SAN DIEGO–(BUSINESS WIRE)–

Biocept, Inc., a privately-held, CLIA certified laboratory testing company focused on detection and analysis of circulating tumor cells (CTCs) in cancer patients, announced that two of its senior scientists, Farideh Bischoff, Ph.D., Vice President of Translational Research, and Lyle Arnold, Ph.D., Senior Vice President, R&D and Chief Scientific Officer, will be making presentations at the 19th Annual Molecular Medicine Tri-Con being held in San Francisco February 19-23.

Dr. Arnold spoke during the “Blood-Based Cancer Diagnostics” session on Monday, February 20th. His talk, entitled “The Capture, Identification and Interrogation of Circulating Tumor Cells,” touched on a proprietary, highly sensitive mutation detection technology developed at Biocept called “SelectorTM.” Dr. Bischoff will speak during the “Clinical Use of Circulating Tumor Cells” session on Wednesday, February 22nd. Her talk, entitled “Capture and Detection of CK+ and CK- CTCs for Subsequent Molecular Analysis Using the OncoCEETM Platform,” will cover in part a continuing clinical study in breast cancer with collaborators at the MD Anderson Cancer Center.

Biocept’s first test, OncoCEE-BRTM for breast cancer, is available through its commercialization partner Clarient, Inc., a GE Healthcare Company. The test includes CTC enumeration and determination of HER2 status by fluorescence in situ hybridization (FISH) from a blood sample. Determination of estrogen receptor (ER) and progesterone receptor (PR) status by immunocytochemical staining will be added to the test later this year. OncoCEE-BR is the first commercially available CTC test to include analysis of a specific, treatment-associated biomarker (HER2).

About Biocept, Inc.

Biocept, Inc., headquartered in San Diego, California, is an advanced laboratory services company specializing in the capture, isolation, detection and analysis of Circulating Tumor Cells (CTCs). Biocept’s mission is to enhance the lives of cancer patients through the development of innovative diagnostic products and services. Biocept utilizes patented and innovative technologies to deliver clinically relevant and actionable information to physicians that enable better patient care. This includes clinical assessments of CTCs, both prognostic and predictive, which may provide physicians with important information for the treatment of their patients with cancer.

Original post:
Biocept to Present at the Molecular Medicine Tri-Conference on Circulating Tumor Cell (CTC) Technologies

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

This news release contains forward-looking statements. You can identify these statements by our use of words such as “may,” “expect,” “believe,” “anticipate,” “intend,” “could,” “estimate,” “continue,” “plans,” or their negatives or cognates. Such statements are valid only as of today, and we disclaim any obligation to update this information. These statements are only estimates and predictions and are subject to known and unknown risks and uncertainties that may cause actual future experience and results to differ materially from the statements made. These statements are based on our current beliefs and expectations as to such future outcomes. Drug discovery and development involve a high degree of risk. Factors that might cause such a material difference include, among others, uncertainties related to the ability to attract and retain partners for our technologies, the identification of lead compounds, the successful preclinical development thereof, the completion of clinical trials, the FDA review process and other government regulation, our pharmaceutical collaborators' ability to successfully develop and commercialize drug candidates, competition from other pharmaceutical companies, product pricing and third-party reimbursement.

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

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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MediVet-America Partners With Butler Schein Animal Health to Distribute World's Leading Animal Stem Cell Technology to …

The American Academy of Neurology and the National Multiple Sclerosis Society are awarding the 2012 John Dystel Prize for MS Research to Richard M. Ransohoff, MD, with the Cleveland Clinic. Ransohoff, a member of the American Academy of Neurology and Associate Editor of Neurology®, the Academy's medical journal, will receive the award at the Academy's 64th Annual Meeting in New Orleans, April 21-28, 2012. The Annual Meeting is the world's largest gathering of neurologists with more than 10,000 attendees and more than 2,300 scientific presentations on the latest research advance in brain disease.

The John Dystel Prize recognizes a significant contribution to research in the understanding, treatment or prevention of multiple sclerosis (MS).

Ransohoff's research has focused on the central nervous system, which includes the brain, optic nerves and spinal cord.

“This award recognizes the superb research done by my colleagues and me, and I'm proud to receive it on their behalf. Support by the National Institutes of Health, the National MS Society and generous individual donors showed confidence in our research and inspired our work,” said Ransohoff. “During the past 15 years, we've identified several new molecules as potential targets for MS treatments by studying how MS lesions begin in the central nervous system. Our research fortifies the rationale for developing new MRI techniques to visualize brain damage in MS and will help us to identify new treatments to address inflammation in the central nervous system.”

The award is presented by the American Academy of Neurology and the National Multiple Sclerosis Society. It is made possible through a special contribution from the John Dystel Multiple Sclerosis Research Fund at the National Multiple Sclerosis Society. Learn more about Ransohoff's contributions to MS research and the Dystel Prize at http://www.nationalmssociety.org/news/news-detail/index.aspx?nid=5975.

“Professor Ransohoff's research has uncovered far-reaching insights on immune activity at work in the brain and spinal cord during the MS disease process,” said Timothy Coetzee, PhD, Chief Research Officer for the National MS Society. “He's a distinguished thought leader whose discoveries could pave the way for totally new approaches to treating the disease.”

Source: American Academy of Neurology

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AAN, National MS Society to honor Cleveland Clinic researcher with John Dystel Prize

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China medicdal tourism– Cirrhosis–Stem cells therapy 3.mp4 – Video

Contact: Linda Brooks
lbrooks@rsna.org
630-590-7762
Radiological Society of North America

OAK BROOK, Ill. ? In a new study published in the March issue of Radiology, functional magnetic resonance imaging (fMRI) shows that cognitive rehabilitation changes brain function and improves cognitive performance in patients with relapsing-remitting multiple sclerosis (MS).

“These results prompt the use of specific computer-based rehabilitation programs to treat deficits in selected neuropsychological domains in patients with relapsing-remitting MS,” said the study's lead author, Massimo Filippi, M.D., professor of neurology at the San Raffaele Vita-Salute University and director of the “BrainMap” interdepartmental research program and the Neuroimaging Research Unit, Department of Neuroscience, Scientific Institute San Raffaele, Milan, Italy. “They also suggest that fMRI might provide useful metrics to monitor the effects of rehab in MS.”

MS is a nervous system disease affecting the brain and spinal cord. MS damages a material called the myelin sheath that surrounds and protects nerve cells. This damage disrupts messages between the brain and other parts of the body, leading to symptoms such as muscle weakness, coordination and balance difficulties, numbness, problems with vision, memory loss and other cognitive issues. MS affects women more than men and often becomes symptomatic between the ages of 20 and 40.

In relapsing-remitting MS, the most common type, patients experience a series of attacks followed by partial or complete disappearance of symptoms. The interval between relapses can range from weeks to years.

Cognitive impairment affects a large proportion of patients with MS in the areas of attention, information processing, executive functions, memory and visual-spatial abilities. Cognitive dysfunction impacts a range of activities, including work, driving and social integration.

For the study, Dr. Filippi and colleagues recruited 20 patients with relapsing-remitting MS. Patients were randomized into two groups of 10. The first group received a 12-week program of computer-assisted cognitive rehabilitation of attention and information processing and executive functions, and the second (control) group received no cognitive rehabilitation.

Aspects of the rehabilitation program included a day-planning task, which employed realistic simulations of a set of scheduled dates and duties to address the patient's ability to organize, plan and develop solution strategies; and an attention task requiring the patient to simulate driving a train, carefully observing the control panel of the train and the countryside while encountering several distractions at increasing levels of difficulty.

All of the patients underwent neuropsychological assessment and MRI exams at baseline and after 12 weeks. As compared to their performance at baseline, the patients in the treatment group improved in tests of attention and information processing and executive functions. The fMRI results showed modifications in activity in several brain regions in the rehabilitation group, compared to the non-rehabilitation group. These fMRI modifications were correlated with cognitive improvement.

Analysis after cognitive rehabilitation found no structural changes in the gray matter or normal-appearing white matter of the brain in the treatment group.

“The findings demonstrated that computer-assisted cognitive rehabilitation in patients with MS results in an improvement of the trained cognitive functions,” Dr. Filippi said. “However, the structural integrity of the brain's gray matter and white matter showed no modifications in these patients, suggesting an impairment of structural plasticity.”

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“Multiple Sclerosis: Effects of Cognitive Rehabilitation on Structural and Functional MR Imaging Measures?An Explorative Study.” Collaborating with Dr. Filippi were Gianna Riccitelli, Ph.D., Flavia Mattioli, M.D., Ruggero Capra, M.D., Chiara Stampatori, Ph.D., Elisabetta Pagani, M.Sc., Paola Valsasina, M.Sc., Massimiliano Copetti, Ph.D., Andrea Falini, M.D., Giancarlo Comi, M.D., and Maria Assunta Rocca, M.D.

Radiology is edited by Herbert Y. Kressel, M.D., Harvard Medical School, Boston, Mass., and owned and published by the Radiological Society of North America, Inc. (http://radiology.rsna.org/)

RSNA is an association of more than 48,000 radiologists, radiation oncologists, medical physicists and related scientists committed to excellence in patient care through education and research. The Society is based in Oak Brook, Ill. (RSNA.org)

For patient-friendly information on fMRI, visit RadiologyInfo.org.

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Cognitive rehabilitation improves brain performance in patients with MS

Contact: Dr. Ian Zagon
isz1@psu.edu
Society for Experimental Biology and Medicine

Researchers at The Pennsylvania State University College of Medicine, Hershey, Pennsylvania have discovered that the presence and integrity of the opioid growth factor receptor (OGFr), which mediates the inhibitory action of opioid growth factor (OGF) on cell proliferation, is a key to understanding the progression and treatment of human ovarian cancer. Transplantation of human ovarian cancer cells that were molecularly engineered to have a reduced expression of OGFr, into immunocompromised mice resulted in ovarian tumors that grew rapidly. This discovery, reported in the February 2012 issue of Experimental Biology and Medicine, provides fresh new insights into the pathogenesis and therapy of a lethal cancer that is the fifth leading cause of cancer-related mortality among women in the USA, and has a death rate that is unchanged for over 75 years.

The OGF (also-termed [Met5]-enkephalin)-OGFr axis plays a fundamental role in cancer, development, and cellular renewal by regulating cell proliferation. An important question addressed in this study relates to the requirement of this peptide-receptor system for the progression of carcinogenesis. Human ovarian cancer cell lines that were genetically modified to underexpress OGFr grew far more rapidly in tissue culture than control (empty vector/wildtype) cell lines. Moreover, the addition of OGF to cultures of these genetically modified cells did not respond to the inhibitory peptide and change cell number, indicating that the loss of OGFr interfered with the function of the OGF-OGFr axis with respect to regulating cell proliferation. Immunocompromised mice injected with ovarian cancer cells that had a reduction in OGFr displayed tumors much earlier than controls, and these tumors grew faster than controls. Putting this information together with knowledge that the pathway for OGF-OGFr regulation of cell proliferation in ovarian cancer is by way of increasing the cyclin-dependent inhibitory kinase proteins p16 and p21, we now can understand that minimizing the quantity of OGFr results in an increase in the number of cells entering the G1/S phase of the cell cycle. This has the net effect of increasing the progression of tumorigenic events. These results reveal the critical nature of OGFr in human ovarian cancer, and that the receptor along with its ligand, OGF, is essential for determining the course of these neoplasias.

The research team was comprised of Dr. Ian S. Zagon, Distinguished University Professor, and Dr. Patricia J. McLaughlin, Professor, along with Dr. Renee N. Donahue in the Department of Neural & Behavioral Sciences. Drs. Zagon and McLaughlin discovered that endogenous opioids serve as growth factors, and have been pioneers in translating their findings from the bench to the bedside. Dr. Zagon states that “Over 75% of women are initially diagnosed with advanced ovarian cancer. Despite excellent initial response to cytoreductive surgery and adjuvant chemotherapy, 65% of these patients relapse within two years. However, only palliative care is available for these patients. With evidence from Phase I and II clinical trials as to the success of OGF for the treatment of advanced pancreatic cancer and knowledge presented herein that the OGF-OGFr axis is a critical determinant of the course of ovarian neoplasia, the present study raises the possibility of using this information to modulate the OGF-OGFr pathway with i) exogenous OGF, ii) imiquimod to upregulate OGFr, and/or iii) low dose naltrexone (LDN) to increase OGF and OGFr, as a therapeutic strategy for ovarian carcinoma.” Co-author Dr. McLaughlin adds that “A major problem in ovarian cancer is the need for diagnostic markers – both for early diagnosis and to monitor treatment modalities. Since some of the signaling pathways for OGF-OGFr are known (e.g., karyopherin ?, Ran, p16, p21), the components of this system would represent a worthwhile focus in designing diagnostic assays.” Dr. Donahue, who conducted the ovarian cancer studies and its relationship to the OGF-OGFr axis for her doctoral dissertation, states that “Ovarian cancers frequently have a methylation of p16 that is associated with an increased progression of ovarian cancer and a loss of OGFr in ovarian tumors. The diminished expression of OGFr and its repercussions on tumorigenesis, only adds to the concern about the need for information concerning genetic and epigenetic changes that may impact the course of disease and its treatment. Our findings also hold potentially ominous overtones for those individuals taking naltrexone for addictive disorders. The dosage used for treatment of addiction blocks opioid receptors continually. The present findings that diminishing the OGF-OGFr axis by depleting the receptor exacerbates tumorigenesis, could place these patients using naltrexone at risk for accelerating disease processes that involve cell proliferation.”

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said “This compelling evidence confirms the absolute requirement for OGFr (and OGF) as a tonically active inhibitory regulatory mechanism in ovarian cancer. As a corollary, amplifying the OGF-OGFr pathway is a novel and highly effective biotherapeutic strategy to suppress the progression of these deadly cancers.”

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Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit www.sebm.org. If you are interested in publishing in the journal please visit http://ebm.rsmjournals.com/.

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

AUSTIN, Texas, Feb. 21, 2012 /PRNewswire/ – Celling Biosciences announces a sponsorship of the 7th Annual Stem Cell Summit being held on February 21st at Bridgewaters New York in New York City. The Stem Cell Summit is consistently the premiere venue for the world's leaders in regenerative medicine to network and promote next generation technologies and cell therapies.

The meeting will feature more than 30 thought leaders in stem cell therapy including Dr. Kenneth Pettine of the Orthopedic Stem Cell Institute in Loveland, Colorado.  Dr. Pettine has teamed up with Celling Biosciences' SpineSmith Division to present “Adult Stem Cell Therapy for Orthopedic and Spine Conditions Resulting from Injury or Aging.”  Dr. Pettine has become an innovator in the regenerative cell therapy market and believes “regenerative therapies will become the next standard of care in treating many orthopedic conditions.” 

Following the Stem Cell Summit, Dr. Pettine will be presenting a discussion on regenerative therapies to the trainers and medical staff attending this year's NFL combine.  The NFL has recently gained attention from Peyton Manning going oversees to receive a cell therapy treatment for his cervical spine condition.  Dr. Pettine envisions a day when these professional athletes stop going to foreign countries to receive medical treatment.

The Orthopedic Stem Cell Institute provides state-of-the-art regenerative cell therapy using Celling Biosciences' ART 21 system. The ART 21 system processes bone marrow from the patient at the point of care to consistently produce a concentrate of regenerative cells with high yields of mononuclear stem cells in less than 15 minutes.  Celling Biosciences provides the cell separation systems along with the biomaterials and devices necessary to recreate the environment to promote healing. 

Kevin Dunworth, founder of Celling Biosciences, believes regenerative cell therapy has more to do with creating the optimal environment then just providing cells.  “We believe autologous cell therapy is a viable solution but physicians need to understand that these cells require the necessary substrate for delivery and the proper techniques for retrieval.  Our focus has been on providing not only cell separation technologies, medical devices and biomaterials but also the registered nurses to deliver the service so physicians can have the most consistent, reliable and predictable regenerative cell therapy for their patients.”

Contact:
Tracy Gladden
Communications Manager
Tgladden@spinesmithusa.com
512-637-2050

About Celling Biosciences
Celling Biosciences, works closely with surgeons, scientists and engineers to research and develop innovative technologies in the field of regenerative medicine. www.cellingbiosciences.com and www.spinesmithusa.com

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Celling Biosciences Sponsors 7th Annual Stem Cell Summit