Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The behavior of two spontaneous transplantable rat tumors and a mouse lymphoma was studied in different hosts. A resistant (eR) subline to Sarcoma E 100 (S-E 100) and a susceptible one (eS) were obtained by divergent selection carried out in an inbred line of rats IIM (e). The phenotypic frequencies of the resistant and susceptible individuals to S-E 100 in the base population e and eR, eS, F1 and F2 fitted with the theoretical frequencies of a model of two independent pairs of genes, one (T) with complete dominance (locus SE1) and the other (R) with partial dominance (locus SE2). Locus SE2 would regulate the antitumoral response. Resistance to S-E 100 was found to be a dominant trait. The subcutaneous challenge of eR and eS rats with Lymphoma TACB (L-TACB) showed a different behavior. Subline eR (resistant to S-E 100) was susceptible to L-TACB while subline eS (susceptible to S-E 100) was resistant. A tumor-host interaction was found, revealing that genotypes resistant to S-E 100 were susceptible to L-TACB; in addition, susceptible animals (eR) developed lymph node metastases. It was observed, using animals of different genotypes, that susceptibility to L-TACB metastases and to local tumor growth, would be conditioned by different genes. Delayed type hypersensitivity (DTH) to tumor antigens (S-E 100 and L-TACB) and humoral immune response and DTH to sheep red blood cells (SRBC) were investigated in eR and eS rats. Differences between both sublines were statistically significant suggesting that genes involved in the divergent selection would regulate the antitumoral immune response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inheritance of susceptibility to tumors and metastases in rodents]. 248 19

A 3-year-old boy presented with pathologic fracture of the left proximal femur. Magnetic resonance imaging revealed an aggressive expansile bony mass associated with cortical destruction and surrounding myositis. Computed tomography-guided biopsy revealed a monomorphic small round blue cell tumor by histology. CD99 immunoreactivity and low-level EWSR1 gene translocation by break-apart fluorescent in situ hybridization initially favored a diagnosis of Ewing sarcoma and chemotherapy commenced. Subsequent molecular evaluation by an anchored multiplex polymerase chain reaction-based assay (Archer FusionPlex Sarcoma Panel) revealed a nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) gene fusion. The diagnosis was then amended to primary bone ALK-positive anaplastic large cell lymphoma and the chemotherapy regimen was modified accordingly. This report illustrates the value of this molecular assay in establishing the correct diagnosis of a very rare malignancy masquerading as another tumor type.
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PMID:Primary Bone Anaplastic Large Cell Lymphoma Masquerading as Ewing Sarcoma: Diagnosis by Anchored Multiplex PCR. 2845 58