The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform
Bruce H. Grahn - One of the best experts on this subject based on the ideXlab platform.
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Lack of detection of Feline leukemia and Feline Sarcoma Viruses in diffuse iris melanomas of cats by immunohistochemistry and polymerase chain reaction.
Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians Inc, 2002Co-Authors: Cheryl L. Cullen, Deborah M. Haines, Marion L. Jackson, Bruce H. GrahnAbstract:Diffuse iris melanoma was confirmed by light-microscopic examination in 10 formalin-fixed, paraffin-embedded globes from 10 cats. To determine if Feline leukemia virus or a replication defective Feline leukemia virus, Feline Sarcoma virus, was present in these anterior uveal melanomas, immunohistochemistry and polymerase chain reaction for Feline leukemia virus were utilized. Immunohistochemical staining for Feline leukemia virus glycoprotein 70 was performed on all 10 tumors using an avidin-biotin complex technique. The DNA was extracted from each specimen and a 166-base pair region of the Feline leukemia virus long terminal repeat was targeted by polymerase chain reaction. Immunohistochemical staining for Feline leukemia virus glycoprotein 70 and polymerase chain reaction amplification of a Feline leukemia virus long terminal repeat region were negative in all cases. Feline leukemia virus/Feline Sarcoma virus was not detected in any neoplasms and therefore was unlikely to play a role in the tumorigenesis of these Feline diffuse iris melanomas.
Sola B - One of the best experts on this subject based on the ideXlab platform.
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Isolation of new oncogenic forms of the murine c-fms gene.
1995Co-Authors: De Parseval N, Bordereaux D, Varlet P, Gisselbrecht S, Sola BAbstract:The c-fms gene encodes the receptor for the macrophage colony-stimulating factor, which plays a key role in the proliferation and differentiation of cells of the myelomonocytic lineage. In order to study the effects of overexpression of the macrophage colony-stimulating factor receptor in hematopoietic cells, a Harvey Sarcoma virus-derived retroviral vector containing the murine c-fms cDNA was pseudotyped with Friend murine leukemia virus and inoculated into newborn DBA/2 mice. This viral complex induced monoclonal or oligoclonal leukemias with a shorter latency than that for Friend murine leukemia virus alone. Unexpectedly, 60% of the integrated fms proViruses had deletions at the 5' end of the c-fms gene. Sequence analysis of seven mutant proViruses indicated that the deletions always included the c-fms ligand binding domain and either occurred within the c-fms sequences, leaving the fms open reading frame unchanged, or joined VL30 sequences located at the 5' end of the parental retroviral vector to internal c-fms sequences, resulting in truncated fms proteins devoid of the canonical signal peptide. In contrast to all tyrosine kinase receptors transduced in retroViruses, no helper gag- or env-derived sequences were fused to the rearranged fms sequences. Viral supernatants isolated from hematopoietic tumors with Viruses with deletions were able to transform NIH 3T3 cells as efficiently as parental fms virus, indicating that deletions resulted in constitutive activation of the c-fms gene. These oncogenic variants differ from those transduced in the Suzan McDonough strain of Feline Sarcoma Viruses (L. Donner, L. A. Fedele, C. F. Garon, S. J. Anderson, and C. J. Sherr, J. Virol. 41:489-500, 1982). The high rate of c-fms rearrangement and its relevance in the occurrence of hematopoietic tumors are discussed
J.c. Neil - One of the best experts on this subject based on the ideXlab platform.
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Feline Leukemia and Sarcoma Viruses
Encyclopedia of Virology, 2008Co-Authors: J.c. NeilAbstract:Feline leukemia virus (FeLV) belongs to the genus Gammaretrovirus of the family Retroviridae. FeLV remains a significant pathogen of the domestic cat although its prevalence has been reduced in some populations by removal of infected animals and the development of effective vaccines. Resistance to FeLV is age related, with later exposure more likely to lead to control of infection via cellular and humoral immunity. This pattern contrasts with Feline immunodeficiency virus where infection rates rise directly with age and infection is not cleared. Animals that become persistently viremic with FeLV are at high risk of succumbing to immunosuppressive or neoplastic diseases, particularly of hematopoietic origin. FeLV isolates can be classified in vitro according to envelope type and host receptor specificity, with alternative host range variants (B, C, and T) arising from the parental subgroup A FeLV by recombination with endogenous FeLV-related sequences in the cat germline or by mutation of receptor-binding domains. Evolution of these variants is important in the pathogenesis of FeLV as they may lead to acute disease onset. FeLV oncogenesis involves insertional mutagenesis and recombination between FeLV and host proto-oncogenes leading to the formation of Feline Sarcoma Viruses or lymphoma-inducing variants. FeLV infection is sustained in cat populations as highly immunosuppressive or oncogenic FeLV variants lead to rapid demise of the host and are generally not transmitted.
Cheryl L. Cullen - One of the best experts on this subject based on the ideXlab platform.
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Lack of detection of Feline leukemia and Feline Sarcoma Viruses in diffuse iris melanomas of cats by immunohistochemistry and polymerase chain reaction.
Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians Inc, 2002Co-Authors: Cheryl L. Cullen, Deborah M. Haines, Marion L. Jackson, Bruce H. GrahnAbstract:Diffuse iris melanoma was confirmed by light-microscopic examination in 10 formalin-fixed, paraffin-embedded globes from 10 cats. To determine if Feline leukemia virus or a replication defective Feline leukemia virus, Feline Sarcoma virus, was present in these anterior uveal melanomas, immunohistochemistry and polymerase chain reaction for Feline leukemia virus were utilized. Immunohistochemical staining for Feline leukemia virus glycoprotein 70 was performed on all 10 tumors using an avidin-biotin complex technique. The DNA was extracted from each specimen and a 166-base pair region of the Feline leukemia virus long terminal repeat was targeted by polymerase chain reaction. Immunohistochemical staining for Feline leukemia virus glycoprotein 70 and polymerase chain reaction amplification of a Feline leukemia virus long terminal repeat region were negative in all cases. Feline leukemia virus/Feline Sarcoma virus was not detected in any neoplasms and therefore was unlikely to play a role in the tumorigenesis of these Feline diffuse iris melanomas.
De Parseval N - One of the best experts on this subject based on the ideXlab platform.
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Isolation of new oncogenic forms of the murine c-fms gene.
1995Co-Authors: De Parseval N, Bordereaux D, Varlet P, Gisselbrecht S, Sola BAbstract:The c-fms gene encodes the receptor for the macrophage colony-stimulating factor, which plays a key role in the proliferation and differentiation of cells of the myelomonocytic lineage. In order to study the effects of overexpression of the macrophage colony-stimulating factor receptor in hematopoietic cells, a Harvey Sarcoma virus-derived retroviral vector containing the murine c-fms cDNA was pseudotyped with Friend murine leukemia virus and inoculated into newborn DBA/2 mice. This viral complex induced monoclonal or oligoclonal leukemias with a shorter latency than that for Friend murine leukemia virus alone. Unexpectedly, 60% of the integrated fms proViruses had deletions at the 5' end of the c-fms gene. Sequence analysis of seven mutant proViruses indicated that the deletions always included the c-fms ligand binding domain and either occurred within the c-fms sequences, leaving the fms open reading frame unchanged, or joined VL30 sequences located at the 5' end of the parental retroviral vector to internal c-fms sequences, resulting in truncated fms proteins devoid of the canonical signal peptide. In contrast to all tyrosine kinase receptors transduced in retroViruses, no helper gag- or env-derived sequences were fused to the rearranged fms sequences. Viral supernatants isolated from hematopoietic tumors with Viruses with deletions were able to transform NIH 3T3 cells as efficiently as parental fms virus, indicating that deletions resulted in constitutive activation of the c-fms gene. These oncogenic variants differ from those transduced in the Suzan McDonough strain of Feline Sarcoma Viruses (L. Donner, L. A. Fedele, C. F. Garon, S. J. Anderson, and C. J. Sherr, J. Virol. 41:489-500, 1982). The high rate of c-fms rearrangement and its relevance in the occurrence of hematopoietic tumors are discussed
