JCI table of contents: December 7, 2006

December 07, 2006

EDITOR'S PICK: T-beta-RIII joins the fight against breast cancer

Although the soluble factor TGF-beta has been shown to suppress the growth of tumor cells in the early stages of breast cancer, high levels of TGF-beta during the later stages of the disease are associated with a poor outcome. A study using human breast cancer samples and mice, which appears online on December 7 in advance of publication in the January print issue of the Journal of Clinical Investigation, indicates that changes in expression of one component of the TGF-beta receptor, T-beta-RIII, might provide a mechanism for the distinct effects of TGF-beta at the different stages of breast cancer.

Gerard Blobe and colleagues from Duke University showed that expression of T-beta-RIII by human breast cancer samples markedly decreased or was lost with disease progression. Conversely, in a mouse model of breast cancer, tumor cells engineered to express high levels of T-beta-RIII were less able to invade the breast tissue and to metastasize to other organs than tumor cells not engineered to express this protein. Further analysis revealed that the mechanism behind these protective effects of T-beta-RIII was likely to be T-beta-RIII cleavage at the cell membrane, which releases soluble T-beta-RIII that blocks TGF-beta signaling. As low levels of T-beta-RIII were found to be associated with decreased recurrence-free survival of patients with breast cancer and loss of T-beta-RIII was found to begin before tumors became invasive, the authors suggest that analysis of T-beta-RIII levels might help clinicians decide how aggressively to treat their patients.

TITLE: The type III TGF-beta receptor suppresses breast cancer progression

AUTHOR CONTACT:
Gerard C. Blobe
Duke University Medical Center, Durham, North Carolina, USA.
Phone: (919) 668-1352; Fax: (919) 668-2458; E-mail: blobe001@mc.duke.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29293




ONCOLOGY: The protein RB could help clinicians decide what breast cancer therapy is best

One protein that is functionally defective in most human cancers, including a third of all breast cancers, is RB. A study using human breast cancer cells, which appears online on December 7 in advance of publication in the January print issue of the Journal of Clinical Investigation, shows that the presence or absence of functional RB influences the efficacy of therapies for breast cancer.

Erik Knudsen and colleagues from the University of Cincinnati showed that decreasing the expression of RB in human breast cancer cells increased their ability to proliferate and their tumorigenic potential. The cells from many breast cancer patients express the receptor for the hormone estrogen, and antiestrogen drugs such as tamoxifen are used to limit the growth of cancer cells in these patients. In this study, decreasing the expression of RB in human breast cancer cells made the cells unresponsive to tamoxifen. By contrast, decreasing the expression of RB in human breast cancer cells increased the sensitivity of the cells to radiation and other anticancer drugs, both of which are treatments given to patients with breast cancer who fail to respond to antiestrogen drugs such as tamoxifen. Importantly, breast cancer cells from patients in whom disease recurred very rapidly after treatment with tamoxifen had characteristics of cells lacking functional RB. This study indicates that analysis of RB functionality might be useful for clinicians to determine the most effective therapy for their patients.

TITLE: The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancer

AUTHOR CONTACT:
Erik S. Knudsen
University of Cincinnati, Cincinnati, Ohio, USA.
Phone: (513) 558-8885; Fax: (513) 558-4454; E-mail: erik.knudsen@uc.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=28803
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