Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tumor inhibitory factor-2 from the conditioned medium of the human rhabdomyosarcoma cell line A673 was purified and sequenced. The 19 N-terminal amino acid residues were identical to those of human interleukin 1 (IL-1), corresponding to the residues 119-137 of the IL-1 alpha precursor. The purified material had an apparent molecular weight similar to that of the mature secreted form of IL-1 alpha (Mr 17,400). In addition, similarly to IL-1, it induced the production of IL-2 by T-cells. The purified protein inhibited the growth of the A673 cells from which it was derived, suggesting that it may act as an autocrine growth inhibitor. It also inhibited the growth of a human adenocarcinoma of the lung and three human mammary carcinomas, but not of two human melanoma cell lines. In contrast, it stimulated the proliferation of normal human fibroblasts. These biological activities, previously assigned to a putative tumor inhibitory factor molecule, are apparently due to the production by the tumor cells of IL-1 alpha.
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PMID:Purification and characterization of tumor inhibitory factor-2: its identity to interleukin 1. 278 51

Adoptive immunotherapy (AIT) of mice bearing the MCA/76-9 rhabdomyosarcoma in combination with cyclophosphamide (CY) injection results in the permanent regression of tumors. This report is concerned with changes in the tumor-associated macrophage (TAM) population and the influence of both CY injection and CY/AIT on their potential functions. Sequential analyses of FcR, MAC-I and Class-II MHC antigen expressed by tumor-associated cells (TAC) showed that CY injection or CY/AIT induced marked increases in the proportions of all 3 parameters as compared with the relatively stable levels in progressing tumors. These changes were time- and treatment-related. The mean MAC-I fluorescence (antigen density per cell) increased nearly 2-fold by 48 hr after CY injection, regardless of subsequent AIT. In contrast, the density of Class-II antigen per cell declined by as much as 75% within 48 hr after CY injection and did not recover by 7 days. This initial decline was also seen after CY/AIT and was followed by a rapid recovery to near-normal values by day 7. Northern analysis of RNA isolated from whole tumor tissue indicated wide fluctuations in expression of the typical macrophage genes encoding the proteins MAC-I, IL-I alpha, IL-I beta, TNF alpha, IA beta and c-fms. However, with the exception of MAC-I and IL-1 alpha/IL-1 beta mRNA, the modifications appeared to be qualitative rather than representing changes in the proportions of TAM. The data suggest that the changes in membrane antigen and gene expression by TAM reflect a complex interaction between TAM and their environment, in particular tumor cells and tumor-infiltrating lymphocytes. In addition, it is evident that CY injection per se is responsible for defined fundamental changes that presumably influence the outcome of AIT.
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PMID:Qualitative and quantitative intratumoral changes in gene expression following cyclophosphamide injection and the adoptive transfer of T cells: the potential contribution of tumor-associated macrophages. 811 93