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JCI online early table of contents: Sept. 12, 2011
Date:9/12/2011

EDITOR'S PICK: BVES butts heads with colorectal cancer

Once a cancer gains the ability to invade local tissues and spread to a distant site it becomes much harder to treat. A team of researchers, led by Min Chang and Christopher Williams, at Vanderbilt University School of Medicine, Nashville, has now identified the protein BVES as a suppressor of colorectal cancer progression to this dangerous state, leading them to suggest that BVES could be a therapeutic or preventative target in colorectal cancer.

Cancers originating from cells covering any of the external and internal surfaces of the body (epithelial cells) are known as epithelial cancers. If such cancers (e.g., colorectal cancer) are to become invasive and spread to distant sites in the body, some of the epithelial cancer cells must acquire the characteristics of a different cell type, a mesenchymal cell. Protein complexes that link epithelial cells together (junctional complexes) are regulators of epithelial-mesenchymal transition (EMT). Chang, Williams, and colleagues found that the junctional protein BVES regulates EMT in human colon cancer cells. Importantly, the team found that BVES expression was reduced in all stages of human colorectal carcinoma and that restoring BVES expression to normal decreased the in vitro and in vivo cancer cell characteristics of human colon cancer cells. These data provide the rational for the suggestion that targeting BVES could be of benefit to individuals with colorectal cancer.

TITLE: BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma

AUTHOR CONTACT:
Min S. Chang
Vanderbilt Eye Institute, Nashville, Tennessee, USA.
Phone: 615.936.6413; Fax: 615.936.6410; E-mail: min.s.chang@vanderbilt.edu.

Christopher S. Williams
Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Phone: 615.322.3642; Fax: 615.343.6229; E-mail: christopher.williams@vanderbilt.edu.

View this article at: http://www.jci.org/articles/view/44228?key=3aac564d108a38a35e37


NEPHROLOGY: Kidney maintains its integrity with the protein Arhgap24

A key function of our kidneys is to filter waste from our blood and to divert this into our urine. Focal segmental glomerulosclerosis (FSGS) is a kidney disease characterized by high levels of protein in the urine. It is caused by breakdown of the filtration barrier in the kidney that prevents proteins in the blood from being lost into the urine. A team of researchers, led by Andrey Shaw, at Washington University School of Medicine, St. Louis, has now linked a mutation in the ARHGAP24 gene to FSGS and uncovered the mechanism by which it could cause disease. The data lead the team to suggest that modulating the activity of the Arhgap24 protein could provide a new way to treat FSGS.

TITLE: Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis

AUTHOR CONTACT:
Andrey S. Shaw
Washington University School of Medicine, St. Louis, Missouri, USA.
Phone: 314.362.4614; Fax: 314.362.9108; E-mail: shaw@pathology.wustl.edu.

View this article at: http://www.jci.org/articles/view/46458?key=f0db4f3a9b1bb81cc4de


ONCOLOGY: New genetic link to lung cancers

Identifying the genetic changes that cause a cancer to form and progress is important for understanding the mechanisms underlying the cancer and for defining candidate therapeutic targets. A team of researchers, led by Aly Karsan, at British Columbia Cancer Agency Research Centre, Vancouver, has now identified an increase in the number of copies of the TRAF6 gene as a genetic change that can contribute to the development of human lung cancers. The team suggests that its data indicating that amplification of the TRAF6 gene is a common event in human lung cancers could explain why the signaling molecule NF-kappa-B is constitutively active in the majority of lung cancers.

TITLE: TRAF6 is an amplified oncogene bridging the RAS and NF-kappa-B pathways in human lung cancer

AUTHOR CONTACT:
Aly Karsan
British Columbia Cancer Agency Research Centre, Vancouver, British Columbia, Canada.
Phone: 604.675.8033; Fax: 604.675.8049; E-mail: akarsan@bccrc.ca.

View this article at: http://www.jci.org/articles/view/58818?key=f98695e6b1517c4b6a58


TUMOR IMMUNOLOGY: Understanding failure: why some anticancer therapies benefit only a few patients

For many years researchers sought to develop approaches to enhance the natural immune response to tumors in the hope that this would be clinically beneficial. As such, there are now several different ways to effectively direct immune responses toward tumor cells. However, surprisingly few patients have benefitted clinically from these approaches. A team of researchers, led by Dmitry Gabrilovich, at the H. Lee Moffitt Cancer Center, Tampa, has now identified one possible explanation as to why therapeutic approaches that induce responses mediated by immune cells known as cytotoxic T lymphocytes (CTLs) are not effective.

For CTLs to kill a cancer cell they must recognize on the cell's surface a protein complex known as an MHC molecule bound to a fragment of a cancer cellspecific protein. In the study, Gabrilovitch and colleagues found that in a mouse model of cancer, cells in the tumor known as MDCs produced a substance (peroxynitrite) that prevented the formation of the MHC/protein fragment complexes that CTLs recognize and that this rendered the tumor cells resistant to killing by CTLs. The clinical relevance of these data was highlighted by the observation that MDCs are a predominant source of peroxynitrite in human lung, pancreatic, and breast cancer samples. The authors therefore suggest that inhibitors of peroxynitrite production might improve the effectiveness of anticancer approaches designed to induce CTL responses.

TITLE: Tumor-infiltrating myeloid cells induce tumor cell resistance to cytotoxic T cells in mice

AUTHOR CONTACT:
Dmitry Gabrilovich
H. Lee Moffitt Cancer Center, Tampa, Florida, USA.
Phone: 813.745.6863; Fax: 813.745.1328; E-mail: dmitry.gabrilovich@moffitt.org.

View this article at: http://www.jci.org/articles/view/45862?key=47083e937e4f504f5fa3


INFECTIOUS DISEASE: The cellular comings and goings in contained M. tuberculosis infection

It is estimated that one-third of the world's population is infected with the bacterium that causes tuberculosis, Mycobacterium tuberculosis. However, only 5󈝶% of those infected develop active disease. In the majority of individuals, the bacteria are prevented from causing disease by being retained inside cell masses known as granulomas. Several cell types are found in granulomas, including immune cells known as inflammatory DCs. In new research, Matyas Sandor and colleagues, at the University of Wisconsin, Madison, have finally gained insight into the function of these cells in 'hidden' (latent) M. tuberculosis infection. Specifically, Sandor and colleagues were able to visualize inflammatory DCs trafficking in and out of granulomas in mice during latent infection and found that they promoted the activation of immune cells known as CD4+ T cells reactive toward M. tuberculosis. These data provide new understanding of events during the late phase of infection and could help us begin to better understand and treat latent M. tuberculosis infections.

TITLE: Inflammatory dendritic cells migrate in and out of transplanted chronic mycobacterial granulomas in mice

AUTHOR CONTACT:
Matyas Sandor
University of Wisconsin, Madison, Wisconsin, USA.
Phone: 608.265.8715; Fax: 608.262.0846; E-mail: msandor@wisc.edu.

View this article at: http://www.jci.org/articles/view/45113?key=650e45f0554a30cdffd2


INFECTIOUS DISEASE: Recapitulating in vivo cellular function in vitro

It is estimated that one-third of the world's population is infected with the bacterium that causes tuberculosis, Mycobacterium tuberculosis. Upon infection, M. tuberculosis often hides in immune cells known as macrophages. Although the macrophages are somehow unable to kill off the invading bacteria, they do not allow the M. tuberculosis to grow. How macrophages restrict the growth of M. tuberculosis has not been determined. This is largely because the macrophages used thus far in in vitro studies fail to recapitulate what happens in vivo they support the growth of infecting M. tuberculosis and then die. However, Guillaume Vogt and Carl Nathan, at Weill Cornell Medical College, New York, have now developed a culture method that generates human macrophages that can survive infection with M. tuberculosis and that severely limit the growth of the bacteria. Vogt and Nathan hope that their new culture method will allow researchers to determine how macrophages keep M. tuberculosis under control.

TITLE: In vitro differentiation of human macrophages with enhanced antimycobacterial activity

AUTHOR CONTACT:
Guillaume Vogt
The Rockefeller University, New York, New York, USA.
Phone: 212.327.7336; Fax: 212.327.7330; E-mail: guillaume.vogt@inserm.fr.

Carl Nathan
Weill Cornell Medical College, New York, New York, USA.
Phone: 212.746.6505; Fax: 212.746.8587; E-mail: cnathan@med.cornell.edu.

View this article at: http://www.jci.org/articles/view/57235?key=adc45d67924205d0a233


NEPHROLOGY: Defining a molecular mechanism that lacks integrity in the kidney

A key function of our kidneys is to filter waste from our blood and to divert this into our urine. Proteinuric kidney diseases, which are characterized by high levels of protein in the urine, are caused by breakdown of the filtration barrier in the kidney that prevents proteins in the blood from being lost into the urine. In particular, these diseases are caused by injury to podocytes, specialized cells that are key to the integrity of the filtration barrier. A team of researchers led by Sanja Sever, at Massachusetts General Hospital, Boston, and Jochen Reiser, at the University of Miami, Miami has now identified a molecular mechanism that impairs key features of mouse and human podocytes that are essential for their function in the filtration barrier of the kidney. The authors conclude that this molecular mechanism could underlie proteinuric kidney disease and suggest that it provides potential new targets for treatment.

TITLE: CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival

AUTHOR CONTACT:
Sanja Sever
Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Phone: 617.724.8922; Fax: 617.726.5669; E-mail: ssever@partners.org.

Jochen Reiser
University of Miami, Miami, Florida, USA.
Phone: 305.243.2349; Fax: 305.243.2309; E-mail: jreiser@med.miami.edu.

View this article at: http://www.jci.org/articles/view/58552?key=b618f54191c2ab2d5ed1


NEPHROLOGY: Cells from outside the kidney link two features of chronic kidney disease

Individuals with chronic kidney disease often suffer from anemia. This is because the cells in the kidney that produce erythropoietin, the hormone that stimulates the production of new red blood cells in the bone marrow, are dysfunctional in these individuals. Dysfunction of these cells (fibroblasts) also causes scarring of the kidney, a condition known as renal fibrosis, which is a central feature of chronic kidney disease. Despite the importance of fibroblasts in chronic kidney disease, little is known about their origin and how they are regulated. Now, a team of researchers, led by Motoko Yanagita, at Kyoto University, Japan, has determined that the majority of erythropoietin-producing fibroblasts in the healthy mouse kidney are derived from cells that originally came from outside the kidney. Importantly, in the diseased kidney, these particular fibroblasts became dysfunctional, decreasing production of erythropoietin and contributing to fibrosis. Further, in a mouse model of renal fibrosis, treatment with tamoxifen (a drug FDA approved to treat breast cancer) increased erythropoietin production and decreased fibrosis. The authors therefore suggest that tamoxifen and related drugs could provide benefit to individuals with chronic kidney disease.

TITLE: Dysfunction of fibroblasts of extrarenal origin underlies renal fibrosis and renal anemia in mice

AUTHOR CONTACT:
Motoko Yanagita
Kyoto University Graduate School of Medicine, Kyoto, Japan.
Phone: 81.75.753.9310; Fax: 81.75.753.9311; E-mail: motoy@kuhp.kyoto-u.ac.jp.

View this article at: http://www.jci.org/articles/view/57301?key=c580cd38514bd32108c5


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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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