Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serologically defined tumor-specific surface antigen (TSSA) of the chemically-induced BALB/c Meth A sarcoma, highly restricted to one of 20 sarcomas of BALB/c origin, has been detected on a Moloney murine sarcoma virus (Mo-MuSV)-transformed BALB/c 3T3 cell lines, designated IIA(v). The immunogenicity of the IIA(v) cell in tumor-rejection assays was specific for the Meth A sarcoma, supporting the evidence for a close relationship between the TSSA and the tumor-associated transplantation antigen (TATA) of this tumor. Infection of SC-I cells with retroviruses present in cultured filtrates of IIA(v) cells resulted in Meth A antigen expression. The retroviruses associated with Meth A antigen expression have been tentatively identified as replication and/or transformation-defective XC- MuLV. The possible roles of Mo-MuSV and cellular genes of the BALB/c strain of mice in the expression of the Meth A antigen are discussed.
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PMID:possible role of a retrovirus in the expression of tumor-specific antigens of the Meth A sarcoma. 710 69

The fibrosarcoma ST2, induced by 3-methylcholanthrene in BALB/c (H-2d) mice, also expressed alien histocompatibility antigens of the C3Hf and B10 background not encoded by the MHC. To examine the relationship between these alien, minor antigens and the tumor-specific transplantation antigen (TSTA) of the tumor, in vivo immunogenicity test were performed in BALB/c mice and in hybrids between BALB/c and C3Hf (H-2k), C3H.OH (H-2o2), C3H.SW (H-2b), BALB.K (H-2k), B10.BR (H-2k), and B10.D2 (H-2d) mice. A significant loss of TSTA immunogenicity was found in (BALB/c x C3Hf) and in (BALB/c x C3H.OH)F1 animals and, to a lesser extent, in (BALB/c x C3H.SW)F1 mice as compared to the immunogenicity of the tumor in BALB/c mice. Immunogenicity tests with ST2 in BALB/c x (BALB/c x C3Hf) or in BALB/c x (BALB/c x B10.D2) backcross mice, respectively, revealed that half of the BALB/c x (BALB/c x C3Hf) and 97% of the BALB/c x (BALB/c x B10.D2) animals were able to mount an immune response to ST2. To see whether the loss of TSTA immunogenicity in (BALB/c x C3Hf) was due to common determinants shared between TSTA and alien non-H-2 C3Hf antigens or to a genetically linked low responsiveness to TSTA introduced by C3Hf and C3H.OH strains, BALB/c mice were immunized with normal tissues of some BALB/c x (BALB/c x C3Hf) backcross, anti-ST2 resistant mice. Normal tissues of anti-ST2 resistant, dd and dk typed backcrosses were able to immunize BALB/c mice against a challenge of an otherwise lethal dose of ST2 cells. Some but not all BALB/c x (BALB/c x B10.D2) anti-ST2 resistant donors had tissues able to immunize BALB/c hosts aginst the ST2 growth. Since resistance to tumor growth and expression of minor "alien" antigens shared with the tumor segregate independently, we concluded that alien, minor C3Hf and B10 antigens of the BALB/c sarcoma ST2 are distinct from the TSTA of this tumor.
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PMID:Expression of alien minor histocompatibility antigens distinct from tumor-specific transplantation antigen on a murine fibrosarcoma. 725 Dec 24

The processes by which the kinase inactive receptor ErbB-3 transmits the signals of its ligand, heregulin (HRG), are incompletely understood. We used a yeast two-hybrid system to identify ErbB-3 interacting proteins that may participate in HRG signal transduction. We found that the protein p23, the human homolog of the mouse transplantation antigen P198, interacted with the cytoplasmic domain of ErbB-3 in the yeast two-hybrid system. P23 bound the 26-amino-acid juxtamembrane domain of ErbB-3 in vitro. The N-terminal end of p23 contained the ErbB-3 interacting region. P23 also bound to ErbB-3 in a human breast cell line. Two p23 mRNA transcripts were detected in normal human epithelial tissues including those of the heart, placenta, lung, brain, kidney, pancreas, skeletal muscle, and liver. These same transcripts were also detected in ErbB-3 overexpressing human tumor cell lines derived from breast and lung carcinomas, and a sarcoma. Transfection of p23 resulted in suppression of colony formation of the ErbB-3 overexpressing human breast cancer cell line, AU565, a decreased rate of cell growth, and induction of differentiation. The interaction of ErbB3 and p23 may play a role in regulation of proliferation of ErbB-3 expressing cells.
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PMID:Interaction of the p23/p198 protein with ErbB-3. 1009 21

Mice allografted with different sarcomas, induced by the Schmidt-Ruppin variant of Rous sarcoma virus (RSV-SR), showed a resistance against subsequent isografting of 9 different Rous sarcomas. Transplantation resistance could also be induced by Rous mouse tumor cells x-irradiated with 8000 r or with cell-free tumor extracts, containing no demonstrable virus. No transplantation resistance could be demonstrated after allograft pretreatment with various polyoma tumors or non-viral tumors. Allograft pretreatment with Rous tumors induced no demonstrable resistance against isografting of polyoma tumors. Inoculation of RSV-SR or Rous chicken sarcoma suspension into adult mice gave no clear cut resistance against isografting of mouse sarcomas. Neither after allografting of Rous tumors nor after virus or chicken sarcoma inoculation into adult mice could virus-neutralizing activity be demonstrated in the sera. The results demonstrate the presence of common, specific transplantation antigen(s) in different Rous sarcomas in mice and speak against an identity between the transplantation antigen(s) and viral antigen(s).
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PMID:FURTHER STUDIES ON SPECIFIC TRANSPLANTATION ANTIGENS IN ROUS SARCOMA OF MICE. 1431 51


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