Public Release:  Other highlights in the Jan. 8 JNCI

Journal of the National Cancer Institute

Statin Use May Be Associated with Reduced Cancer Risk

Patients taking cholesterol-lowering drugs known as statins may be at lower risk for developing cancer, especially lung and colorectal cancers. However, it is unknown whether statins directly prevent cancer.

Laboratory studies have shown that statins may inhibit cancer cell growth, but evidence from observational studies has been inconsistent.

To investigate the association between statin use and cancer incidence, Wildon Farwell, M.D., of the Veterans Affairs Boston Healthcare System and colleagues collected data on patients in the VA healthcare system who were using statins and/or blood pressure-lowering medications.

Statin users had a reduced risk of all cancer types compared with non-statin users. The incidence of cancer was 9.4 percent among statin users and 13.2 percent among non-statin users.

"Our findings support the hypothesis that statins may reduce the risk of cancer, in particular lung and colorectal cancers. This relationship may be affected by the [statin dose]," the authors write.

Contact: Wildon Farwell, wildon.farwell@va.gov, (857) 364-6182


Receptor May Be New Target for Colon Cancer Drugs

A receptor on the surface of colorectal cancer cells is involved in tumor growth and could be a potential target for anticancer drugs.

Neuropilin-2 (NRP2) is a vascular endothelial growth factor (VEGF) receptor. VEGF is a protein that is involved in angiogenesis--the formation of blood vessels, which tumors need to survive--and it is a target for some cancer drugs. Recently, VEGF has been shown to directly affect cancer cells, with actions independent of that on blood vessels.

Lee Ellis, M.D., of the University of Texas M. D. Anderson Cancer Center in Houston and colleagues assessed the expression of NRP2 in colorectal cancer cells and tried to determine its role of NRP2 in cancer growth and cell growth, death, and migration.

NRP2 was expressed in primary and metastatic cancers but was not detectable in surrounding non-cancerous tissue. Blocking NRP2 reduced cell growth, migration, and invasiveness, as well as tumor growth. The researchers also demonstrated that inhibiting NRP2 was effective in treating tumors in mice.

"The use of anti-NRP2 therapeutic targeting in conjunction with anti-VEGF therapy may improve on existing antiangiogenesis treatments and may provide a unique opportunity to circumvent the ability of NRP2-expressing tumors, such as colorectal cancers, to grow and metastasize," the authors write.

In an accompanying editorial, Giovanna Tosato, M.D., of the National Cancer Institute in Bethesda, Md., and colleagues discuss how this "groundbreaking work" by Ellis and colleagues furthers the understanding of the role of NRP2 in colon cancer.

"This is welcome new information. Let us hope that targeting neuropilin-2 can hit double punches against the cancer microenvironment and the cancer itself," the editorialists write.

Contact:


Mouse Model of Rare Disorder Shows Parallel to Human Kidney Cancer

A new mouse model may be useful for studying kidney cancer development.

Birt-Hogg-Dubé (BHD) syndrome is a rare genetic disorder that is associated with an increased risk of kidney cancer. Patients with BHD carry mutations in the BHD tumor suppressor gene. Masaya Baba, M.D., Ph.D., of the National Cancer Institute in Frederick, Md., used a knockout mouse model to examine the role of the BHD gene in kidney function and tumor development.

The mice without the BHD gene had enlarged kidneys filled with cysts and died from kidney failure by the time they were three weeks old. Treatment with the drug rapamycin reduced kidney size and increased survival time.

"Because BHD-targeted mice develop a striking kidney phenotype over a very short time, this model may be useful for the development and testing of new therapies or drugs...with which to treat BHD patients and BHD-associated kidney cancers," the authors write.

Contact: National Cancer Institute press office, ncipressofficers@mail.nih.gov, (301) 496-6641


Tumor Viruses Regulate Telomeres to Assure Cell Proliferation

Human tumor viruses employ a variety of strategies for maintaining telomere length, which assist in the growth and survival of tumor cells.

Telomeres are the sections of DNA at the end of chromosomes that protect them from being degraded. Each time a cell divides, the telomeres shorten, giving normal cells a finite lifespan. Tumor cells are able to achieve cellular immortality by increasing the production of enzymes known as telomerase that can lengthen the telomeres.

In a review, Christophe Nicot, Ph.D., and graduate student Marcia Bellon and of the University of Kansas Medical Center in Kansas City discuss the many ways that human tumor viruses regulate these enzymes in order to maintain telomere stability and promote tumor cell survival and proliferation.

"The diversity of strategies used by tumor viruses underscores the complexity of...telomerase regulation," the authors write.

Contact: Christophe Nicot, cnicot@kumc.edu, (913) 588-6724


Also in the January 8 JNCI:

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