Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtypes were validated that were strongly influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating translocations and hyperdiploidy. Indicative of the deregulation of common pathways by gene orthologs, common gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation, the latter consisting of 2 subgroups, one characterized by expression of the early B-cell markers CD20 and PAX5. A low incidence of focal bone disease distinguished one and increased expression of proliferation-associated genes of another novel subgroup. Comprising varying fractions of each of the other 6 subgroups, the proliferation subgroup dominated at relapse, suggesting that this signature is linked to disease progression. Proliferation and MMSET-spike groups were characterized by significant overexpression of genes mapping to chromosome 1q, and both exhibited a poor prognosis relative to the other groups. A subset of cases with a predominating myeloid gene expression signature, excluded from the profiling analyses, had more favorable baseline characteristics and superior prognosis to those lacking this signature.
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PMID:The molecular classification of multiple myeloma. 1672 3

Rheumatoid arthritis (RA) is a representative bone disease. TNF-alpha plays a pivotal role in the pathological processes of RA, leading to cartilage and bone destruction. Although biologics targeting TNF have brought about a marked reduction of progression of bone destruction, the rate of remission induction is about 30% and the rest of the patients require alternative biologics such as B cell targeting (chimeric anti-CD20 antibody : rituximab) or T cell targeting (CTLA [cytotoxic T-lymphocyte antigen]-4-Igfusion protein : abatacept) therapies. To date, the efficacy of these new biologics on the disease activity and bone destruction was confirmed by randomized control trials. Then abatacept and rituximab were recommended for the treatment of the patients who do not respond adequately to TNF inhibitors.
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PMID:[Efficacy of new biologics on bone destruction in rheumatoid arthritis]. 1925 47