JCI early table of contents for Dec. 9, 2013
Contact information: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
JCI early table of contents for Dec. 9, 2013 Breast cancer prognosis associated with oncometabolite accumulation The metabolic profile of cancer cells can be used to develop therapies and identify biomarkers associated with cancer outcome. In this issue of the Journal of Clinical Investigation Stefan Ambs and colleagues at the National Cancer Institute discovered an association between the oncometabolite 2-hydroxyglutarate (2-HG) levels, DNA methylation patterns, and breast cancer prognosis. The authors identified a breast cancer subtype with high levels of 2-HG, and a district DNA methylation pattern that was associated with reduced survival. This breast cancer subtype was common in African-American breast cancer patients, who as a group have a high prevalence of aggressive breast cancers. This study indicates that evaluation of 2-HG along with DNA methylation may be a useful biomarker for breast cancer diagnosis and prognosis TITLE: MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis AUTHOR CONTACT: Stefan Ambs
National Cancer Institute, Bethesda, MD, USA
Phone: 301-496-4668; E-mail: ambss@mail.nih.gov View this article at: http://www.jci.org/articles/view/71180?key=e428ff2ab0218ea590e1 Choloroquine reduces formation of bone resorbing cells in murine osteoporosis Bone homeostasis requires precise balance between deposition of new bone by osteoblasts and resorption of old bone by osteoclasts. Bone diseases, including osteoporosis and rheumatoid arthritis, are the result of increased osteoclast activity and formation, which allows bone resorption to outpace deposition. In this issue of the Journal of Clinical Investigation, Brendan Boyce and colleagues at the University of Rochester evaluated the role of TNF receptor–associated receptor 3 (TRAF3) in promoting osteoclast formation. Mice lacking TRAF3 in osteoclast precursor cells had mild osteoporosis that was associated with increased osteoclast formation. The authors found that chloroquine treatment increased TRAF3 in osteoclast precursor cells and limited osteoclast generation. Furthermore, treatment of mouse models of osteoporosis with chloroquine inhibited osteoclast formation. These studies implicate that therapies aimed at increasing TRAF3 in osteoclast precursor cells may limit bone loss for those with bone diseases. TITLE: Chloroquine reduces osteoclastogenesis in murine osteoporosis by preventing TRAF3 degradation AUTHOR CONTACT: Brendan Boyce
University of Rochester Medical Center, Rochester, NY, USA
Phone: 585-275-5837; Fax: 585-276-2832; E-mail: brendan_boyce@urmc.rochester.edu View this article at: http://www.jci.org/articles/view/66947?key=5187dc887c5491664800 ALSO IN THIS ISSUE TITLE: Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways AUTHOR CONTACT: Mina Bissell Lawrence Berkeley National Laboratory, Berkeley, CA, USA Phone: 510 486-4365; E-mail: mjbissell@lbl.gov View this article at: http://www.jci.org/articles/view/63146?key=7749b0e936bffa996011 TITLE: Hematopoietic stem cells are acutely sensitive to Acd shelterin gene inactivation AUTHOR CONTACT: Ivan Maillard
University of Michigan, Ann Arbor, MI, USA
Phone: 734-763-3599; Fax: 734-615-5493; E-mail: imaillar@umich.edu View this article at: http://www.jci.org/articles/view/67871?key=ca7546ee3f58d0b2e096 TITLE: Embryonic exposure to excess thyroid hormone causes thyrotrope cell death AUTHOR CONTACT: Ksenia Tonyushkina
Baystate Medical Center, Springfield, MA, USA
Phone: 413-794-3510; E-mail: ksenia.tonyushkina@bhs.org View this article at: http://www.jci.org/articles/view/70038?key=4e70d4504e09ce632a0f TITLE: Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis AUTHOR CONTACT: Dorina Avram
Albany Medical College, Albany, NY, USA
Phone: 518-262-6731; E-mail: avramd@mail.amc.edu View this article at: http://www.jci.org/articles/view/70103?key=9a540eeb2b0b19f8798b TITLE: Combined SFK/MEK inhibition prevents metastatic outgrowth of dormant tumor cells AUTHOR CONTACT: Jeff Green
National Cancer Institute, Potomac, MD, USA
Phone: 301-435-5193; Fax: 301-496-8709; E-mail: jegreen@nih.gov View this article at: http://www.jci.org/articles/view/70259?key=f6260391d44effc936ab TITLE: LRIG1 inhibits STAT3-dependent inflammation to maintain corneal homeostasis AUTHOR CONTACT: Takahiro Nakamura
Kyoto Prefectural University of Medicine, Kyoto, , JPN
Phone: +81-75-251-5578; Fax: +81-75-251-5663; E-mail: tnakamur@koto.kpu-m.ac.jp View this article at: http://www.jci.org/articles/view/71488?key=d1957df2c922a9a9a9fb ### END
press_releases@the-jci.org
Journal of Clinical Investigation
JCI early table of contents for Dec. 9, 2013 Breast cancer prognosis associated with oncometabolite accumulation The metabolic profile of cancer cells can be used to develop therapies and identify biomarkers associated with cancer outcome. In this issue of the Journal of Clinical Investigation Stefan Ambs and colleagues at the National Cancer Institute discovered an association between the oncometabolite 2-hydroxyglutarate (2-HG) levels, DNA methylation patterns, and breast cancer prognosis. The authors identified a breast cancer subtype with high levels of 2-HG, and a district DNA methylation pattern that was associated with reduced survival. This breast cancer subtype was common in African-American breast cancer patients, who as a group have a high prevalence of aggressive breast cancers. This study indicates that evaluation of 2-HG along with DNA methylation may be a useful biomarker for breast cancer diagnosis and prognosis TITLE: MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis AUTHOR CONTACT: Stefan Ambs
National Cancer Institute, Bethesda, MD, USA
Phone: 301-496-4668; E-mail: ambss@mail.nih.gov View this article at: http://www.jci.org/articles/view/71180?key=e428ff2ab0218ea590e1 Choloroquine reduces formation of bone resorbing cells in murine osteoporosis Bone homeostasis requires precise balance between deposition of new bone by osteoblasts and resorption of old bone by osteoclasts. Bone diseases, including osteoporosis and rheumatoid arthritis, are the result of increased osteoclast activity and formation, which allows bone resorption to outpace deposition. In this issue of the Journal of Clinical Investigation, Brendan Boyce and colleagues at the University of Rochester evaluated the role of TNF receptor–associated receptor 3 (TRAF3) in promoting osteoclast formation. Mice lacking TRAF3 in osteoclast precursor cells had mild osteoporosis that was associated with increased osteoclast formation. The authors found that chloroquine treatment increased TRAF3 in osteoclast precursor cells and limited osteoclast generation. Furthermore, treatment of mouse models of osteoporosis with chloroquine inhibited osteoclast formation. These studies implicate that therapies aimed at increasing TRAF3 in osteoclast precursor cells may limit bone loss for those with bone diseases. TITLE: Chloroquine reduces osteoclastogenesis in murine osteoporosis by preventing TRAF3 degradation AUTHOR CONTACT: Brendan Boyce
University of Rochester Medical Center, Rochester, NY, USA
Phone: 585-275-5837; Fax: 585-276-2832; E-mail: brendan_boyce@urmc.rochester.edu View this article at: http://www.jci.org/articles/view/66947?key=5187dc887c5491664800 ALSO IN THIS ISSUE TITLE: Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways AUTHOR CONTACT: Mina Bissell Lawrence Berkeley National Laboratory, Berkeley, CA, USA Phone: 510 486-4365; E-mail: mjbissell@lbl.gov View this article at: http://www.jci.org/articles/view/63146?key=7749b0e936bffa996011 TITLE: Hematopoietic stem cells are acutely sensitive to Acd shelterin gene inactivation AUTHOR CONTACT: Ivan Maillard
University of Michigan, Ann Arbor, MI, USA
Phone: 734-763-3599; Fax: 734-615-5493; E-mail: imaillar@umich.edu View this article at: http://www.jci.org/articles/view/67871?key=ca7546ee3f58d0b2e096 TITLE: Embryonic exposure to excess thyroid hormone causes thyrotrope cell death AUTHOR CONTACT: Ksenia Tonyushkina
Baystate Medical Center, Springfield, MA, USA
Phone: 413-794-3510; E-mail: ksenia.tonyushkina@bhs.org View this article at: http://www.jci.org/articles/view/70038?key=4e70d4504e09ce632a0f TITLE: Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis AUTHOR CONTACT: Dorina Avram
Albany Medical College, Albany, NY, USA
Phone: 518-262-6731; E-mail: avramd@mail.amc.edu View this article at: http://www.jci.org/articles/view/70103?key=9a540eeb2b0b19f8798b TITLE: Combined SFK/MEK inhibition prevents metastatic outgrowth of dormant tumor cells AUTHOR CONTACT: Jeff Green
National Cancer Institute, Potomac, MD, USA
Phone: 301-435-5193; Fax: 301-496-8709; E-mail: jegreen@nih.gov View this article at: http://www.jci.org/articles/view/70259?key=f6260391d44effc936ab TITLE: LRIG1 inhibits STAT3-dependent inflammation to maintain corneal homeostasis AUTHOR CONTACT: Takahiro Nakamura
Kyoto Prefectural University of Medicine, Kyoto, , JPN
Phone: +81-75-251-5578; Fax: +81-75-251-5663; E-mail: tnakamur@koto.kpu-m.ac.jp View this article at: http://www.jci.org/articles/view/71488?key=d1957df2c922a9a9a9fb ### END