CytRx Corporation (Nasdaq:CYTR), a biopharmaceutical company engaged in the development and commercialization of human therapeutics, today announced that INNO-406, CytRx’s potent, orally available, rationally designed, dual Bcr-Abl and Lyn-kinase inhibitor, demonstrated clinical responses in patients with Chronic Myeloid Leukemia (CML). INNO-406 is being evaluated for the treatment of patients with CML and other leukemias that have a certain mutation called the Philadelphia Chromosome (Ph+) and are intolerant of or resistant to imatinib (Gleevec®) and second line tyrosine kinase inhibitors (i.e. dasatinib (Sprycel®) and nilotinib (Tasigna®)).

CML is a type of cancer that starts in blood-forming cells of the bone marrow and invades the blood. In 2007, the American Cancer Society estimated that approximately 4,600 new cases of CML were diagnosed in the US and that the number will increase as the population ages. Current estimates are that worldwide CML prevalence will increase by 10,000 patients a year, reaching a population of 110,000 in 2010. The global market is estimated to be $5.5 billion by 2012.
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Doctors know that you’re at a higher risk for breast, colon and prostate cancers if they’ve been found in your family. Brain cancer can now be placed on that same list, says a new study by Tel Aviv University and the University of Utah.

Dr. Deborah Blumenthal, co-director of Tel Aviv University’s Neuro-oncology Service at the Tel-Aviv Sourasky Medical Center, says that a family history of brain cancer, like those of other cancers, should be reported to the family doctor during a routine medical checkup.

The new study, using data from the Utah Population Data Base (UPDB) at the University of Utah in Salt Lake City, was unique in the large number of cases examined, which tracked back at least three generations and as far as ten generations in some families. The brain tumors studied by the researchers include glioblastoma, the same tumor afflicting Sen. Edward Kennedy, who has been undergoing treatment since June.
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Cancer Research UK scientists have discovered the molecular basis for tamoxifen response in breast cancer cells - and the reason why some women can develop resistance to the treatment, according to a study published in Nature*.

Tamoxifen is given to most women for five years after they are first diagnosed with breast cancer to help prevent the disease from coming back but some women develop resistance to the treatment after time, meaning their cancer is more likely to return.

Researchers at the Cancer Research UK Cambridge Research Institute have discovered for the first time the mechanism by which the breast cancer therapy tamoxifen operates. It switches off a breast cancer gene ErbB2 via a protein called Pax2. Pax2 acts as a ’switch’ to keep ErbB2 switched off. Tamoxifen resistance occurs when ErbB2 remains switched on.

Previously it was known that tamoxifen worked by blocking oestrogen from causing unchecked cell growth in breast cancer by switching certain genes on but the mechanism by which this occurred was unknown.

Lead author, Dr Jason Carroll said: “We knew that women developed resistance to tamoxifen but previously our understanding of why this occurred could be compared with trying to fix a broken car without knowing how the engine worked. Now we understand how all the engine parts operate and we can try to think about ways to make repairs.

“We have discovered that for tamoxifen to work it has to block the gene ErbB2 and it does this by using a control switch that is hidden in the background of the genome, within the ErbB2 gene itself. In order for tamoxifen to be effective, this switch must be held in the off position by Pax2. Now we understand how women can develop tamoxifen resistance.”

The production of oestrogen can cause breast cancer cells to grow and divide but tamoxifen prevents oestrogen from causing breast cancer cells to grow, helping to lower the risk of the disease returning. Most women have breast cancers that are stimulated to grow by oestrogen but not all.**

Breast cancer is the most common cancer in women in the UK. More than 45,500 women are diagnosed with the disease each year - 125 women a day, and the disease causes almost 12,500 deaths each year. Eight in 10 cases of breast cancer are diagnosed in women over the age of 50.

Professor Sir David Lane, Cancer Research UK’s chief scientist said: “Cancer Research UK’s early clinical trials of tamoxifen helped transform the way that women were treated for early breast cancer saving ten’s of thousands of lives, and this work is yet another step forward.

“More women are surviving breast cancer than ever before thanks to improvements in diagnosis and treatment as well as important fundamental science discoveries like this.”

He added: “Tamoxifen has been a huge success story helping to prevent breast cancer recurring for many women.

“Understanding why it occasionally stops working is really important because it allows us to identify new targets for drug development and who will need such treatments.”

Notes

Antoni Hurtado et al. *ERBB2 regulation by Estrogen Receptor-Pax2 determines tamoxifen response. (2008) Nature. Wednesday 12 November.

The scientists used microarray technology (genomic technology) to define a genomic map of where oestrogen receptor interacts with the genome. The oestrogen receptor was found to interact with unexpected areas in the genome, which were then identified as the ’switches’ for gene regulation. This provided insight into how oestrogen receptor worked. Using this information, the scientists could find the switch for the important cancer related gene, ErbB2.
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A new study of people in Europe found that having a large waist nearly doubled the risk of premature death regardless of whether they were overweight or not and supports the idea that waist size or waist to hip ratio should be used to assess risk of death.

The study was conducted by researchers from Imperial College London, the German Institute of Human Nutrition, and other research institutions across Europe and was published on 13 November in the New England Journal of Medicine.

The researchers wrote that previous studies relied heavily on BMI (body mass index, a person’s weight in kilos divided by the square of their height in metres) to assess the link between body fat (adiposity) and risk of death, but not many had looked into the effect of how the body fat is distributed.

For the study the researchers used data from 359,387 participants from 9 countries that were taking part in the European Prospective Investigation into Cancer and Nutrition (EPIC), one of the largest long-term prospective studies in the world. The average age of the participants when data were first collected was 51.5 years, and 65.4 per cent were women.
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Based on current estimates, 8,420 people are expected to die from melanoma this year. In an effort to reverse this sobering trend, dermatologists and the scientific community alike are continually developing new diagnostics, refining detection guidelines and providing patients with the tools they need to properly examine their own skin for signs of skin cancer.

Speaking today at the American Academy of Dermatology’s SKIN academy (Academy), dermatologist Ellen S. Marmur, MD, FAAD, chief of the division of dermatologic and cosmetic surgery at The Mount Sinai Medical Center in New York, presented the latest advances in diagnosing skin cancer and the Academy’s new detection strategies that emphasize the importance of patient involvement.

“There are some exciting innovations in diagnosing skin cancer that can help us detect skin cancer early, when it is most treatable,” said Dr. Marmur. “Even simple detection tools designed by the Academy that patients can use in their own homes can save thousands of lives.”

New Technologies for Diagnosing Skin Cancer

Dermatologists traditionally diagnose skin cancer by evaluating the skin using a clinical examination and, if necessary, a magnifying device and then biopsying any suspicious lesions. Now, technological advances in computers, lasers and other polarizing light sources are providing dermatologists with tools to enhance the evaluation of suspicious lesions and, in some cases, decreasing the number of biopsies needed for an accurate diagnosis. The idea is to hone in on suspicious lesions earlier and with more specificity.

One of the newest technological developments in the fight against skin cancer is the use of sophisticated imaging to scan and enhance certain features of suspected lesions. Similar to how a computerized tomography (CT) scan highlights areas of the brain for abnormalities, imaging devices can now work on the skin to help detect cancerous tissue.

Another exciting technology dermatologists are using to evaluate suspected skin cancers is a hand-held light device known as dermascopy that can look at the pigment of the skin through specialized filters that magnify and polarize lesions. For example, similar to how filters are used on cameras to create certain backgrounds, filters are used on this device to enhance certain features of lesions such as brown or red background colors that could indicate a melanoma (the deadliest form of skin cancer).
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Researchers at the University of California, San Diego School of Medicine, led by Ajit Varki, M.D., have shown a new mechanism for how human consumption of red meat and milk products could contribute to the increased risk of cancerous tumors. Their findings, which suggest that inflammation resulting from a molecule introduced through consumption of these foods could promote tumor growth, are published online this week in advance of print publication in the Proceedings of the National Academy of Sciences (PNAS).

Varki, UC San Diego School of Medicine distinguished professor of medicine and cellular and molecular medicine, and co-director of the UCSD Glycobiology Research and Training Center, and colleagues studied a non-human cellular molecule called N-glycolylneuraminic acid (Neu5Gc). Neu5Gc is a type of glycan, or sugar molecule, that humans don’t naturally produce, but that can be incorporated into human tissues as a result of eating red meat. The body then develops anti-Neu5Gc antibodies - an immune response that could potentially lead to chronic inflammation, as first suggested in a 2003 PNAS paper by Varki.
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She’s travelled between Brisbane and Paris to better understand skin cancer, and now UQ PhD student Marina Kvaskoff has been awarded a top French prize for her research.

Ms Kvaskoff, from St Lucia, is one of only 10 academics to win a 2008 L’Oreal France-UNESCO For Women in Science Award, with the prizes presented in Paris next week.

The awards are worth 10,000 Euros each and are given to French women completing PhDs in the life sciences to enable greater recognition for their work and to build a career in their chosen fields.
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A new cross-Canada study has found that breast and prostate cancer treatment can foster bone loss. In the online edition of the American Society of Clinical Oncology, the scientists explain how loss of bone mass might affect 46,000 people diagnosed with breast and prostate cancer each year* and place them at increased risk for osteoporosis and fractures.

“Our study also looked at possible medications that can reverse or halt bone loss,” says Dr. Fred Saad, lead author and director of urologic oncology at the Université de Montréal’s Faculty of Medicine and the Centre Hospitalier de l’Université de Montréal (CHUM), who completed the exhaustive study with colleagues from McMaster University, the Université Laval, the University of Toronto and the University of British Columbia.
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A small, antibody-like molecule created by researchers at Fox Chase Cancer Center can successfully attack two separate molecules on the surface of cancer cells at the same time, halting the growth of breast cancer cells in laboratory tests, the researchers say. The molecule, nickname “ALM,” might be a means of slowing cancer spread or, as the researchers believe, a guidance system for delivering more aggressive drugs directly to cancer cells. Their findings appear in this month’s British Journal of Cancer.

Unlike naturally occurring antibodies, which only bind to one specific target at a time, ALM is bispecific, meaning it attaches to two separate targets simultaneously. ALM’s targets are two signaling proteins, ErbB2 and ErbB3, which connect to form a growth-promoting complex on the surface of many cancer cells, including head and neck cancer and drug-resistant breast cancer.
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For the first time in a clinical study, researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and the Charité - Universitätsmedizin Berlin, Germany, have tested a new technology enabling them to transfer genetic material directly into a tumor by means of high pressure. As Assistant Professors Wolfgang Walther, together with Professor Peter M. Schlag report in Clinical Cancer Research (Vol. 14, Nr. 22, pp. 7545-7553)*, their results show that jet injection delivers genes into the tumor tissue safely and in a targeted manner. The application was well tolerated by all 17 patients enrolled in this study. No adverse events were experienced.
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