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Doctors Haeck, Eaves, and Rohrich write joint ASAPS/ASPS statement calling for more research into stem cell facelift and stem cell breast augmentation.

Dallas, TX (PRWEB) February 22, 2012

There is little evidence to support the safety and effectiveness of procedures, equipment and treatments that have been advertised using adult stem cells for aesthetic reconstruction, including plastic surgery and facial rejuvenation, according to physicians writing in Plastic and Reconstructive Surgery.

Dr. Rod J. Rohrich, chairman of the Department of Plastic Surgery at UT Southwestern Medical Center and editor-in-chief of the journal, published a position statement on “stem cell facelifts” and “stem cell breast augmentation,” also known as “natural breast augmentation.” Dr. Felmont F. Eaves III of Chapel Hill, N.C., and Dr. Phillip C. Haeck of Seattle, Wash.,collaborated on the statement on behalf of the American Society for Aesthetic Plastic Surgery (ASAPS) and the American Society of Plastic Surgeons (ASPS).

“There are encouraging data from studies in laboratories to suggest that the use of adult stem cells is a very promising field and may produce beneficial medical therapies to treat a variety of diseases,” the doctors said in the statement. They emphasized that there is a lack of consistency in the way stem cell facelift procedures are performed, and pointed out that many procedures are being advertised by physicians who are not board-certified for this type of treatment, and devices being sold for aesthetic stem cell treatments have not been approved for human use in the U.S.

In the report, the doctors encourage their peers to continue reporting clinic results and experimental research to peer-reviewed plastic surgery journals to both promote good science and to foster safety and best practices for stem cell use in aesthetic procedures. “Much more research needs to be conducted before any definitive statements can be made,” the report said. “[Until then,] stem cell based procedures should be performed in compliance with FDA regulatory guidelines.”

Dr. Rohrich said many of the advertisements claiming stem cells can aid in restoring facial and body youthfulness come from outside the U.S. “Further direct, approved clinical research is needed to validate those claims,” he said, “but the future is potentially bright for the use of adult stem cells in both plastic surgery and facial rejuvenation, as well as in medical procedures, such as restoring nerve and brain damage resulting from trauma or cancer, as well as reversing the severe effects of auto immune disease.”

To read the complete joint ASAPS/ASPS position statement on stem cell use in aesthetic surgery, including stem cell facelifts and natural breast augmentation, visit the ASPS, at their website.

About Rod J. Rohrich, M.D., F.A.C.S.

Dr. Rod J. Rohrich holds the Betty and Warren Woodward Chair in Plastic and Reconstructive Surgery at UT Southwestern Medical Center in Dallas, Texas. He also holds the UT Southwestern Medical Center Crystal Charity Ball Distinguished Chair in Plastic Surgery. He is a graduate of the Baylor College of Medicine with high honors, with residencies at the University of Michigan Medical Center and fellowships at the Massachusetts General Hospital/Harvard (hand/microsurgery) and Oxford University (pediatric plastic surgery). He has served as president of the American Society of Plastic Surgeons. He repeatedly has been selected by his peers as one of America's best doctors, and twice has received one of his profession's highest honors, the Plastic Surgery Educational Foundation Distinguished Service Award, which recognizes his contributions to education in his field. Dr. Rohrich participates in and has led numerous associations and councils for the advancement of plastic and reconstructive surgery. He is a native of North Dakota. He is married to Dr. Diane Gibby, also a plastic surgeon. They live in Texas with their two children.

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Rod J. Rohrich, M.D.
Rod J. Rohrich M.D.
(214) 821-9114
Email Information

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Surgeons Urge Caution: Stem Cell Treatments Untested in Aesthetic Surgery

Global leader in animal stem cell technology is poised for significant expansion through new partnership with top U.S. companion animal health distribution company.

Las Vegas, Nevada (PRWEB) February 22, 2012

MediVet-America, the global leader in veterinary stem cell technology and regenerative medicine, has entered into a distribution partnership with Butler Schein Animal Health, a division of Henry Schein, the leading companion animal health distribution company in the U.S., to sell and distribute stem cell kits and equipment to veterinarians serving the nation’s fast-growing $50 billion pet industry.

The announcement was made today at the Western Veterinary Conference in Las Vegas by Jeremy Delk, CEO of MediVet-America.

The two companies will partner to sell and distribute MediVet-America’s advanced stem cell technology to more than 26,000 veterinary clinics nationwide. Adult animal stem cell technology uses the body’s own regenerative healing power to help treat dogs, cats, horses and other animals suffering from painful arthritis, hip dysplasia and tendon, ligament and cartilage injuries and other ailments.

The Adipose-Derived Stem Cell Procedure Kit and state of the art equipment, co-developed with Medical Australia, enable veterinarians to remove a small sample of fat, separate the stem cells, then activate and inject them into affected areas.

“We are pleased to be teaming up with Butler Schein, the largest companion animal health distribution company in the nation,” said Delk. “Their strong track record in sales and distribution will further fuel our rapid growth and bring this breakthrough technology to more leading veterinary practices across the country.”

To introduce the distribution partnership, Delk said MediVet-America has developed an exclusive program of product and service offers that will be made available only to Butler Schein customers.

Veterinary practitioners in more than 200 markets throughout 42 states now perform the drug-free procedure entirely in their own clinics more quickly, effectively and economically than earlier generation animal stem cell therapy. MediVet-America’s new treatment, developed in Australia, is available in 26 countries worldwide.

“This exciting partnership will allow even more of our colleagues unparalleled access to MediVet-America’s superior technology, providing the most affordable and efficacious stem cell therapy in the industry,” said Mike Hutchinson, D.V.M., the world’s leading animal stem cell practitioner. Dr. Hutchinson, who has spoken around the world about stem cell therapy, most recently in Tokyo, has performed more than 300 procedures over the last 18 months in his practice near Pittsburgh, PA.

Partnering with the leading animal health manufacturers in the world, Butler Schein maintains an order-fill ratio greater than 98 percent, and is positioned to bring the broadest selection of veterinary products and strategic business solutions to veterinarians, including:

    A comprehensive product offering for companion animal, equine and large animal practices including biologicals, diagnostics, nutritionals, parasiticides and pharmaceuticals

    Technology hardware and software solutions     Capital equipment, supply products and repair services     Practice design and remodeling, client marketing and financial solutions

Stem cells are basic biological cells with the ability to differentiate into specialized tissue cells and regenerate new cells to replace or repair damaged tissue. The stem cells used in veterinary medicine are not embryonic, which have attracted controversy over the years, but are taken from adipose (fat) tissue of the adult animal.

Americans spent an estimated $50.8 billion in 2011 on their companion animals, according to the American Pet Products Association, up from $28.5 billion in 2001. MediVet-America’s stem cell treatment costs about $1,800 for small animals, $2,400 for horses. Stem cells also can be frozen and banked for future use through MediVet Lab Services.

MEDIVET-AMERICA

A research and development company and global leader in veterinary stem cell technology, MediVet-America provides innovative cell applications for the therapeutic care of animals. Headquartered in Nicholasville, Kentucky, MediVet-America develops advanced cellular designed kits and services for the treatment of arthritis and degenerative joint disease. The company also offers MediVet Lab Services in multiple locations around the world that provides technical support for in-house stem cell vets, as well as regional and national Adipose stem cell processing and cryo banking services for pets at a young age or for a maintenance program, autologous conditioned serum processing, and cell counting for in-house stem cell procedures. http://www.MediVet-America.com

BUTLER SCHEIN ANIMAL HEALTH

Butler Schein Animal Health is the leading U.S. companion animal health distribution company. Headquartered in Dublin, Ohio, the company operates through 18 distribution centers and 12 telecenters. Approximately 900 Butler Schein Animal Health team members, including 300 field sales representatives and 200 telesales and customer support representatives, serve animal health customers in all 50 states. http://www.ButlerShein.com

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Dick Roberts
Roberts Communications
(412) 535-5000
Email Information

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Committed to funding the most innovative minds in the field of prostate cancer research, the Prostate Cancer Foundation (PCF) expanded its global knowledge exchange in 2012 and will be expanding its research efforts in new countries later this year. A total of 15 competitive research grants have been awarded to-date in 2012, bringing the total of young investigators awarded to 89.

Young Investigator awards are designed to promote long-term careers in the field of prostate cancer by providing three year grants for transformational research focused on prostate cancer treatments to improve patient outcomes. Since 2007, PCF has invested more than $20 million in Young Investigator grants.

“PCF-supported young investigators have changed the scope of prostate cancer research, advancing treatment sciences and improving the lives of patients worldwide,” said Howard Soule, PhD, chief science officer and executive vice president of PCF. “It is with great pride and appreciation that PCF can now announce our young investigator program spans across six countries and 42 research institutes.”

Each Young Investigator recipient is awarded $225,000 over a three-year period. Funding is also matched dollar-for-dollar by each recipient’s research institution, making the total award worth $450,000. A total of 148 applicants applied for 2012 PCF Young Investigator funding and over 74 global professionals reviewed these applications, which addressed 29 specialized scientific areas within prostate cancer research.

Buoyed by PCF support and the research it enables, many funded researchers go on to win additional government and privately funded grants to help advance the field of prostate cancer research.

The Prostate Cancer Foundation (PCF) is the world’s leading philanthropic organization funding and accelerating research. Founded in 1993, PCF has raised more than $475 million and provided funding to over 1,600 research projects at nearly 200 institutions in 15 countries around the world. PCF advocates for greater awareness of prostate cancer and more efficient investment of governmental research funds supporting transformational cancer research. Our efforts have helped produce a 20-fold increase in government funding for prostate cancer. More information about PCF can be found at pcf.org.

The 2012 Robbins Family – PCF Young Investigator Award

Tarek Bismar, MD

University of Calgary

Mentor: Peter Forsyth, MD  

The two most common genomic aberrations in prostate cancer are the ERG gene rearrangements and PTEN deletion. TMPRSS2-ERG represents the most common form of ERG rearrangements. It is an aberration in the genome of prostate cancer cells created when two distinct genes, TMPRSS2 and ERG (found in two different regions of DNA), are shuffled around and erroneously juxtaposed. PTEN is a tumor suppressor gene (a gene that protects against cancer) and is often deleted from the DNA code of prostate cancer cells. Dr. Bismar’s work centers on identifying the molecular differences between prostate cancer cells that harbor these genetic alterations and prostate cancer cells that do not. To understand how TMPRSS2-ERG and PTEN deletion change the behavior of prostate cancer cells, Dr. Bismar compared the molecular profile of tissue samples from patients who were either positive or negative for the two genetic alterations. In his comparative analysis he has identified a list of genes that are either elevated or depleted in prostate cancers in relation to their TMPRSS2-ERG and PTEN status. So far, Dr. Bismar has discovered 5 novel, candidate prostate cancer biomarkers (a molecule that indicates a biological process or pathogenesis) that are discriminate benign tissue, from localized prostate cancer and lethal prostate cancer. Some of these genes may also represent new therapeutic targets for patients with prostate cancer. Dr. Bismar and his team are currently working on validating their findings in larger studies.

The 2012 Sternlicht Family Foundation – PCF Young Investigator Award

Dimple Chakravarty, PhD, DVM

Weill Medical College of Cornell University

Mentor: Mark Rubin, MD  

Androgens and Androgen Receptor (AR) fuel prostate cancer. Therefore, androgen deprivation therapy (ADT) is usually the preferred treatment modality. However, prostate tumors employ multiple alternate mechanisms to bypass the need for androgens or AR, progressing on the path to castration-resistance. Several recent studies in Dr. Mark Rubin’s laboratory and others have shown that prostate tumors express the Estrogen Receptor ? (ER?) at early onset of the disease. However, the role of ER? in prostate cancer still remains unclear. Dr. Dimple Chakravarthy proposes to study this ER?-lncRNA axis in prostate cancer. She will validate the relevance of ER? and ER?-regulated lncRNA as prognostic biomarkers of tumor progression and therapy response. Dr. Chakravarthy will also evaluate the therapeutic potential of knocking down lncRNAs using nanoparticles. She will test the combinatorial therapy with anti-androgens and anti-lncRNA medications to control prostate cancer growth and metastasis.

The 2012 John A. Moran – PCF Young Investigator Award

Junjie Feng, PhD

Wake Forest University

Mentor: Jiangfeng Xu, MD, PhD  

Androgen Receptor (AR) mediates the action of the male hormones, androgens by binding to genomic DNA and regulating gene expression. The precise sites on the genome to which AR binds are called AR Response Elements (AREs) or AR binding sites. Recent reports have shown that approximately 1/3 of all known prostate cancer risk-associated genetic variants reside in these AR binding sites. Genetic variations that predispose a man to prostate cancer are usually found to be concentrated in the specific DNA regions to which AR binds. Other PCF-funded studies have shown that AR signaling is causally related to the formation and/or expression of recurrent oncogenic gene fusions (e.g. TMPRSS2-ERG), suggesting that altered AR signaling caused by inherited genetic changes may have a profound impact on the pathogenesis and progression of prostate cancer. To test this hypothesis, Dr. Junjie Feng proposes to 1) identify genome-wide AR binding sites and prostate cancer-specific fusion genes; 2) prostate cancer risk/aggressiveness-associated genetic variants that are located within AR binding sites, and 3) assess whether these genetic variants cause altered AR signaling and influence the formation and/or expression of fusion genes.

The 2012 Steve Wynn – PCF Young Investigator Award

Stephen Finn, MBBS, PhD

University of Dublin, Trinity College

Mentors: John O’Leary, MD, PhD and Lorelei Mucci, ScD, MPH  

Genetic information flows from genes on DNA as follows: gene (DNA)-> RNA-> protein. RNAs, which are the products of DNA, either give rise to proteins (coding RNAs) or do not produce proteins (non-coding RNAs). However, these non-coding RNAs (ncRNAs) are functional molecules that perform specialized roles in the cell, such as regulation of gene expression. Recent reports have provided evidence for the role of small ncRNAs in the development and progression of prostate cancer. Dr. Stephen Finn proposes to identify the ncRNA repertoire associated with aggressive prostate cancer (defined by failure to respond to Androgen Deprivation Therapy (ADT); disease specific mortality etc.). Dr. Finn’s research will identify the role of ncRNAs in aggressive prostate cancer and correlate these to prostate cancer-specific outcome, laying the groundwork for the design of novel ncRNA-targeting therapeutics. These studies will also provide reliable biomarkers of aggressiveness which can help in patient stratification for therapy and more efficient disease monitoring.

The 2012 Lowell Milken – PCF Young Investigator Award

Terence Friedlander, MD

University of California, San Francisco

Mentors: Charles Ryan, MD and Pamela Paris, PhD  

One of the medications used for androgen deprivation therapy (ADT) is the recently FDA-approved Abiraterone (Zytiga) which targets the biosynthesis of androgens in the adrenal glands and more importantly, in the tumor itself. Though patients respond well to Abiraterone and other ADT medications, almost all develop resistance to this therapy and their cancers progress. This stage of treatment resistance is termed castration resistant prostate cancer (CRPC). CRPC is hypothesized to develop due to either 1) the increased production of androgens by the tumor itself, or 2) mutations in the AR that make it independent of the presence/absence of androgens. Dr. Terence Friedlander proposes to investigate the specific genetic changes in prostate cancer cells that occur during the development and progression of castration resistance. During the course of these investigations, Dr. Friedlander will collect metastatic tumor biopsies and circulating tumor cells from patients to evaluate the precise mechanisms underlying Abiraterone resistance. A better understanding of the mechanisms that cause CRPC development will allow clinicians to optimize and sequence the new therapies available for the treatment of CRPC.

The 2012 Mortimer Sackler – PCF Young Investigator Award

Matthew Galsky, MD

Mt. Sinai School of Medicine

Mentors: William Oh, MD and Michael Ohlmeyer, PhD  

The protein FOXO1 regulates cellular growth and survival pathways in normal cells. To effect its function, FOXO1 has to move from its location outside the nucleus (the cellular compartment that harbors the genome (DNA)) to inside the nucleus. Prostate cancer (PCa) cells, however, redirect the cellular localization of FOXO1 and sequester it outside of the nucleus, in its inactive form. Scientific approaches to relocalize FOXO1 to the nucleus represent a novel strategy for the treatment of prostate cancer, especially treatment resistant PCa. A group of chemical compounds called the tricyclic neuroleptics have previously been shown to inhibit the transport of FOXO1 proteins from the nucleus.

  Under this PCF-funded study, Dr. Galsky will explore the anti-cancer effects and mechanism of action of these novel compounds in preclinical prostate cancer models. He will also study circulating tumor cells from castration-resistant prostate cancer (CRPC) patients to identify suitable pharmacodynamic markers that can efficiently report the localization of FOXO1 in patient tumors. Dr. Galsky’s research will set the stage for early phase clinical trials of these experimental medications for the treatment of advanced prostate cancer.  

The 2012 Leon and Debra Black – PCF Young Investigator Award

Kalpana Kannan, PhD

Baylor College of Medicine

Mentors: Laising Yen, PhD and Michael Ittman, MD, PhD   Chimeric RNAs are the fused products of two different genes. Recent studies have shown that chimeric RNAs are present in normal cells and their presence allows the limited number of human genes to encode a substantially larger number of RNAs and proteins, forming an additional layer of cellular complexity. Dr. Kalpana Kannan and her team recently identified 27 novel, highly recurrent chimeric RNAs in prostate cancer. Their results showed that these chimeric RNAs occurred at a higher frequency in cancer compared to normal cells. These preliminary findings show that chimeric RNAs form a potentially unique class of molecular alterations in prostate cancer. She will also evaluate the significance of these chimeric RNAs in prostate cancer diagnosis and prognosis. If validated, these chimeric RNAs will serve as useful biomarkers for the identification of prostate cancer subtypes. New therapeutic targets for advanced prostate cancer may also emerge from this work. Dr. Kannan proposes to study the biological significance and potential clinical applications of these recurrent RNAs in prostate cancer.  

The 2012 Michael Milken – PCF Young Investigator Award

Stacey Kenfield, ScD

Brigham and Women's Hospital, Harvard University

Mentors: June Chan, ScD and Meir Stampfer, MD   Under the mentorship of Dr. Chan and Dr. Stampfer, Dr. Kenfield has evaluated whether diet and lifestyle factors after prostate cancer diagnosis are associated with disease progression in men with localized disease. This proposal is a natural extension of this work and will focus specifically on men with advanced and recurrent prostate cancer and whether diet and lifestyle factors can reduce risk of distant metastasis or prostate cancer-specific mortality. The ultimate goal of this work is to translate these results into cancer survivorship tools for the community. First, Dr. Kenfield will develop a prognostic score for prostate cancer mortality and other outcomes that will incorporate clinical, pathological, and lifestyle variables. The analyses will be performed in two large studies with extensive data available on lifestyle factors: the Health Professionals Follow-Up Study and CaPSURE (Cancer of the Prostate Strategic Urologic Research Endeavor) and the findings could be important in guiding physician counseling of men with prostate cancer. Second, she will examine whether diet and other lifestyle factors may reduce progression in men with advanced or recurrent prostate cancer, which may elucidate strategies for reducing progression of disease. Third, she will build novel web-based cancer survivorship tools and use them in a clinical trial to determine if a web-based intervention program can help men with prostate cancer adopt healthier behaviors associated with reduced prostate cancer mortality. If successful, it could be administered efficiently in a variety of settings and scaled up to reach larger populations of men with prostate cancer.  

The 2012 Steve Wynn – PCF Young Investigator Award

Hung-Ming Lam, PhD

University of Cincinnati

Mentor: Shuk-Mei Ho, PhD   The protein G-protein coupled receptor 30 (GPR30) regulates several signaling pathways governing cell growth, migration, etc. In previous studies, Dr. Hung-Ming Lam has shown that the chemical compound G1 tightly binds GPR30 in highly selective manner and this G1-GPR30 complex inhibits the growth of prostate cancer cells. In this study, Dr. Lam proposes to evaluate the efficacy of GPR30 inhibition by G1 for the treatment of castration-resistant prostate cancer (CRPC). Previous studies have shown that the expression of GPR30 in cells shows an inverse correlation with the levels of androgens. The recently FDA-approved medication Abiraterone acetate (Zytiga) inhibits androgen synthesis. Dr. Lam proposes to evaluate combinatorial therapy with G1 and Abiraterone to treat prostate cancer in a two-pronged fashion: 1) delaying cancer relapse and the emergence of metastatic CRPC and, 2) extending the time to chemotherapy in patients with advanced cancer. Dr. Lam also aims to determine the levels of GPR30 before and after ADT in human specimens with bone and lymph node metastases. Her studies will help define a group of patients most suitable for GPR30-targeted therapy.  

The 2012 John A. Moran – PCF Young Investigator Award

Heather Montie, PhD

Thomas Jefferson University, Jefferson Medical College

Mentors: Diane Merry, PhD and Karen Knudsen, PhD   Prostate cancer is driven by the male hormones, androgens which mediate their activity through the androgen receptor (AR). Unfortunately most prostate cancerous tumors progressively become resistant to the preferred treatment modality, androgen deprivation therapy. One of the mechanisms proposed to enhance the activity of androgen receptors in castration-resistant prostate cancer, even in the absence of androgens, is the addition of a small chemical group/moiety to the AR protein. This modification of AR is termed ‘acetylation’ and is proposed to convert the protein to a ‘super AR.’ However, there is currently no experimental data to show that AR acetylation directly enhances AR-dependent prostate cancer cell viability. Dr. Heather Montie proposes to evaluate the role of AR acetylation in the enhanced AR functional activity central to CRPC. She will study the precise mechanisms by which this modification of AR enhances its cancer-promoting activity. Dr. Montie will also validate the potential of AR acetylation as a therapeutic target for castrate-resistant prostate cancer.  

The 2012 Lori Milken – PCF Young Investigator Award

David Mulholland, PhD

University of California, Los Angeles

Mentor: Hong Wu, MD, PhD   The use of anti-androgens is standard treatment for prostate cancer patients in the management of PSA recurrence and metastatic disease. However, all men with metastatic prostate cancer become castrate resistant (CRPC) during which time conventional androgen deprivation therapy is no longer effective. This indicates that cancerous cells may become less reliant upon androgen or androgen receptor (AR) mediated signaling and more dependent upon alternative survival pathways either as a consequence of treatment or during the natural disease evolution.  

Recent studies on stem cells in in vitro experimental systems have shown that the deletion of important housekeeping genes can give rise to castration-resistant prostate cancerous tumors. In an extension to these observations, Dr. Mulholland proposes to study whether stem/progenitor cells with tumorigenic capabilities may acquire independence from the androgen/AR signaling axis and whether such cells are a potential source of the initiation of prostate cancer or the progression of aggressive metastatic prostate cancer. The short term goal of this proposal is to ascertain whether cancer initiating cells with impaired AR function can reconstitute disease progression in a manner that is entirely autonomous from AR function. The long term goal is the identification of alternative survival pathways, and therefore relevant targets, for cancers that are non-responsive to anti-androgen therapy.

The 2012 Heritage Medical Research Institute – PCF Young Investigator Award

Paul Nguyen, MD

Dana Farber Cancer Institute, Harvard University

Mentors: Anthony D’Amico, MD, PhD and Phillip Kantoff, MD   One of the most pressing dilemmas in the care of patients with prostate cancer is the ability to distinguish indolent from aggressive disease. However, considering the complexity of the disease, it is important to note that no single marker or diagnostic modality will likely account for all of the variability in prostate cancer outcome. In this proposal, Dr. Nguyen proposes to combine multiple markers of disease outcome into a single prognostic model to achieve maximum predictive accuracy. The overall goal of Dr. Nguyen’s efforts is to identify and integrate underlying genetic differences (polymorphisms), serum biomarkers, imaging characteristics and novel clinical factors to enhance the predictive ability of the current tools. He will study prostate cancer patient blood and tissue samples to identify biological and clinical predictors of outcome. Dr. Nguyen’s research will potentially provide a single unified system that integrates multiple types of prognostic information. These results will ultimately allow patients to understand their risk of cancer recurrence with greater certainty, and make better treatment choices.  

The 2012 Foundation 14 – PCF Young Investigator Award

Luke Selth, PhD

University of Adelaide, Dame Roma Mitchell Cancer Research Laboratories

Mentor: Wayne Tilley, PhD  

Androgen receptors mediate the action of the male sex hormone and fuel prostate cancer—which is why the primary treatment for prostate cancer is androgen deprivation therapy. Unfortunately, almost all patients develop resistance to ADT and their cancers resume growth despite hormone therapy. Recent research has revealed that highly active variants of AR rather than the normal AR protein may be the key drivers of CRPC and androgen receptor variants usually lack the ability to bind androgens. Therefore, androgen receptor variants (ARVs) can easily drive prostate cancer, even during ADT. Dr. Luke Selth proposes to study the molecular mechanisms by which AR variants initiate and drive CRPC. He will identify the precise genes activated by AR variants to promote CRPC. Dr. Selth will also determine the co-factors that regulate ARV-driven CRPC. Dr. Selth’s research will be a crucial next step in the development of strategies to counter the role of AR variants in CRPC development.

The 2012 Chris and Felicia Evensen – PCF Young Investigator Award

Karen Sfanos, PhD

Johns Hopkins University School of Medicine

Mentors: Angelo DeMarzo, MD, PhD and William Nelson, MD, PhD   The major risk factors for the development of prostate cancer are advanced age, family history, and African-American race; however, there is also a distinct geographic distribution to prostate cancer incidence, and an apparent increase in risk with the adoption of a “Westernized” lifestyle. Therefore, there is a high probability that prostate cancer development involves environmental factors in addition to hereditary factors. Two major environmental factors shown to have a strong linkage with prostate cancer are dietary carcinogens, and chronic infections that cause inflammation, which over time leads to the initiation of prostate cancer. Dr. Sfanos proposes to study the combined effects of dietary carcinogens and tumor-promoting inflammation in preliminary prostate cancer initiation and/or tumor progression.  

The 2012 David A. Koch – PCF Young Investigator Award

Hans David Ulmert, MD, PhD

Memorial Sloan Kettering Cancer Center

Mentor: Jason Lewis, PhD   The androgen receptor (AR) signaling pathway is a key component in the progression of prostate cancer to its lethal form, castration resistant prostate cancer (CRPC). Several, recently developed, potent inhibitors of AR-signaling have shown encouraging, though highly variable responses in patients. One of the reasons for this inconsistent response is the biological heterogeneity of different cancerous lesions in the same patient. Therefore, documenting the response of individual tumor lesions to therapy is important for prostate cancer clinical management (e.g. understanding the overall patient therapeutic response; decision-making for dose escalation or designing therapy combinations that more completely suppress AR-signaling etc.). Dr. Ulmert aims to evaluate the efficiency of 89Zr-5A10-PET for measuring tumor response to next-generation androgen-deprivation therapeutics such as MDV3100 and Abiraterone. Dr. Ulmert also proposes to conduct first-in-man studies to determine if 89Zr-5A10 can detect CRPC.  

If successful, this radiotracer (89Zr-5A10) will potentially be an important molecular imaging tool to definitively measure AR inhibition in individual tumor lesions in response to AR pathway-directed therapies. Since the complexities of metastatic CRPC still remain unclear, understanding the biology of responsive and resistant lesions could provide a clear rationale for the individualization of patient care, impacting decisions for dose escalation and/or combination therapy to completely suppress AR signaling.

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Nearing Goal of 100 Young Investigators, the Prostate Cancer Foundation Expands Global Research Enterprise

MADISON, WI–(Marketwire -02/22/12)- Novelos Therapeutics, Inc. (OTCQX: NVLT.OB – News) a pharmaceutical company developing novel drugs for treatment and diagnosis of cancer, today announced that the University of Wisconsin Carbone Cancer Center, a leading medical oncology research institution, has enrolled the first patient in a Phase 1-2 positron emission tomography (PET) imaging trial of I-124-CLR1404 (LIGHT), a cancer-targeted PET imaging agent, in patients with advanced non-small cell lung cancer (NSCLC). Details of the trial design are available at www.clinicaltrials.gov ID: NCT00582283, or at www.novelos.com in the 'Clinical Trials' section. Anne M. Traynor, M.D., is the trial's principal investigator.

“Surgical resection in properly selected NSCLC patients offers the best chance for long-term survival and may be curative. Consequently, accurate pre-operative assessment of local, regional and distant metastatic spread is critical for effective disease management,” said Dr. Traynor. “If metastatic spread can be more accurately detected, we may be able to customize and optimize treatment decisions.”

“We are very pleased to be expanding our collaboration with the UW Carbone Cancer Center,” said Harry Palmin, President and CEO of Novelos. “We look forward to obtaining initial LIGHT imaging data in the second quarter of 2012 in lung cancer patients. We believe positive data would establish proof-of-concept for LIGHT as a PET imaging agent for NSCLC, could advance our partnering discussions and could be used to calculate effective doses for Phase 2 clinical trials of HOT. HOT is our chemically identical small-molecule, broad-spectrum, cancer-targeted molecular radiotherapeutic that delivers cytotoxic radiation directly and selectively to cancer cells and cancer stem cells.”

About LIGHT
LIGHT is a small molecule imaging agent that we believe has first-in-class potential for selective detection of tumors and metastases in a broad range of cancers. LIGHT is comprised of a small, non-pharmacological quantity of CLR1404 (COLD, acting as a cancer-targeted delivery and retention vehicle) labeled with the short-lived radioisotope, iodine-124, a new PET imaging isotope. PET imaging used in conjunction with CT scanning has now become the imaging method of choice in oncology. In studies to date, LIGHT selectively illuminated malignant tumors in 52 of 54 animal models of cancer, demonstrating broad-spectrum, cancer-selective uptake and retention. Investigator-sponsored Phase 1-2 trials of LIGHT as a PET imaging agent are ongoing. The trials include brain metastases, lung cancer and starting in the second quarter of 2012 other solid tumors. These human trials, if successful, will serve two important purposes. First, they would provide proof-of-concept for LIGHT itself as a PET imaging agent with the potential to supplant the current “gold standard” agent, 18-fluoro-deoxyglucose (FDG), due to what we believe to be LIGHT's superior cancer-specificity and more favorable logistics of clinical use. Second, favorable results would accelerate clinical development of HOT by predicting efficacy and enabling calculation of efficacious doses of HOT for Phase 2 trials.

About the UW Carbone Cancer Center in Madison
The University of Wisconsin Carbone Cancer Center (UWCCC) is recognized throughout the nation as one of the leading innovators in cancer research, quality patient care and active community involvement. It is the only comprehensive cancer center, as designated by the National Cancer Institute, in Wisconsin. An integral part of the UW School of Medicine and Public Health, the UWCCC unites physicians and scientists who work together in translating discoveries from research laboratories into new treatments that benefit cancer patients. To learn more about clinical studies and other initiatives, visit www.uwhealth.org/uw-carbone-cancer-center/for-researchers/uwccc/28373

About Novelos Therapeutics, Inc.
We are a pharmaceutical company developing novel drugs for the treatment and diagnosis of cancer. Our three cancer-targeted compounds are selectively taken up and retained in cancer cells (including cancer stem cells) versus normal cells. Thus, our therapeutic compounds appear to directly kill cancer cells while minimizing harm to normal cells. This offers the potential for a paradigm shift in cancer therapy by providing efficacy versus all three major drivers of mortality in cancer: primary tumors, metastases and stem cell-based relapse. LIGHT is a small-molecule cancer-targeted PET imaging agent. We believe LIGHT has first-in-class potential and Phase 1-2 clinical trials are ongoing. HOT is a small-molecule, broad-spectrum, cancer-targeted molecular radiotherapeutic that delivers cytotoxic radiation directly and selectively to cancer cells and cancer stem cells. We believe HOT also has first-in-class potential. HOT Phase 1b dose-escalation trial is ongoing and we expect HOT to enter Phase 2 trials in the first quarter of 2013 as a monotherapy for solid tumors with significant unmet medical need, subject to additional funding. COLD, a cancer-targeted non-radioactive chemotherapy, works primarily through Akt inhibition. We plan to file an IND for COLD in the first quarter of 2013, subject to additional funding. Together, we believe our compounds are able to “find, treat and follow” cancer anywhere in the body in a novel, effective and highly selective way. For additional information please visit www.novelos.com

INVESTOR CONTACTS
J. Patrick Genn, Vice President of IR
Novelos Therapeutics, Inc.
Ph: (858) 775-7456
Email: jpgenn@novelos.com

Anne Marie Fields, Senior Vice President
Lippert/Heilshorn & Associates, Inc.
Ph: (212) 838-3777
Email: afields@lhai.com

Novelos Therapeutics, Inc.
Madison, WI
Boston, MA

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Novelos Therapeutics Announces Enrollment of First Patient in Lung Cancer Trial With I-124-CLR1404 (Light) Cancer …

Contact: Jennifer Wenger
wengerj@nidcd.nih.gov
301-496-7243
NIH/National Institute on Deafness and Other Communication Disorders

What: NIH-supported scientists will be presenting their latest research findings at the 2012 Midwinter Meeting of the Association for Research in Otolaryngology (ARO).

When: February 25-29, 2012

Where: The Manchester Grand Hyatt Hotel, San Diego, California, USA

Additional Information: Research topics to be presented by NIDCD-funded scientists will include:

Bilateral ? Binaural: Can the Ability to Localize Sounds Be Regained After Bilateral Cochlear Implantation?
Ruth Litovsky, Ph.D., University of Wisconsin-Madison

Bilateral cochlear implants?one implant for each ear?are becoming more common as a treatment for children who are deaf or hard-of-hearing. Many children with cochlear implants attain spoken language skills that are comparable to their hearing peers, but even with two implants children often appear to perform significantly worse on tasks that involve hearing in complex listening environments (a busy classroom, for example) where they need to distinguish a teacher's or classmate's voice from competing background noise. According to NIDCD-grantee Ruth Litovsky, Ph.D., this is a function of the difference between how cochlear implants and the natural hearing ear process sound. Cochlear implants have not been designed to provide binaural cues?the cues that two normal ears provide to the brain. Binaural cues help listeners localize (know where the sound happens) and segregate (identify the meaning of a sound source) incoming sounds. In normal hearing, each ear sends its own unique information up the auditory pathway to the brainstem, and specialized neurons are able to decode the timing and intensity difference between sounds at the two ears to establish location and meaning. Cochlear implants don't provide the same kind of coordinated information to the brain. Dr. Litovsky's lab is working with three different groups of children and adults with bilateral cochlear implants to learn more about the binaural pathway in the brain. The investigators are working with a desktop research processor that attempts to recapture lost binaural cues by using a microphone in each ear and combining both streams of information, which it then sends back to each cochlea. The researchers are hoping that this technique will offer a way to preserve acoustic cues that are currently degraded because of lack of coordination between the two implants.

The Presidential Symposium, “Listening with the Brain: Cochlear Implants and Central Auditory System Plasticity,” takes place on Saturday, Feb. 25, 8:00 a.m.????:00 p.m. in the Elizabeth Ballroom

Spotlight on Spiral Ganglion Cells? New Research in Regeneration
Alain Dabdoub, Ph.D., University of California School of Medicine, San Diego (organizer); Robin Davis, Ph.D., Rutgers University; Albert Edge, Ph.D., Harvard Medical School, Massachusetts Eye and Ear Infirmary; Bernd Fritzsch, Ph.D., University of Iowa (among the presenters)

Spiral ganglion neurons (SGNs) transmit sound information in the form of electrical signals from the sensory cells in the inner ear, called hair cells, to the cochlear nucleus of the brainstem. Once lost due to noise or aging, SGNs and hair cells in mammals are never recovered. The most common therapies for hearing loss either use hearing aids to increase hair cell stimulation or use cochlear implants as an electronic substitute for damaged hair cells, but both therapies depend on the presence of functional SGNs. However, recent evidence shows that exposure to loud noise over time can lead to hearing loss caused not by damage to hair cells, but by loss of SGNs, and interest is rising in looking at strategies for replacing damaged or missing SGNs in the cochlea. This symposium features presentations from some of the most prominent investigators in the field of SGN regeneration, whose findings could play a significant role in future advances in cochlear implant technology and the medical treatment of hearing loss and deafness. Dr. Bernd Fritzsch will share findings from his laboratory, where they are elucidating the molecular mechanisms that regulate hair cell and SGN formation, particularly the factors that appear to regulate the growth and guidance of SGN fibers. Dr. Robin Davis will describe the diversity of organization, protein expression, and electrophysiological characteristics of neurons in the SGN family?not all SGNs are alike. Dr. Albert Edge will discuss his laboratory's efforts to generate SGNs using mouse embryonic stem cells and to reconnect healthy hair cells to the stem cell-derived neurons. Dr. Dabdoub will also be discussing how he and his colleagues are working to reprogram cochlear non-sensory epithelial cells to become functional SGNs.

The symposium, “The Spiral Ganglion: Neurogenesis and Concepts for Regeneration,” takes place on Saturday, Feb. 25, 2:00 p.m.????:35 p.m. in the Elizabeth Ballroom

Auditory Training of Older Adults Improves Speech Understanding in Noisy Environments
Samira Anderson, Au.D., Northwestern University

As we age we tend to have difficulty hearing in crowds and in other noisy environments, which isn't entirely the result of age-related hearing loss. There are also age-related changes in the neural circuits of the brain in coding the rapidly-changing speech signal, which make it much more difficult to follow speech in background noise. Amplifying sound, which is what hearing aids do, does not restore the precise neural timing needed for speech perception. Samira Anderson, Au.D., a graduate student at Northwestern University, and her colleagues have been working with older adults using a commercially available cognitive-based auditory training program to determine if intensive auditory training can improve temporal processing and increase speech-in-noise performance. Participants are older adults (ages 58 to 65) with normal to mild hearing loss, who were randomly assigned to one of two treatment groups. The experimental group completed eight weeks of cognitive-based auditory training, the control group completed eight weeks of general interest education training, and a third group received no training. Ms. Anderson will be discussing the results of the study, which showed significant improvements in the ability of the auditory trained group to process the time-changing speech signal and to understand speech in noisy environments. The findings offer a method of treatment, above and beyond sound amplification, to improve the hearing abilities of older adults.

The poster “Neural precision with auditory training in older adults,” takes place from Saturday, Feb. 25 at 1:00 p.m. to Sunday, Feb. 26, at 12:00 p.m. in the Manchester Ballroom

Novel Photokinetic Transducer Technology Drives New, Experimental Hearing Device
Sunil Puria, Ph.D., EarLens Corporation and Stanford University

In this podium presentation, Dr. Sunil Puria will be presenting findings from a recent small FDA-approved clinical trial. The trial tested a new class of hearing device that applies vibrations directly to the eardrum, rather than amplifying sound in the ear canal, to improve hearing in noise and sound quality. The EarLens Photokinetic transducer prototype uses a small solar cell that turns light pulses into the energy needed to remotely drive the motor and avoids the need for a hardwired connection, found in other surgically implanted systems. A key technical advantage is that the Photonic Hearing Device has a 10 kHz bandwidth, while acoustic hearing aids are limited to about 5 kHz. Subjects in the trial were fitted with the device and exposed to four different hearing conditions using noise and speech maskers to simulate difficult listening environments. Results indicate an improvement in hearing in noisy situations. EarLens Corporation, the developer of the prototype device, is planning to build a more refined clinical prototype for a multicenter clinical trial.

The podium presentation “The EarLens Photonic Hearing Aid,” takes place on Monday, Feb. 27, 11:45 a.m.????:00 p.m. in the Elizabeth Ballroom

Steroid Treatments in the Inner Ear Impact Thousands More Genes than Expected
Dennis Trune, Ph.D., M.B. A., Oregon Health & Science University

Corticosteroids, usually in the form of prednisone, prednisolone, or dexamethasone, have become the treatment standard for sensorineural hearing loss. However, little is known about how steroids work in the inner ear to restore hearing. The prevailing view has been that steroids reduce inflammation, which is believed to be what causes the hearing loss. In previous studies, Dr. Trune's laboratory has shown in mice that although steroids do suppress circulating inflammatory factors, their key function in restoring hearing appears to be in turning on genes involved in maintaining the proper concentration of potassium and sodium ions in the endolymph, a fluid contained in the inner ear. These studies also showed that, in spite of having no anti-inflammatory properties, the mineralocorticoid aldosterone (a naturally occurring steroid hormone) can also activate the genes responsible for ion balance and recover hearing. Taking advantage of an NIDCD supplemental grant, Dr. Trune and his colleagues have used gene chip technology to scan the entire mouse genome to establish the full array of inner ear genes that are switched on or off by traditional steroid treatments versus aldosterone treatment. In light of recent clinical activities?which favor a local injection of steroids to the middle ear to lower the risk for the side effects that accompany systemic steroid use?they treated either systemically or by injection across the eardrum (transtympanic). Dr. Trune will be discussing the findings of the genome scan, which indicate that steroids turn on or off 55 to 82 percent of the approximately 17,500 genes that are expressed in the inner ear. In addition, these numbers increase significantly when steroids are delivered transtympanically. These findings could offer a way to finetune sensorineural hearing loss treatments to target ion balance pathways instead of immunosuppressive pathways.

The podium presentation “Transtympanically Delivered Steroids Impact Thousands of Inner Ear Genes over Conventional Systemic Delivery,” takes place on Tuesday, Feb. 28, 11:45 a.m. in the Elizabeth Ballroom

###

For more information about the Association for Research in Otolaryngology, visit their website at www.aro.org.

NIDCD supports and conducts research and research training on the normal and disordered processes of hearing, balance, taste, smell, voice, speech and language and provides health information, based upon scientific discovery, to the public. For more information about NIDCD programs, see the website at www.nidcd.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH?Turning Discovery Into Health

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NIH-funded science on hearing research at annual ARO meeting

DUBLIN–(BUSINESS WIRE)–

Research and Markets (http://www.researchandmarkets.com/research/a12f57/basic_neurochemist) has announced the addition of Elsevier Science and Technology's new report “Basic Neurochemistry. Edition No. 8″ to their offering.

This is a classic advanced neurochemistry and neurobiology textbook that has a renewed focus on clinical applications. The early chapters focus on fundamental membrane chemistry, cellular signaling, and development of the nervous system. Later chapters cover cell injury and inflammation, neurodegenerative diseases, sensory transduction, and neural processing/behavior. By understanding mechanisms at the molecular and systems level, scientists can develop new pharmacotherapies to treat diseases such as Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis as well as neuropsychiatric diseases (e.g., schizophrenia, depression, pain, addictions). This book provides a foundation of all key principles of neurochemistry and neurobiology–within the context of human diseases–for advanced students and graduate students in neuroscience, biomedical sciences, as well as clinical neuroscientists and neurologists.

Includes clinical perspective boxes in each chapter that make connections between molecular processes and disease states, between biochemistry and drug discovery enabling students to better understand neurological diseases Presents cutting-edge advances in neuroscience in context of principles of brain chemistry and biology Companion Web site features animations to illustrate critical biochemical processes

Key Topics Covered:

Part I: Cellular Neurochemistry and Neural Membranes Neuronal Cell Biology Cell Membrane Structures and Functions Membrane Transport Electrical Excitability and Ion Channels Lipids The Cytoskeleton of Neurons and Glia Intracellular Trafficking Axonal Transport Cell Adhesion Molecules Myelin Structure and Biochemistry Energy Metabolism of the Brain

PART II: Intercellular Signaling Synaptic Transmission and Cellular Signaling: An Overview Acetylcholine Catecholamines Serotonin Histamine Glutamate GABA Purinergic Systems Peptides

PART III: Intracellular Signaling G Proteins Cyclic Nucleotides in the Nervous System Phosphoinositides Calcium Serine and Threonine Phosphorylation Tyrosine Phosphorylation Transcription Factors in the Central Nervous System

PART IV: Growth, Development and Differentiation Development Growth Factors Stem Cells in the Nervous System Formation and maintenance of myelin Axonal Growth in the Adult Mammalian Nervous System

PART V: Cell Injury and Inflammation Neuroimmunology Neuroinflammation Hypoxic'Ischemic Brain Injury and Oxidative Stress Lipid Mediators: Eicosanoids, Docosanoids, Platelet-Activating Factor and Inflammation Apoptosis and Necrosis

PART VI: Inherited and Neurodegenerative Diseases Peripheral Neuropathy Diseases Involving Myelin The Epilepsies: Phenotype and Mechanisms Genetics of Neurodegenerative Diseases Disorders of Amino Acid Metabolism Diseases of Carbohydrate, Fatty Acid and Mitochondrial Metabolism, including Lysosomal and Peroxisomal Diseases Disorders of Muscle Excitability Motor Neuron Diseases Neurobiology of Alzheimer's Disease Neurodegenerative alpha-Synucleinopathies and Tauopathies Trinucleotide repeat diseases Neurotransmitters and Disorders of the Basal Ganglia Molecular Basis of Prion Diseases

PART VII: Sensory Transduction Molecular Biology of Vision Molecular Biology of Olfaction and Taste Molecular Biology of Hearing and Balance Pain

PART VIII: Neural Processing and Behavior Endocrine Effects on the Brain and Their Relationship to Behavior Learning and Memory Sleep The Neurochemistry of Schizophrenia Autism Neurobiology of Severe Mood and Anxiety Disorders Addiction

For more information visit http://www.researchandmarkets.com/research/a12f57/basic_neurochemist

Link:
Research and Markets: Basic Neurochemistry. Edition No. 8

Within each cell, mitochondria are constantly splitting in two, a process called fission, and merging back into one, called fusion. Before a cell can divide, the mitochondria must increase their numbers through fission and separate into two piles, one for each cell.

By reversing an imbalance of the signals that regulate fusion and fission in rapidly dividing cancer cells, researchers were able to dramatically reduce cell division, thus preventing the rapid cell proliferation that is a hallmark of cancer growth. Increasing production of the signal that promotes mitochondrial fusion caused tumors to shrink to one-third of their original size. Treatment with a molecule that inhibits fission reduced tumor size by more than half.

“We found that human lung cancer cell lines have an imbalance of signals that tilts them towards mitochondrial fission,” said Stephen L. Archer, MD, the Harold Hines Jr. Professor of Medicine at the University of Chicago Medicine and senior author of the study. “By boosting the fusion signal or blocking the fission signal we were able to tip the balance the other way, reducing cancer cell growth and increasing cell death. We believe this provides a promising new approach to cancer treatment.”

“This could be a potential new Achilles' heel for cancer cells,” said the study's lead author, Jalees Rehman, MD, an associate professor of medicine and pharmacology at the University of Illinois at Chicago. “Many anticancer drugs target cell division. Our work shifts the focus to a distinct but necessary step: mitochondrial division. The cell division cycle comes to a halt if the mitochondria are prevented from dividing. This new therapy may be especially useful in cancers which become resistant to conventional chemotherapy that directly targets the cycle.”

The researchers found that the mitochondrial networks within several different lung cancer cell lines were highly fragmented, compared to normal lung cells. Cancer cells had low levels of mitofusin-2 (Mfn-2), a protein that promotes fusion by tethering adjacent mitochondria, and high levels of dynamin-related protein (Drp-1), which initiates fission by encircling the organelle and squeezing it into two discrete fragments. The Drp-1 in cancer cells also tended to be in its most active form.

The researchers tested several ways to enhance fusion and restore the mitochondrial network, both in cell culture and in animal models. They used gene therapy to increase the expression of Mfn-2, injected a small molecule (mdivi-1) that inhibits Drp-1, and used genetic techniques to block the production of Drp-1. All three interventions markedly reduced mitochondrial fragmentation, increased networking and reduced cancer cell growth.

Although the authors identify mitochondrial fission and Drp-1 activation as a potential therapeutic target in lung cancer, “this is not a cure,” Archer emphasized. The treatment drastically reduced tumor size but the tumors did not completely disappear. They continued to use high levels of glucose as fuel, a hallmark of cancer metabolism that can be seen on PET scans. “This remnant could be either a central cluster of cancer stem cells,” Archer said, “or an inflammatory response, the immune system infiltrating the tumor.”

“Inhibiting mitochondrial fission”, Archer said, “did not show any significant toxicity in mice or rats, so we are quite optimistic that our findings can lead to the development of novel, clinically feasible therapies.”

The substances used to block fusion are commercially available for research purposes, but they have not been tested in humans. Mdivi-1 has been used in animals to prevent kidney injury.

Although the focus on mitochondria is fairly new to cancer biologists—despite a flurry of interest in the 1920s stimulated by the German Nobel Prize laureate Otto Warburg—this organelle has long been a central focus for physicians and scientists interested in muscle biology, especially cardiac muscle.

Archer, a cardiologist, specializes in pulmonary hypertension. In this disorder, as in cancer, excessive cellular growth causes disease. The death of his cousin and close friend from lung cancer made him start thinking about the connections. Rehman is a German scientist and became interested in studying mitochondria after reading some of the historical Warburg papers in German.

The fact that two cardiologists, Archer and Rehman, decided to study cancer and collaborated with a team of basic scientists, a cancer physician and a pathologist is “an indicator of how interconnected modern biomedical research has become,” Rehman said.

Provided by University of Chicago Medical Center

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Energy network within cells may be new target for cancer therapy

DUBLIN–(BUSINESS WIRE)–

Research and Markets (http://www.researchandmarkets.com/research/b93d9c/evolutionary_biolo) has announced the addition of John Wiley and Sons Ltd's new book “Evolutionary Biology: Cell-Cell Communication, and Complex Disease” to their offering.

Evolutionary Biology: Cell-Cell Communication, and Complex Disease – An Integrative View of the Evolution of Genetics and the Natural World

Even in this advanced age of genomics, the evolutionary process of unicellular and multicellular organisms is continually in debate. Evolutionary Biology, Cell-Cell Communication, and Complex Disease challenges current wisdom by using physiology to present an integrative view of the nature, origins, and evolution of fundamental biological systems.

Providing a deeper understanding of the way genes relate to the traits of living organisms, this book offers useful information applying evolutionary biology, functional genomics, and cell communication studies to complex disease. Examining the 4.5 billion-year evolution process from environment adaptations to cell-cell communication to communication of genetic information for reproduction, Evolutionary Biology hones in on the “why and how” of evolution by uniquely focusing on the cell as the smallest unit of biologic structure and function.

Based on empirically derived data rather than association studies, Evolutionary Biology covers:

A model for forming testable hypotheses in complex disease studies The integrating role played by the evolution of metabolism, especially lipid metabolism The evolutionary continuum from development to homeostasis Regeneration and aging mediated by signaling molecules

Key Topics Covered:

1 THE CELLULAR ORIGIN OF VERTEBRATES

2 REDUCING LUNG PHYSIOLOGY TO ITS MOLECULAR PHENOTYPES

3 A CELL-MOLECULAR STRATEGY FOR SOLVING THE EVOLUTIONARY PUZZLE

4 THE EVOLUTION OF CELL-CELL COMMUNICATION

5 HOW TO INTEGRATE CELL-MOLECULAR DEVELOPMENT, HOMEOSTASIS, ECOLOGY, AND EVOLUTIONARY BIOLOGY: THE MISSING LINKS

6 FROM CELL-CELL COMMUNICATION TO THE EVOLUTION OF INTEGRATED PHYSIOLOGY

7 EXPLOITING CELL-CELL COMMUNICATION ACROSS SPACETIME TO DECONSTRUCT EVOLUTION

8 THE PERIODIC TABLE OF BIOLOGY

9 VALUE ADDED BY THINKING IN TERMS OF THE CELL-CELL COMMUNICATION MODEL FOR EVOLUTION

10 CELL-CELL COMMUNICATION AS THE BASIS FOR PRACTICING CLINICAL MEDICINE

Author:

John Torday, PhD, is Professor of Pediatrics and Ob/Gyn at Harbor-UCLA Medical Center where he is also Director of The Henry L. Guenther Laboratory for Cell/Molecular Research and Director of Laboratory for Evolutionary Preventive Medicine.

V.K. Rehan, MD, is Professor of Pediatrics and Director of the Neonatal Intensive Care Unit at Harbor-UCLA Medical Center. The recipient of numerous teaching honors, Dr. Rehan is involved both in treating patients and continuing research on neo and peri-natal respiratory issues and lung development.

For more information visit http://www.researchandmarkets.com/research/b93d9c/evolutionary_biolo

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Research and Markets: Evolutionary Biology: Cell-Cell Communication, and Complex Disease – An Integrative View of the …