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Jurgen Vielkind, PhD

Emeritus Scientist - Genetics Unit, Integrative Oncology

jvielkin@bccrc.ca  Rm 10-112 ▪ 675 West 10th Avenue, Vancouver, B.C., V5Z 1L3, Canada  

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juergen

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Current Appointments

  • Emeritus Scientist, Integrative Oncology, BCCA
  • Member, Genetics Program, UBC.
  • Senior Scientist, Cancer Endocrinology, B.C. Cancer Agency/Cancer Research Centre
  • Habilitation (Genetics, Mol Genetics), Justus Liebig University, Giessen, FRG, 1979
  • Associate Professor, Pathology and Laboratory Medicine, UBC 
  • Associate Member, Dermatology, UBC

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Training

  • Diploma (Biology), Justus Liebig University, Giessen, FRG, 1969
  • PhD (Genetics, Virology, Zoology), Justus Liebig University, Giessen, FRG, 1971

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Research Interests

Major goals are to identify genetic factors and to understand the mechanisms that mediate the genesis of cancers such as melanoma and carcinoma of the prostate. With regard to melanoma we have studied the hereditary melanomas that occur in small tropical fish Xiphophorus. This melanoma formation is well recognized as a model for human melanoma. Previous formal genetic studies by this laboratory have identified an oncogenic sex-linked, multigenic locus and an autosomal tumour suppressor locus, Diff, that mediate melanoma formation in Xiphophorus.

We have attempted to identify candidate genes for the multigenic locus and have cloned a closely linked, duplicated gene, Xmrk-2. It encodes a novel growth factor receptor tyrosine kinase which has similarities to, but is distinct from. the epidermal growth factor receptor (EGFR). Evidence indicates that this gene is related to pigment cell formation and that it mediates melanoma formation when overexpressed at the transcriptional and protein levels. Recently, we have cloned another gene, a putative nicotine choline receptor, which also maps to this complex locus. Electron microscopic studies of normal and melanomatous pigment cell development provided evidence that the Diff tumour suppressor gene may play a role in final pigment cell differentiation. When homozygously lost, pigment cells fail to differentiate and proliferate in an uncontrolled fashion. Ongoing research is aimed at further understanding the molecular mechanism of Xmrk-2 and at the cloning of the tumour suppressor gene; the latter would allow us to understand how this gene may function in the differentiation of pigment cells and in hindering melanoma formation.

As part of the functional analysis of Xmrk-2 we have raised a monoclonal antibody, XMEL, against an extracellular domain of the Xmrk-protein. Consistent with the evidence that these fish melanomas are very similar to human melanoma we were able to show that XMEL specifically recognized human melanoma. In a large study of 200 different cancers the antibody showed essentially no cross reactivity with other cancers but surprisingly exhibited specificity for prostatic carcinoma. Ongoing research is aimed at investigating the diagnostic as well as the prognostic value of this antibody for melanoma and prostate cancer. The major goal however is, to clone the human gene(s) encoding the antigen recognized by XMEL. This would allow the study of their function in human melanoma and prostate cancer formation and could be a major breakthrough since no gene has been detected to be significant in the formation of these malignancies. In the long run we would be able to develop tools for early diagnosis, prognosis, and perhaps for treatment, of melanoma and prostatic carcinoma.

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Personnel

  • Barbara Schmidt

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Recent Publications

  • Ekuni D, Firth JD, Nayer T, Tomofuji T, Sanbe T, Irie K, Yamamoto T, Oka T, Liu Z, Vielkind J, Putnins EE. (2009) Lipopolysaccharide-induced epithelial monoamine oxidase mediates alveolar bone loss in a rat chronic wound model. Am J Pathol. 175(4):1398-409.
  • Watson SK, Woolcock BW, Fee JN, Bainbridge TC, Webber D, Kinahan TJ, Lam WL, Vielkind JR.(2009) Minimum altered regions in early prostate cancer progression identified by high resolution whole genome tiling path BAC array comparative hybridization. Prostate 69(9):961-75.
  • Ma S, Chan YP, Woolcock B, Hu L, Wong KY, Ling MT, Bainbridge T, Webber D, Chan TH, Guan XY, Lam W, Vielkind J, Chan KW. (2009) DNA fingerprinting tags novel altered chromosomal regions and identifies the involvement of SOX5 in the progression of prostate cancer. Int J Cancer 124(10):2323-32.
  • Noorali S, Kurita T, Woolcock B, de Algara TR, Lo M, Paralkar V, Hoodless P, Vielkind J. (2007) Dynamics of expression of growth differentiation factor 15 in normal and PIN development in the mouse. Differentiation. 75(4):325-36.
  • Ma S, Guan XY, Beh PS, Wong KY, Chan YP, Yuen HF, Vielkind J, Chan KW. (2007) The significance of LMO2 expression in the progression of prostate cancer. J Pathol. 211(3):278-85.
  • Pugh TJ, Bebb G, Barclay L, Sutcliffe M, Fee J, Salski C, O'Connor R, Ho C, Murray N, Melosky B, English J, Vielkind J, Horsman D, Laskin JJ, Marra MA. (2007) Correlations of EGFR mutations and increases in EGFR and HER2 copy number to gefitinib response in a retrospective analysis of lung cancer patients. BMC Cancer 7:128.
  • Woolcock B, Kazianis S, Lucito R, Walter RB, Kallman KD, Morizot DC, Vielkind JR. (2006) Allele-specific marker generation and linkage mapping on the Xiphophorus sex chromosomes. Zebrafish 3(1):23-37.
  • Kazianis S, Nairn RS, Walter RB, Johnston DA, Kumar J, Trono D, Della-Coletta L, Gimenez-Conti I, Rains JD, Williams EL, Pino BM, Mamerow MM, Kochan KJ, Schartl M, Vielkind JR, Volff JN, Woolcock B, Morizot DC. (2004) The genetic map of Xiphophorus fishes represented by 24 multipoint linkage groups. Zebrafish 1(3):287-304.
  • Cheung PK, Woolcock B, Adomat H, Sutcliffe M, Bainbridge TC, Jones EC, Webber D, Kinahan T, Sadar M, Gleave ME, Vielkind J. (2004) Protein profiling of microdissected prostate tissue links growth differentiation factor 15 to prostate carcinogenesis. Cancer Res. 64(17):5929-33.

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Links 

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