American Association for Cancer Research

October 1, 2008 Cancer Research Highlights

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Selected Articles from the October 1, 2008 Issue

The articles referenced in this Highlights section will be available online in HTML and PDF formats to all interested users at no charge until the next issue of Cancer Research is published. Click on the article title to view the complete article.

View the Table of Contents for the October 1 issue of Cancer Research.


Mammary Cancer Stem Cells and CD61

Vaillant et al.

Page 7711

This study examines changes in epithelial cellular subpopulations in preneoplastic and neoplastic mammary lesions in three mouse models (MMTV-wnt-1, MMTV-neu, and p53+/−) to gain insight into the cells of origin and cellular mechanisms underlying tumor propagation. Vaillant and colleagues found that constitutive wnt-1 signaling in the preneoplastic stage perturbs the epithelial hierarchy, leading to the appearance of aberrant multipotential stem-like cells. The authors also identified a population of cancer stem cells expressing the luminal mammary progenitor marker CD61 in p53+/− and MMTV-wnt-1 mammary tumors, while no cancer stem cell population could be defined from the more homogeneous MMTV-neu model. These data provide further evidence that some breast cancers can develop according to a cancer stem cell model of mammary tumorigenesis and highlight the importance of the progenitor marker CD61 in defining a cellular hierarchy within some types of tumors. 
 

Hypomethylation of P-Cadherin and Crypt Fission

Milicic et al.

Page 7760

In colorectal cancer, ectopic P-cadherin is present within the earliest morphologically recognized neoplastic lesion, the aberrant crypt focus. Milicic and colleagues analyzed the CpG methylation status of the P-cadherin (CDH3) promoter as well as mRNA and protein expression levels in familial and sporadic colorectal cancers and found ectopic expression of P-cadherin in the colon mucosa from the early stages of colorectal cancer that correlated with abnormal gene activation through CDH3 gene promoter hypomethylation. Forced ectopic expression of P-cadherin in a transgenic mouse model accompanied by indomethacin-induced inflammation resulted in a 3-fold higher crypt fission rate in the small and large intestines in homozygous mice compared with wild-type animals. The authors conclude that epigenetic demethylation of the P-cadherin promoter in the human intestine permits its ectopic expression very early in the development of colorectal cancer and that induced P-cadherin expression leads to an increased rate of crypt fission, a common feature of clonal expansion in gastrointestinal dysplasia.


Dietary Induction of Colon Tumors

Yang et al.

Page 7803

Epidemiologic studies show a profound effect of diet on the incidence and progression of colon cancer. Yang and colleagues report that a defined new Western diet (NWD) that mimics dietary risk factors for colon cancer in human Western populations induced colonic tumors when fed to wild-type C57Bl/6 mice for ~ 2 years beginning at age 6 weeks (two-thirds of their average life span). Tumors were prevented by increasing dietary calcium and vitamin D3 to levels comparable to upper levels consumed by humans. Unsupervised clustering of gene expression profiles showed that profiles from mice fed the NWD were similar to that initiated by inheritance of a mutant Apc allele, which is often associated with human colon cancer. This mouse model of dietary induction of colon cancer recapitulates the etiology and pattern of formation of human sporadic colon cancer, the form of the disease responsible for >90% of cases in the United States and other Western countries.


The NF2 gene is mutated in neurofibromatosis type 2, a dominantly inherited cancer disorder. Merlin, the protein coded by the NF2 gene, has been shown to function as an inhibitor of the p21-activated kinases (Paks). Thus, it is plausible that merlin’s tumor suppressive function might be mediated, at least in part, via inhibition of the Paks. Yi and colleagues show that Pak1 activity is increased in a significant fraction of primary schwannomas. Inhibition of Pak1–3 significantly reduced cell growth rates in NIH3T3 cells expressing a dominant-negative form of merlin and inhibited the ability of these cells to form tumors in vivo. These results suggest that inhibiting Paks would be a beneficial approach for the development of therapeutics for the treatment of neurofibromatosis type 2. 


NVP-BEZ235 Prevents Oncogenic PI3K Signaling

Serra et al.

Page 8022

The PI3K signaling pathway plays a central role in diverse cellular functions including proliferation, growth, survival, and metabolism, and genetic aberrations of this pathway are among the most commonly encountered in human cancer. Serra and colleagues show that NVP-BEZ235, a dual inhibitor of PI3K and downstream mammalian target of rapamycin (mTOR), inhibited proliferation and inhibited the activation of several downstream effectors in a panel of breast cancer cells of different origin and mutation status. NVP-BEZ235 was also able to inhibit proliferation of trastuzumab-resistant modified HER2-amplified BT474 cells. In xenografts of one of these, BT474 H1047R, NVP-BEZ235 inhibited PI3K signaling and had potent antitumor activity. In treated animals, there was complete inhibition of PI3K signaling in the skin at pharmacologically active doses, suggesting that skin may serve as a surrogate tissue for pharmacodynamic studies.

 


Fc-Engineered Anti-CD19 Antibody for B-Cell Neoplasms

Horton et al.

Page 8049

CD19 is an excellent target for antibody-based therapies of B-cell neoplasms due to its pan–B cell expression profile. To develop a highly cytotoxic anti-CD19 antibody (XmAb5574), Horton and colleagues employed protein engineering to increase the affinity of the Fc domain for Fcγ receptors on immune effector cells. In vitro, XmAb5574 displayed dramatically increased tumor cytotoxicity via direct and indirect effector functions relative to the wild-type Fc analog antibody and, in vivo, significantly reduced tumor growth in lymphoma xenograft mouse models. These results suggest that the humanized antibody XmAb5574 warrants clinical evaluation as an immunotherapeutic for CD19+ hematological malignancies. 


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