Studies on tumor markers in the pathogenesis of lymphoid leucosis in poultry

R.V.S. Pawaiya, Ram Kumar, O.P. Paliwal and T.R. Mohanty
Division of Pathology Indian Veterinary Research institute
Izatnagar (UP) - 243 122

Molecular markers have been earlier employed for purpose of differential diagnosis of human and animal neoplasm. Present communication describes the role of molecular tumor markers, such as proliferating cell nuclear antigen (PCNA), C – myc proto-oncogene, P56 – tumor suppressor gene, human telomerase reverse transcriptase (hTERT) and fibronectin (FN) cell adhesion glycoprotein with the help of specific monoclonal antibodies in the study of pathogenesis of lymphoid leucosis in poultry. Four specimens of avian lymphoid leucosis (large swollen liver, spleen and heart with multiple diffuse gray white nodules) from adult birds formed the materials of study after histopathological diagnosis.

Histopathologically, liver tissue exhibited massive nodular areas of proliferating cells mainly large lymphoblasts and lymphocytes growing expansively by compressing the surrounding hepatic parenchyma. The uniformed lymphoblastoid cells having darkly stained round or oval nuclei were arranged in loose sheet of connective tissue stroma. Mitotic figures were absent. Hepatocytes in the vicinty of tumor masses were flattened and atrophied. The thin connective tissue stroma intersected to the cell masses to divide into pseudolobulations. Islands of individual or small groups of hepatocytes were also observed amongst the large diffuse tumor cells. In the spleen, tumor cells showed more or less similar features with distorted trabeculae and red pulps. In the heart, the cells appeared as cord like loose mass and were extensively infiltrated between the cardiac muscle fibers.

Proliferative activity of growing lymphoid tumor cells was evidenced by numerous strongly stained PCNA positive nuclei with very high PCNA index (327.97 + nuclei per high field). Most of the tumor cells revealed strongly positive nuclear stain for P53 and hTERT and conspicuously negative for C – myc along with weak intercellular staining for FN but strong pericellular FN positive staining. These molecular characteristics were suggestive of aggressively malignant and metastatic behaviour. The negative C –myc staining in the present study might be due to fact that monoclonal anti C –myc antibody used in this investigation was raised against the human C – myc, which possibly did not react with the avian counterpart. Further, a different pathway of viral oncogenesis was evident since lymphoid tumor cells were labelled strongly for P53 and h TERT. The study indicated the possibility of either P 53 gene mutation and / or hTERT gene activation leading to their over expression which resulted neoplastic transformation of cells followed by marked proliferation and immortalization (hTERT), The reduced intercellular FN might have contributed to the wide spread dissemination of the tumor.

Source : IPSACON-2005

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