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(Chest. 2004;125:102S-103S.)
© 2004 American College of Chest Physicians

Evaluation of H37, a Candidate 3p21.3 Tumor Suppressor Gene, as a Therapeutic and Diagnostic Marker in Lung Cancer*

Juliana J. Oh, PhD; Michael C. Fishbein, MD; Baher Boctor, BS; Cynthia A. Jimenez, BS{dagger}; Robert Lopez, BS{dagger} and Dennis J. Slamon, MD, PhD

* From the Division of Hematology/Oncology and Pathology & Laboratory Medicine, UCLA School of Medicine, Los Angeles, CA.

Correspondence to: Juliana Oh, PhD, 5–535 MRL (UCLA), 675 Charles E. Young Dr South, Los Angeles, CA 90095; e-mail: joh{at}ucla.edu

Allelic loss at chromosome 3p21.3 is the most frequent and the earliest genetic alteration in lung cancer, implying the presence of one or more critical tumor suppressor genes (TSGs) in this region.1 Identifying these genes and translating the knowledge into clinical practice should facilitate the development of novel therapeutics, and new early detection and prevention strategies for lung cancer. H37, also known as Luca15/RBM5, is one of the approximately 35 genes located in this 370-kilobase tumor suppressor locus.2 We have demonstrated that H37 has the characteristics of a TSG. There is reduced expression of the H37 gene and/or reduced protein expression in 80% of primary non-small cell lung cancers, and the transfection of H37 shows growth-inhibitory properties both in vivo and in vitro.3 Currently, we are trying to confirm H37 as a bona fide TSG and to evaluate the potential of H37 as a therapeutic or molecular marker in lung cancer by implementing the following three strategies. First, we are examining the methylation status of the H37 gene promoter in lung cancer patient samples to determine whether H37 has utility as a tumor diagnostic/prognostic marker. Second, we are generating conditional knockout mice to study the roles of H37 in normal lung development and lung cancer formation in an animal model. Last, we are investigating the molecular mechanism of H37 growth regulation and the interactions of H37 with other important molecules in lung cancer, with a long-term goal of developing rationally designed, targeted therapies. Ultimately, our present studies may serve as a foundation for developing new diagnostic and therapeutic regimens for human lung cancers containing alterations in the H37 gene.


   Footnotes
 
Abbreviation: TSG = tumor suppressor gene

{dagger} Current affiliation: University of California, San Francisco, School of Medicine, San Francisco, CA. Back

This study was supported by funds from the Revlon/UCLA Women’s Cancer Research Program and by UCLA Lung Cancer SPORE grants.


   References
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 References
 

  1. Lerman, MI, Minna, JD (2000) The 630-kb lung cancer homozygous deletion region on human chromosome 3p21.3: identification and evaluation of the resident candidate tumor suppressor genes; The International Lung Cancer Chromosome 3p21.3 Tumor Suppressor Gene Consortium. Cancer Res 60,6116-6133[Abstract/Free Full Text]
  2. Wei, MH, Latif, F, Bader, S, et al Construction of a 600-kilobase cosmid clone contig and generation of a transcriptional map surrounding the lung cancer tumor suppressor gene (TSG) locus on human chromosome 3p21.3: progress toward the isolation of a lung cancer TSG. Cancer Res 1996;56,1487-1492[Abstract/Free Full Text]
  3. Oh, JJ, West, AR, Fishbein, MC, et al A candidate tumor suppressor gene, H37, from the human lung cancer tumor suppressor locus 3p21.3. Cancer Res 2002;62,3207-3213[Abstract/Free Full Text]




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