February 15 Cancer Research Highlights

Selected Articles from the February 15, 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 February 15 issue of Cancer Research.

EMT Is Highly Associated with Basal Phenotype Breast Cancer

Sarrío et al.

Page 989

In carcinoma cells, the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype [epithelial-mesenchymal-transition (EMT)] are associated with aggressiveness and invasive potential. To explore the occurrence of EMT in human breast cancer, Sarrió and colleagues performed an immunohistochemical study in 491 invasive breast tumors, and demonstrated that coordinated up-regulation of a variety of EMT markers, together with reduction of epithelial characteristics, preferentially occur in breast tumors with the "basal-like phenotype." Further molecular studies confirmed the potential transformation via EMT of basal-like cells. These data suggest that EMT relates to the high aggressiveness and metastatic potential of basal-like tumors.

STK31 Is a Novel Cancer/Testis Antigen

Yokoe et al.

Page 1074

Yokoe and colleagues adopted a new methodology to identify a novel cancer/testis (CT) antigen with high frequency of expression in colorectal cancer as follows: a combination of laser microdissection and cDNA microarray was used to analyze the gene expression profile of colorectal cancer cells; genes overexpressed in testis and underexpressed in normal colon epithelium were analyzed using cDNA microarray; and the gene expression profile of colorectal cancer cells was compared with that of normal testis. The results show that the new methodology in this study facilitated identification of CT antigens and that STK31 may be a candidate for cancer immunotherapy against gastrointestinal cancer.

Pten Inactivation Accelerates Oncogenic K-ras–Induced Lung Neoplasia

Iwanaga et al.

Page 1119

Findings from studies in humans and mice indicate that K-ras somatic mutations are sufficient to cause lung premalignant lesions, which require additional genetic events to progress into lung adenocarcinomas. Iwanaga and colleagues investigated whether mutant K-ras acts cooperatively with Pten inactivation to promote lung tumorigenesis in mice. Although Pten inactivation alone caused no morphologic evidence of lung premalignancy, it accelerated the onset and increased the number and histologic severity of lung lesions that developed due to mutant K-ras. This cooperativity suggests that Pten inactivation might be a crucial secondary event in K-ras–induced lung neoplasia.

Androgen Receptor Promotes Invasiveness of Prostate Cancer

Hara et al.

Page 1128

Neither the role of androgen receptor (AR) in invasion/metastasis nor the relationship between invasiveness and androgen-refractory status has been established. Hara and colleagues used the androgen-dependent prostate cancer cell line MDA PCa 2b, derived from a human bone metastasis, to generate an invasive subline (MDA-I) using a Matrigel chamber. Their results suggest that AR promotes the invasiveness of both androgen-dependent and androgen-refractory prostate cancer, and that a more invasive phenotype might develop through AR activation during cancer progression. These findings potentially support the use of adjuvant hormonal therapy and the future development of more potent androgen blockade therapy.

An Inhibitor of a Phosphatase from Regenerating Liver Suppresses Cell Growth

Daouti et al.

Page 1162
Daouti et al.

The phosphatase of regenerating liver (PRL), a unique class of oncogenic phosphatases, has been found to be dysregulated in many tumors. In light of a causative role of PRL-3 in tumorigenesis, targeting PRL may provide a novel approach to cancer therapy. Daouti and co-investigators identified a potent selective PRL inhibitor that suppressed tumor cell anchorage-independent growth via a novel p53-independent mechanism involving p130Cas cleavage and anoikis. The PRL inhibitor and PRL-targeting siRNAs resulted in similar cellular consequences. This study provides a new insight into a role of PRL in tumor progression and supports PRL as an attractive target for cancer intervention.

February 15 Cancer Research Highlights

Selected Articles from the February 15, 2008 Issue

EMT Is Highly Associated with Basal Phenotype Breast Cancer

STK31 Is a Novel Cancer/Testis Antigen

Pten Inactivation Accelerates Oncogenic K-ras–Induced Lung Neoplasia

Androgen Receptor Promotes Invasiveness of Prostate Cancer

An Inhibitor of a Phosphatase from Regenerating Liver Suppresses Cell Growth

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