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Posts Tagged ‘Jonsson Comprehensive Cancer Ctr.’

PI3K Pathway: A Potential Ovarian Cancer Therapeutic Target?

Posted by Paul Cacciatore on November 20, 2009

…[T]here are several PI3K signaling pathway targeting drugs in clinical development for use against ovarian cancer and solid tumors, including GDC-0941, BEZ235, SF1126, XL-147, XL-765, BGT226, and PX-866.  The results of two recent medical studies suggest that the use of PI3K-targeted therapies may offer an effective therapeutic approach for patients with advanced-stage and recurrent ovarian cancer, including a generally chemotherapy-resistant histological subtype of epithelial ovarian cancer known as “ovarian clear cell cancer” (OCCC).  The targeting of the PI3K pathway in endometrial, ovarian, and breast cancer is also being investigated by a Stand Up To Cancer “Dream Team.” …

PI3K Cellular Signaling Pathway — An Overview

PI3K/AKT cellular signaling pathway (Photo: Cell Signaling Technology(R))

In 2004 and 2005, multiple researchers identified mutations in the PIK3CA  gene with respect to multiple cancers.[1]  The PIK3CA gene encodes the PI3K catalytic subunit p110α. PI3K (phosphoinositide 3- kinase) proteins have been identified in crucial signaling pathways of ovarian cancer cells. PI3Ks are also part of the PI3K-AKT-mTOR signaling pathway which promotes cellular glucose metabolism, proliferation, growth, survival, and invasion and metastasis in many cancers. PIK3CA gene mutations can increase PI3K signaling, thereby activating the PI3K-AKT-mTOR pathway within cancer cells.

As of this writing, there are several PI3K signaling pathway targeting drugs in clinical development for use against ovarian cancer and solid tumors, including GDC-0941, BEZ235, SF1126, XL-147, XL-765, BGT226, and PX-866. [2]  The results of two recent medical studies suggest that the use of PI3K-targeted therapies may offer an effective therapeutic approach for patients with advanced-stage and recurrent ovarian cancer, including a generally chemotherapy-resistant histological subtype of epithelial ovarian cancer known as “ovarian clear cell cancer” (OCCC).  The targeting of the PI3K pathway in endometrial, ovarian, and breast cancer is also being investigated by a Stand Up To CancerDream Team.”

Frequent Mutation of PIK3CA Gene In Recurrent & Advanced Clear Cell Ovarian Cancer

OCCC is one of the five major subtypes of epithelial ovarian cancer. OCCC accounts for only 4% to 12% of epithelial ovarian cancer in Western countries and, for unknown reasons, it comprises more than 20% of such cancers in Japan [3,4,5]. OCCC possesses unique clinical features such as a high incidence of stage I disease, a large pelvic mass, an increased incidence of venous thromboembolic complications, and hypercalcemia. It is frequently associated with endometriosis.  Compared to serous ovarian cancer, OCCC is relatively resistant to conventional platinum and taxane-based chemotherapy. For these reasons, new effective therapies are desperately needed for OCCC.

Researchers from Johns Hopkins and the University of California, Los Angeles (UCLA) analyzed 97 OCCC tumors for genetic sequence mutations in KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog), BRAF (v-raf murine sarcoma viral oncogene homolog B1), PIK3CA (phosphoinositide-3-kinase, catalytic, alpha polypeptide), TP53 (tumor protein p53), PTEN (phosphatase and tensin homolog), and CTNNB1 (Catenin, Beta-1) as these mutations frequently occur in other major types of ovarian cancers.[6] The samples tested included the following:

  • 18 OCCCs for which affinity-purified tumor cells from fresh specimens were available;
  • 10 OCCC tumor cell lines.

Upon test completion, the researchers discovered that sequence mutations of PIK3CA, TP53, KRAS, PTEN, CTNNB1, and BRAF occurred in 33%, 15%, 7%, 5%, 3%, and 1% of OCCC cases, respectively.

Clear cell carcinoma of the ovary (Photo: Geneva Foundation For Medical Education & Research)

The sequence analysis of the 18 affinity purified OCCC tumors and the 10 OCCC cell lines showed a PIK3CA mutation frequency of 46%. Based upon these findings the researchers concluded that the use of PIK3CA-targeting drugs may offer a more effective therapeutic approach compared with current chemotherapeutic agents for patients with advanced-stage and recurrent OCCC. As noted above, there are several PI3K-targeting drugs in clinical development for use against ovarian cancer and solid tumors.[2]

Notably, one of the researchers involved with this OCCC study is Dennis J. Slamon, M.D., Ph.D. Dr. Slamon serves as the Director of Clinical/Translational Research, and as Director of the Revlon/UCLA Women’s Cancer Research Program at the Jonsson Comprehensive Cancer Center. Dr. Slamon is also a professor of medicine, chief of the Division of Hematology/Oncology and Executive Vice Chair of Research for UCLA’s Department of Medicine. Dr. Slamon is a co-discoverer of the breast cancer drug Herceptin®. Herceptin is a monoclonal antibody targeted therapy used against HER-2 breast cancer, an aggressive breast cancer subtype that affects 20% to 30% of women with the disease. Herceptin’s development was based, in part, upon the unique genetic profile of HER-2 breast cancer as compared to other forms of breast cancer. Herceptin® revolutionized the treatment of HER-2 postive breast cancer and is recognized worldwide as the standard of care for that subtype of breast cancer.  The approach taken by Johns Hopkins and UCLA researchers in this study — the identification of  a subtype within a specific form of cancer that may be susceptible to a targeted therapy –  bears a striking similarity to the overarching approach taken in the development of Herceptin®.

Ovarian Cancer & Other Solid Tumors With PIK3CA Gene Mutations Respond To PI3K-AKT-mTOR Pathway Inhibitors In Phase I Clinical Testing.

Testing patients with cancer for PIK3CA gene mutations is feasible and may allow targeted treatment of the PI3K-AKT-mTOR cellular signaling pathway, according to the results of a University of  Texas, M.D. Anderson Cancer Center study presented on November 17, 2009 at the 2009 AACR (American Association for Cancer Research)-NCI (National Cancer Institute)-EORTC (European Organization For Research & Treatment of Cancer) International Conference on Molecular Targets and Cancer Therapeutics.[7]

mTOR cellular signaling pathway (Photo: Cell Signaling Technology(R))

Filip Janku, M.D., Ph.D, a clinical research fellow with the M.D. Anderson Cancer Center’s department of investigational cancer therapeutics, and colleagues conducted a mutational analysis of exon 9 and exon 20 of the PI3KCA gene using DNA from the tumors of patients referred to targeted therapy clinical trials. Patients with PIK3CA mutations were preferably treated whenever possible with regimens utilizing PI3K-AKT-mTOR signaling pathway inhibitors.

As part of this study 117 tumor samples were analyzed. PIK3CA mutations were detected in 14 (12%) patients.  In tumor types with more than 5 patients tested, PIK3CA mutations were identified in endometrial cancer (43%, 3 out of 7 patients), ovarian cancer (22%, 5 out of 23 patients), squamous head and neck cancer (14%, 1 out of 7 patients), breast cancer (18%, 2 out of 11 patients), and colon cancer (15%, 2 out of 13 patients). No mutations were identified in patients with melanoma or cervical cancer.

Of the 14 patients found to possess PIK3CA mutations, 10 were treated based upon a clinical trial protocol that included a drug targeting the PI3K-AKT-mTOR pathway.  A partial response to treatment was experienced by 4 (40%) patients. Although the total number of patients is small, there were 2 (67%) patient responses in 3 endometrial cancer cases, 1 (25%) patient response in 4 ovarian cancer cases, 1 (100%) patient response in 1 breast cancer, and no patient response in 1 colorectal cancer case.  Although the total number of study patients is small, the researchers conclude that the response rate appears high (40%) in tumors with PIK3CA mutations treated with PI3K-AKT-mTOR pathway inhibitors.

“The implications of this study are twofold,” said Dr. Janku.  “We demonstrated that PIK3CA testing is feasible and may contribute to the decision-making process when offering a patient a clinical trial. Although this study suffers from low numbers, the response rate observed in patients treated with inhibitors of PI3K/AKT/mTOR pathway based on their mutational status was well above what we usually see in phase-1 clinical trials.”  “These results are intriguing but at this point should be interpreted with caution,” said Janku. “The promising response rate needs to be confirmed in larger groups of patients. We expect to learn more as this project continues to offer PIK3CA screening to patients considering a phase-1 clinical trial.”

Stand Up 2 Cancer Dream Team: Targeting the PI3K Pathway in Women’s Cancers

The potential importance of the PI3K pathway in the treatment of ovarian cancer is emphasized by the two medical studies above.  This issue is also receiving considerable attention from one of the Stand Up 2 Cancer (SU2C) “Dream Teams,” which is going to evalute  the potential for targeting the PI3K pathway in women’s cancer.  SU2C assigned $15 million of cancer research funding to this critical issue.  The scientists involved in this SU2C Dream Team are the pioneers who discovered the PI3K pathway and validated its role in human cancers, and they will focus on breast, ovarian and endometrial cancers, all of which possess the PI3K mutation.

The leader and co-leaders of the PI3K pathway SU2C team are set forth below.

Leader:

Lewis C. Cantley, Ph.D., Director, Cancer Center at Beth Israel Deaconess Medical Center.

Co-Leaders:

Charles L. Sawyers, M.D., Director, Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center.

Gordon B. Mills, M.D., Ph.D., Chair, Department of Systems Biology, University of Texas, M.D. Anderson Cancer Center.

The specific SU2C Dream Team research goal with respect to targeting the PI3K pathway in women’s cancers is stated as follows:

The PI3K pathway is mutated in more cancer patients than any other, and these mutations are the most frequent events in women’s cancers, making it an attractive molecular target for agents that inhibit these genetic aberrations. If successful, this project will allow clinicians to use biomarkers and imaging techniques to predict which patients will benefit from PI3K pathway inhibitors and lead to the development of therapeutic combinations that will hit multiple targets in the complex pathways that contribute to cancer cell growth.  This work will help assure that these therapies are given to patients who will benefit from them, and it will also increase the overall pace of clinical trials targeting PI3K inhibitors.

Based upon the two studies discussed, and the creation and funding of the SU2C Dream Team for the purpose of targeting the PI3K pathway in women’s cancer, the future holds great promise in the battle against ovarian cancer (including OCCC).  It is our hope that more clinical study investigators will offer PI3K pathway mutation screening to all ovarian cancer patient volunteers.  Libby’s H*O*P*E*™ will continue to monitor the clinical development of PI3K pathway inhibitors, and make our readers aware of all future developments.

________________________________

References:

1/Yuan TL, Cantley LC. PI3K pathway alterations in cancer: variations on a theme. Oncogene. 2008 Sep 18;27(41):5497-510. PubMed PMID: 18794884
Samuels Y, Ericson K. Oncogenic PI3K and its role in cancer. Curr Opin Oncol. 2006 Jan;18(1):77-82. PubMed PMID: 16357568.
Levine DA, Bogomolniy F, Yee CJ, et. al. Frequent mutation of the PIK3CA gene in ovarian and breast cancers. Clin Cancer Res. 2005 Apr 15;11(8):2875-8. PubMed PMID: 15837735.
Samuels Y, Wang Z, Bardelli A, et. al. High frequency of mutations of the PIK3CA gene in human cancers. Science. 2004 Apr 23;304(5670):554. Epub 2004 Mar 11. PubMed PMID: 15016963.

2/For open ovarian cancer clinical trials using a PI3K-targeted therapy; CLICK HERE; For open solid tumor clinical trials using a PI3K-targeted therapy, CLICK HERE.

3/ Itamochi H, Kigawa J & Terakawa N.  Mechanisms of chemoresistance and poor prognosis in ovarian clear cell carcinoma. Can Sci 2008 Apr;99(4):653-658. [PDF Document]

4/Schwartz DR, Kardia SL, Shedden KA, et. alGene Expression in Ovarian Cancer Reflects Both Morphology and Biological Behavior, Distinguishing Clear Cell from Other Poor-Prognosis Ovarian CarcinomasCan Res 2002 Aug; 62, 4722-4729.

5/Sugiyama T & Fujiwara K.  Clear Cell Tumors of the Ovary – Rare Subtype of Ovarian Cancer, Gynecologic Cancer, American Society of Clinical Oncology (ASCO) Educational Book, 2007 ASCO Annual Meeting, June 2, 2007 (Microsoft Powerpoint presentation).

6/Kuo KT, Mao TL, Jones S, et. al. Frequent Activating Mutations of PIK3CA in Ovarian Clear Cell Carcinoma. Am J Pathol. 2009 Apr 6. [Epub ahead of print]

7/Janku F, Garrido-Laguna I, Hong D.S.  PIK3CA mutations in patients with advanced cancers treated in phase I clinical trials, Abstract #B134, Molecular Classification of Tumors, Poster Session B, 2009 AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics Conference. [PDF Document].

Posted in Biological Therapies, Clinical Trials, Conferences, Discoveries, Genetics, Medical Study Results, Meeting Highlights, Novel Therapies, Pipeline Drugs, Targeted Therapies | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 4 Comments »

UCLA Researchers Significantly Inhibit Growth of Ovarian Cancer Cell Lines With FDA-Approved Leukemia Drug Dasatinib (Sprycel®)

Posted by Paul Cacciatore on November 11, 2009

The drug dasatinib (Sprycel®), approved for use by the U.S. Food and Drug Administration in patients with specific types of leukemia, significantly inhibited the growth and invasiveness of ovarian cancer cells and also promoted their death, say UCLA researchers in the November 10th issue of the British Journal of Cancer. The drug, when paired with a chemotherapy regimen, was even more effective in fighting ovarian cancer cell lines in which signaling of the Src family kinases — associated with approximately one-third of ovarian cancers– is activated. Clinical trials that involve the testing of dasatinib against ovarian cancer and solid tumors are currently ongoing.

Researchers affiliated with the University of California, Los Angeles (UCLA), Mayo Clinic and Harvard Medical School announced that they have established a biological rationale to support the clinical study of the U.S. Food & Drug Administration (FDA)-approved leukemia drug dasatinib (U.S. brand name: Sprycel®), either alone or in combination with chemotherapy, in patients with ovarian cancer. The study appears in the November 10th edition of the British Journal of Cancer.

Background

Dasatinib is an FDA-approved drug for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (ALL). Dasatinib is a small-molecule inhibitor that targets several tyrosine kinases, including the Src kinase family, Ephrin type-A receptor 2 ( EphA2) , and the focal adhesion kinase (FAK).

Src is the prototypic member of a family of nine non-receptor tyrosine kinases (Src, Lyn, Fyn, Lck, Hck, Fgr, Blk, Yrk, and Yes). The Src family kinase (SFK) proteins regulate four main cellular fuctions that ultimately control the behavior of transformed cancer cells:  cell proliferation, adhesion, invasion, and motility.

Eph receptors and ephrins are integral players in cancer formation and progression, and are associated with advanced ovarian cancer and poor clinical outcome.

FAK is a non-receptor tyrosine kinase involved in the regulation of cell adhesion, survival, and migration.  Preclinical studies indicate that FAK plays a signficant role in ovarian cancer cell migration and invasion.

Dasatinib Study Methodology & Findings

slamon1

One of the dasatinib study authors is Dennis J. Slamon, M.D. Ph.D. Dr. Slamon is the Director of Clinical/Translational Research & Director of the Revlon/UCLA Women's Cancer Research Program, at the UCLA Jonsson Comprehensive Cancer Center. He is also the co-discoverer of Herceptin®, a targeted therapy that revolutionized the treatment of HER-2 positive breast cancer.

The researchers carried out the study by testing the effects of dasatinib on human ovarian cancer cells in vitro, using a panel of 34 established human ovarian cancer cell lines.  The 34 cell lines selected were representative of the major epithelial ovarian cancer subtypes:

On this basis, the researchers examined the effects of dasatinib on ovarian tumor cell proliferation, invasion, apoptosis, and cell-cycle arrest.  To more fully understand the activity of dasatinib, the researchers also studied the efficacy of chemotherapeutic drugs (i.e., carboplatin and paclitaxel) in combination with dasatinib against ovarian cancer cells that were previously determined to be dasatinib-sensitive.

The overarching goals of the study were (i) to provide a rationale to test dasatinib as a single agent or in combination with chemotherapy in patients with ovarian cancer, and (ii) to identify molecular markers that may help define subsets of ovarian cancer patients most likely to benefit from treatment with dasatinib.

Significant findings reported in the dasatinib study are summarized below.

  • Concentration-dependent, anti-proliferative effects of dasatinib were seen in all ovarian cancer cell lines tested.
  • Dasatinib significantly inhibited tumor cell invasion, and induced tumor cell death, but was less effective in causing tumor cell-cycle arrest.
  • At a wide range of clinically achievable drug concentrations, additive and synergistic interactions were observed for dasatinib plus carboplatin or paclitaxel.
  • 24 out of 34 (71%) representative ovarian cancer cell lines were highly sensitive (i.e.,  ≥ 60% growth inhibition) to dasatinib.
  • 6 cells lines were moderately sensitive (i.e., 40% – 59% growth inhibition) to dasatinib.
  • 4 cell lines were resistant (i.e., < 40% growth inhibition) to dasatinib.
  • When comparing dasatinib sensitivity between cell lines based solely upon histological subtype (i.e., serous papillary, clear cell, endometrioid, mucinous, and undifferentiated ovarian cancer cell lines), no single histological subtype was more sensitive than another.
  • Ovarian cancer cell lines with high expression of Yes, Lyn, Eph2A, caveolin-1 and 2, moesin, annexin-1 and 2 and uPA (urokinase-type Plasminogen Activator), as well as those with low expression of IGFBP2 (insulin-like growth factor binding protein 2), were particularly sensitive to dasatinib.
  • Ovarian cancer cell lines with high expression of HER-2 (Human Epidermal growth factor Receptor 2), VEGF (Vascular endothelial growth factor) and STAT3 (Signal Transducer and Activator of Transcription 3) were correlated with in vitro resistance to dasatinib.

Based upon the findings above, the researchers concluded that there is a clear biological rationale to support the clinical study of dasatinib, as a single agent or in combination with chemotherapy, in patients with ovarian cancer.

Konecny

Gottfried E. Konecny, M.D., UCLA Assistant Professor of Hematology/Oncology, UCLA Jonsson Comprehensive Cancer Center Researcher & First Author of the Dasatinib Study

Ovarian cancer, which will strike 21,600 women this year and kill 15,500, causes more deaths than any other cancer of the female reproductive system. Few effective therapies for ovarian cancer exist, so it would be advantageous for patients if a new drug could be found that fights the cancer, said Gottfried E. Konecny, M.D., a UCLA assistant professor of hematology/oncology, a Jonsson Comprehensive Cancer Center researcher, and first author of the study.

“I think Sprycel® could be a potential additional drug for treating patients with Src dependent ovarian cancer,” Konecny said. “It is important to remember that this work is only on cancer cell lines, but it is significant enough that it should be used to justify clinical trials to confirm that women with this type of ovarian cancer could benefit.”

Recent gene expression studies have shown that approximately one-third of women have ovarian cancers with activated Src pathways, so the drug could potentially help 7,000 ovarian cancer patients every year. Notably, a gene expression study published in 2007 reported Src activation in approximately 50% of the ovarian cancer tumors examined.

In the dasatinib study, the UCLA team tested the drug against 34 ovarian cancer cell lines and conducted genetic analysis of those lines. Through these actions, the researchers were able to identify genes that predict response to dasatinib. If the work is confirmed in human studies, it may be possible to test patients for Src activation and select those who would respond prior to treatment, thereby personalizing their care.

“We were able to identify markers in the pre-clinical setting that would allow us to predict response to Sprycel®,” Konecny said. “These may help us in future clinical trials in selecting patients for studies of the drug.”

Dasatinib is referred to as a “dirty” kinase inhibitor, meaning it inhibits more than one cellular pathway. Konecny said it also inhibits the focal adhesion kinase (FAK) and ephrin receptor, also associated with ovarian cancer, in addition to the Src cellular pathway.

The next step, Konecny said, would be to test the drug on women with ovarian cancer in a clinical trial. The tissue of responders would then be analyzed to determine if the Src and other pathways were activated. If that is confirmed, it would further prove that dasatinib could be used to fight ovarian cancer. In studies, women would be screened before entering a trial and only those with Src dependent cancers could be enrolled to provide further evidence, Konecny said, much like the studies of the molecularly targeted breast cancer drug Herceptin® enrolled only women who had HER-2 positive disease.

“Herceptin® is different because we knew in advance that it only worked in women with HER-2 [gene] amplification,” he said. “In this case, we don’t clearly know that yet. The data reassures us that the drug works where the targets are over-expressed but we need more testing to confirm this.”

The tests combining the drug with chemotherapy are significant because chemotherapy, namely carboplatin and paclitaxel, is considered the standard first line treatment for ovarian cancer patients following surgery. Because dasatinib proved to have a synergistic effect when combined with chemotherapy, it may be possible to add this targeted therapy as a first line treatment if its efficacy is confirmed in future studies.

Dasatinib Study Significance

The dasatinib study is potentially significant to the area of ovarian cancer treatment for several reasons.

First, although this study only tested dasatinib in vitro against ovarian cancer cell lines, the drug is already FDA-approved.  Accordingly, the general safety of the drug has already been established by the FDA.

Second, 71% of the ovarian cancer lines were highly sensitive to dasatinib.

Third, dasatinib was additive to, or synergistic with, the standard of care chemotherapy drugs used in first line ovarian cancer treatment, i.e., carboplatin and paclitaxel.

Fourth, the study established molecular markers that may be predictive of dasatinib effectiveness in particular patients.  In theory, a patient’s tumor biopsy could be tested for the presence of those molecular markers to determine whether a patient will benefit from dasatinib.

Fifth, one of the dasatinib study authors is Dennis J. Slamon, M.D. Ph.D. Dr. Slamon is the director of Clinical/Translational Research, and director of the Revlon/UCLA Women’s Cancer Research Program, at the UCLA Jonsson Comprehensive Cancer Center. Dr. Slamon is also the co-discoverer of Herceptin®, a targeted therapy that revolutionized the treatment of HER-2 positive breast cancer.  Herceptin® is a targeted therapy that kills HER-2 positive breast cancer cells while leaving normal cells unaffected.  The potential use of dasatinib to treat select ovarian cancer patients who test “positive” for specific molecular markers (e.g., Src cellular pathway activation) is similar to the extremely successful drug development approach used for Herceptin®.

Open Clinical Trials Testing Dasatinib (Sprycel®) Against Ovarian Cancer & Solid Tumors

As of this writing, there are several open (i.e., recruiting) clinical trials that involve testing dasatinib against ovarian cancer and solid tumors.

For a list of open clinical trials that involve testing dasatinib against ovarian cancer, CLICK HERE.

For a list of open clinical trials that involve testing dasatinib against solid tumors, CLICK HERE.

All potential volunteers must satisfy the clinical trial entrance criteria prior to enrollment.  Depending on the drug combination being tested, one or more of the solid tumor clinical trials may not be appropriate for an ovarian cancer patient.

About the UCLA Jonsson Comprehensive Cancer Center

UCLA’s Jonsson Comprehensive Cancer Center (JCCC) has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation’s largest comprehensive cancer centers, JCCC is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2009, JCCC was named among the top 12 cancer centers nationwide by U.S. News & World Report, a ranking it has held for 10 consecutive years. For more information on JCCC, visit the website at http://www.cancer.ucla.edu.

Sources:

Posted in Biomarker, Chemotherapy, Discoveries, Medical Study Results, Molecular Diagnostics, Novel Therapies, Preclinical Testing, Targeted Therapies | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 2 Comments »

Stand Up To Cancer Funded Research Dream Team Takes Aim At Women’s Cancers

Posted by Paul Cacciatore on May 29, 2009

Stand Up To Cancer (SU2C), the Entertainment Industry Foundation’s charitable initiative supporting groundbreaking research aimed at getting new cancer treatments to patients in an accelerated timeframe, has reached a significant milestone, awarding the first round of three-year grants — that total $73.6 million — to five multi-disciplinary, multi-institutional research Dream Teams. … Each Dream Team’s project, funded for three years pending satisfactory achievement of stated milestones, is “translational” in nature, geared toward moving science from “bench to bedside” where it can benefit patients as quickly as possible. …

A Dream Team of leading cancer researchers will accelerate development of drugs to attack a mutated [PI3K] molecular pathway that fuels endometrial, breast and ovarian cancers, funded by a three-year $15 million grant awarded today by [SU2C] … Genetic aberrations in the network, known as the PI3K pathway, are found in half of all breast cancer patients, 60 percent of all cases of endometrial cancer and 20 percent of ovarian cancer patients. Other cancers that include a mutationally activated PI3K pathway include melanoma, colon and prostate cancers, brain tumors, and leukemia.

Read the rest of this entry »

Posted in Inspirational, Novel Therapies, Research Grant | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | Leave a Comment »

 
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