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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.625 5-Year IF: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvPathToxOncol.v22.i3.10
19 pages

Mechanisms of Metastasis as Related to Receptor Tyrosine Kinases in Small-Cell Lung Cancer

Nazia F. Jafri
Lowe Center for Thoracic Oncology,Dept.of Medical Oncology,Dana-Farber Cancer Institute;Div.of Medical Oncology and Dept.of Medicine,Brigham and Women's Hospital;Harvard Medical School; Boston University Medical School, Boston, Massachusetts, USA
Patrick C. Ma
Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute; Brigham and Women’s Hospital; Harvard Medical School; Tufts-New England Medical Center, Boston, Massachusetts;University of Chicago, Pritzker School of Medicine, Chicago, Illinois, USA
Ravi Salgia
Department of Medical Oncology and Therapeutics Research, Comprehensive Cancer Center, City of Hope National Medical Center


Small-cell lung cancer (SCLC) is an aggressive, malignant neoplasm with a 5-year survival of less than 10%. This poor survival rate is related to a high propensity for recurrence and a high rate of metastases. Metastases initially occur in the lymph nodes and thereafter in other organs such as the lung itself, liver, adrenal glands, brain, bone, and bone marrow. The mechanisms of metastases have been better understood recently and are described in this review. Receptor tyrosine kinases (RTKs) have been identified as important therapeutic targets in non-small-cell lung cancer (such as the EGF-receptor). We have begun to identify RTKs in SCLC and have shown that c-Kit and c-Met are expressed and functional in SCLC. RTKs have also been shown to be important in the metastasis of cancer cells. The roles of RTKs in the mechanism of metastasis are detailed in this review, with special emphasis on downstream signal transduction from RTK signaling.

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