ANN ARBOR, Mich. - Even though cigarette smoking accounts for up to half of all bladder cancer cases, few people are aware of the connection - including more than three-quarters of patients who have bladder cancer, according to a new study from the University of Michigan Comprehensive Cancer Center.

This knowledge vacuum suggests that urologists and other physicians need to do a much better job of telling patients about the risk of smoking and encourage them to quit, the study authors say.

"The general public understands that cigarette smoking can lead to lung cancer, but very few people understand that it also can lead to bladder cancer," says senior author James E. Montie, M.D., Valassis Professor of Urologic Oncology at the U-M Health System.

Counting the number of tumor cells circulating in the bloodstream of patients with castration-resistant prostate cancer can accurately predict how well they are responding to treatment, new results show.

At the ESMO Conference Lugano (ECLU) organized by the European Society for Medical Oncology, researchers showed that changes in the number of circulating tumor cells predicted the outcome after chemotherapyterm in this hard to treat cancer.

"The results add to a growing body of evidence showing that counting these cells is a valuable method for predicting survival and for monitoring treatment benefit in these patients", said Dr. David Olmos from The Royal Marsden NHS Foundation Trust in the UK.

Barcelona, Spain: Researchers have shown for the first time that it is possible to stimulate a woman's ovaries to produce eggs for collection during the final phase of the menstrual cycle. The finding offers the chance for more women who have been diagnosed with cancer to restore their fertility following chemotherapyterm or radiotherapy – cancer treatments that can seriously damage the ovaries, often permanently. The findings were presented at the 24th annual meeting of the European Society of Human Reproduction and Embryology in Barcelona today (Monday).

At present, women who have been diagnosed with cancer may want to have some of their eggs collected and frozen in order to give them an opportunity of having children once their cancer treatment has finished. However, conventional protocols involve starting ovarian stimulation only at the beginning of a woman's menstrual cycle (the day that menstruation starts). Therefore, if the cancer diagnosis is made at any other time in the cycle, a woman could wait up to six weeks before it would be possible to collect eggs (or oocytes) after ovarian stimulation. For many women, six weeks is too long to wait before starting cancer treatment.

The American poet E. E. Cummings lionized the singular 'i', creating a persona standing apart from the crowd and, without power, scoffing at pretentious authority. Capitalist marketeers and scientists alike have repopularized the poetic 'i', perhaps innocently, in iMac and iPhone, Wii and RNAi. Biology's latest 'i' acronym is iPS cells, for induced pluripotent stem cells — antithetically one of the most potent of all cell types¹. To produce iPS cells, drab adult cells are induced into a rejuvenated, embryonic stem (ES)-cell-like state by a puissant cocktail of just four genes — a process known as direct reprogramming. But exactly how this remarkable process works, and why it is so inefficient, has been a mystery. On page 49 of this issue, Mikkelsen et al.² explain why many of the cells get stuck in a woolly intermediate state during reprogramming, and show how to put them back on the path to pluripotency (the ability of a cell to differentiate into all adult cell types).

Emisphere Technologies, Inc. (NASDAQ:EMIS) announced today that Novartis Pharma AG has launched a Phase I study in postmenopausal women to determine the safety and tolerability of oral PTH134, a combination of human PTH-1-34 and the absorption enhancer 5-CNAC using Emisphere's proprietary Eligen(R) technology, for the treatment of postmenopausal osteoporosis. The study is designed to assess the bioavailability profile of increasing doses of PTH-1-34 combined with different amounts of 5-CNAC administered orally. The trial is being conducted in Switzerland and is estimated to yield first interpretable results by the end of the year.

HOUSTON - Thyroid cancer that has spread to distant sites has a poor prognosis, but an experimental drug that inhibits tumor blood vessel formation can slow disease progression in some patients, a research team led by investigators from The University of Texas M. D. Anderson Cancer Center reports in the July 3rd edition of The New England Journal of Medicine.

The investigational drug, motesanib diphosphate, is a VEGFterm inhibitor, a biologic agent that targets receptors on a protein known as vascular endothelial growth factor (VEGF). VEGF is instrumental in angiogenesis (formation of new blood vessels), a process that allows tumors to grow and spread.

Massachusetts General Hospital (MGH) investigators have shown that an MGH-developed, microchip-based device that detects and analyzes tumor cells in the bloodstream can be used to determine the genetic signature of lung tumors, allowing identification of those appropriate for targeted treatment and monitoring genetic changes that occur during therapy. A pilot study of the device called the CTC-chip will appear in the July 24 New England Journal of Medicine and is receiving early online release.

"The CTC-chip opens up a whole new field of studying tumors in real time," says Daniel Haber, MD, director of the MGH Cancer Center and the study's senior author. "When the device is ready for larger clinical trials, it should give us new options for measuring treatment response, defining prognostic and predictive measures, and studying the biology of blood-borne metastasisterm, which is the primary method by which cancer spreads and becomes lethal."

HOUSTON - Thyroid cancer that has spread to distant sites has a poor prognosis, but an experimental drug that inhibits tumor blood vessel formation can slow disease progression in some patients, a research team led by investigators from The University of Texas M. D. Anderson Cancer Center reports in the July 3rd edition of The New England Journal of Medicine.

The investigational drug, motesanib diphosphate, is a VEGFterm inhibitor, a biologic agent that targets receptors on a protein known as vascular endothelial growth factor (VEGF). VEGF is instrumental in angiogenesis (formation of new blood vessels), a process that allows tumors to grow and spread.

Dr. Alan List Named Physician-In-Chief Of Moffitt Cancer Center

Dr. Eduardo Sotomayor to lead Malignant Hematology Program

Tampa, FL (July 1, 2008) — Dr. Alan F. List, formerly the division chief of Malignant Hematology at Moffitt Cancer Center, has been named Executive Vice President, Physician-in-Chief. He will take over for the retired Dr. Clifford Schold Jr.

A new large, prospective population-based study confirms an inverse relationship between coffee consumption and liver cancer risk. The study also found that higher levels of gamma-glutamyltransferase (GGT) in the blood were associated with an increased risk of developing the disease. These findings are published in the July issue of Hepatology, a journal published by John Wiley & Sons on behalf of the American Association for the Study of Liver Diseases (AASLD). The article and an accompanying editorial are also available online at Wiley Interscience (www.interscience.wiley.com).

NEW YORK (June 26, 2008) - The Mesothelioma Center within the Herbert Irving Comprehensive Cancer Center at NewYork-Presbyterian Hospital and Columbia University Medical Center is now recruiting patients for a clinical research study of a new targeted radiation and chemotherapyterm protocol for pleural mesothelioma, a cancer of the lung's lining that is almost always caused by previous exposure to asbestos.

The standard treatment for pleural mesothelioma is currently surgery to remove the patient's lung - a potentially debilitating consequence.

"Current surgical and chemotherapy treatments of patients with malignant pleural mesothelioma are unsatisfactory, and have not been shown to significantly prolong survival. In this study, we will investigate whether a combination of chemotherapy and radiation targeted directly at the lung's lining can improve outcomes while avoiding surgery," says Dr. Robert Taub, the study's principal investigator, director of the Mesothelioma Center at NewYork-Presbyterian/Columbia and professor of clinical medicine at Columbia University College of Physicians and Surgeons. "In addition, this approach has shown to have minimal toxic side effectsterm compared to systemic chemotherapy."

BOSTON--Scientists at Dana-Farber Cancer Institute report they have blocked the development of prostate tumors in cancer-prone mice by knocking out a molecular unit they describe as a "powerhouse" that drives runaway cell growth.

In an article that is being published today as an advanced online publication by the journal Nature, the researchers say the growth-stimulating molecule called p110beta -- part of a cellular signaling network disrupted in several common cancers -- is a promising target for novel cancer therapies designed to shut it down. The report's lead authors are Shidong Jia, MD, PhD, Zhenning Liu, PhD, Sen Zhang PhD, and Pixu Liu, MD, PhD.

A set of promising new anticancer agents could have unforeseen risks in individuals with heart disease, suggests research at Washington University School of Medicine in St. Louis. The anticancer drugs — which go by the strange name of hedgehog antagonists — interfere with a biochemical process that promotes growth in some cancer cells. But the researchers showed that interfering with this biochemical process in mice with heart disease led to further deterioration of cardiac function and ultimately death.

"This finding should serve as a warning that these drugs might have adverse effects on the heart and that it could be very important to monitor patients' cardiovascular health when using this type of anticancer drug," says senior author David Ornitz, M.D., Ph.D., the Alumni Endowed Professor and head of Developmental Biology. The research was reported June 20, 2008, in advance online publication in the Journal of Clinical Investigation.

Cells with irreparable DNA damage normally induce programmed cell death, or apoptosis. However, this mechanism often fails in tumor cells so that transformed cells are able to multiply and spread throughout the body. Scientists at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have now discovered a possible cause of this failure. Tumor cells simply degrade a protein that triggers apoptosis in the case of DNA damage. Blocking this protein degradation might set apoptosis back in operation and, thus, increase the effectiveness of radiotherapy or chemotherapyterm. The researchers have now published their results in Nature Cell Biology.