we detected an up-regulation of the cytochrome c oxidase II gene (COX-II), the ND-IV gene, and the SET oncogene by Northern blot hybridization in three SIV-associated NHLs of different histomorphological classification. All these genes have not previously been found to be overexpressed in B-NHL.
 ...
PMID:Differential gene expression in B-cell non-Hodgkin's lymphoma of SIV-infected monkey. 1065 56

Functioning mitochondria are crucial for cancer metabolism, but aerobic glycolysis is still considered to be an important pathway for energy production in many tumor cells. Here we show that two well established, classic Hodgkin lymphoma cell lines (cHL) harbor deleterious variants within mitochondrial DNA (mtDNA) and thus exhibit reduced steady state levels of respiratory chain complexes. However, instead of resulting in the expected bioenergetic defect, these mtDNA variants evoke a retrograde signaling response that induces mitochondrial biogenesis and ultimately results in increased mitochondrial mass as well as function and enhances proliferation in vitro as well as tumor growth in mice in vivo. When complex I assembly was impaired by knock-down of one of its subunits, this led to further increased mitochondrial mass and function and, consequently, further accelerated tumor growth in vivo. In contrast, inhibition of mitochondrial respiration in vivo by the mitochondrial complex I inhibitor metformin efficiently slowed down growth. We conclude that, as a new mechanism, mildly deleterious mtDNA variants in cHL cancer cells cause an increase of mitochondrial mass and enhanced function as a compensatory effect using a retrograde signaling pathway, which provides an obvious advantage for tumor growth.
 ...
PMID:Mitochondrial DNA mutations induce mitochondrial biogenesis and increase the tumorigenic potential of Hodgkin and Reed-Sternberg cells. 3225 84