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Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.241 5年インパクトファクター: 1.349 SJR: 0.519 SNIP: 0.613 CiteScore™: 1.61

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v20.i3.30
9 pages

Enhanced Sequential Expression of G1/S Cyclins During Experimental Hepatocarcinogenesis and Tyrosine Phosphorylation

Monisha Sundarrajan
Cellular Carcinoge'nesis Laboratory, Cancer Research Institute, Tata Memorial Centre,. Parel, Mumbai, India
Aaron Z. Fernandis
Biotechnology Centre, Indian Institute of Technology, Powai, Mumbai, India
Gosukonda Subrahmanyam
Biotechnology Centre, Indian Institute of Technology, Powai, Mumbai, India
Shilpa Prabhudesai
Department of Pathology, Tata Memorial Hospital, Tata Memorial Centre, Parel, Mumbai, India
Shanta C. Krishnamurthy
Department of Pathology, Tata Memorial Hospital, Tata Memorial Centre, Parel, Mumbai, India
K. V. K. Rao
Cellular Carcinogenesis Laboratory, Cancer Research Institute, Tata Memorial Centre, Parel, Mumbai 400012, India

要約

It is now widely accepted that cancer development is a multistage process, starting from the original cell population and ending with a malignant tumor. However, the mechanisms involved in the progressive growth of cells from normalcy to preneoplasia, and from preneoplasia to malignancy are not clear. Because tyrosine phosphorylation and dephosphorylation reactions are known to play critical roles during normal and abnormal cellular growth, we have studied the tyrosine phosphorylation, tyrosine phosphorylated proteins, and protein phos-phatases during the sequential development of liver cancer. The present investigation indicated that enhanced tyrosine phosphorylation and tyrosine phosphorylated proteins, with no change in the levels of tyrosine protein phosphatases may contribute to abnormal cellular proliferation during liver carcinogenesis. We have also seen an increase in the expression of proliferating cell nuclear antigen and G1/S cyclins during tumor development.


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