Carrboro man to get stem cell transplant

Stem Cell Medical Center | Posted by admin
Feb 22 2012

Published: Feb 22, 2012 02:00 AM
Modified: Feb 20, 2012 10:41 PM


Carrboro man to get stem cell transplant
Treatment a first at UNC

BY ELIZABETH SWARINGEN, Special to The Chapel Hill News

CHAPEL HILL – Three infusions of your own stem cells – each infusion over a 21-day hospitalization – can seem daunting. But, when it's your best chance for beating a recurrence of testicular cancer, you look forward to it.”It doesn't seem intimidating to me at all,” said David Alston, 42, of Carrboro. “You don't normally think of stem cell bone marrow transplants as treatment for testicular cancer, but it has been done in New York with success. I'm pleased it's available to me here at UNC Hospitals.”This month Alston is having the first triple-tandem transplant done in an adult at UNC Hospitals.The process involves harvesting and freezing his own stem cells, receiving high-dose chemotherapy to attack the cancer, then having the stem cells infused over three back-to-back hospitalizations.”He's young and otherwise healthy, and we think this is the right thing for him,” said Dr. Paul M. Armistead, assistant professor of medicine in the Division of Hematology/Oncology, a member of the UNC Lineberger Comprehensive Cancer Center and leader of Alston's transplant team. “This is his best chance for being cured.”Alston, a Charlotte native, was diagnosed with aggressive testicular cancer in March 2011 after experiencing an “avalanche of symptoms.”"I didn't have a lump, but I had some weird back pain and loss of feeling in one leg,” David said. “By the time I had some scans, we found lymph node involvement in a lot of places. Essentially, the cancer had gone on vacation all over my body.”Testicular cancer is one of the more curable cancers, often cured in the first round of chemotherapy, said Dr. Kim Rathmell, associate professor of medicine, a member of UNC Lineberger Comprehensive Cancer Center and Alston's medical oncologist.Aggressive chemotherapy sent the cancer into remission, and by August Alston returned to his long-time job at Weaver Street Market in Chapel Hill's Southern Village.Routine blood test results in December surprised everyone: the cancer was back.”Because of the way David's cancer came back, a more aggressive approach than chemotherapy alone was needed,” said Rathmell, adding how hard it was knowing Alston faced treatment again. “I shop that store, and I had seen him back at work.”Dr. Matthew Milowsky, who participated in the development of the triple-tandem transplant for testicular cancer at Memorial Sloan Kettering in New York City, joined UNC Lineberger Comprehensive Cancer Center last fall as co-director of UNC's urologic oncology program. Rathmell quickly recruited him to Alston's team.”We have everything we need here at UNC to treat David,” Rathmell said. “Had David come to us five years ago, when this recommended treatment was newer and we didn't have local expertise, I would likely have referred him elsewhere. Today, we are very comfortable doing this transplant here. And it's a total team approach.”In January, Alston began receiving two types of chemotherapy to mobilize his stem cells in preparation for collection.This chemotherapy featured one less drug than what he endured after initial diagnosis and yielded fewer side effects.”It was night and day difference,” he said, remembering the physical and mental side effects that sent him into the ICU last spring. “By comparison, what I'm doing in preparation for the transplant has been rather effortless.”But the process is complicated and has many moving parts.”David will have five chemotherapy infusions administered by two separate medical teams that have to work together through a lot of logistics about what happens when,” said Armistead. “That David is organized and intelligent and sends a lot of questions to Dr. Rathmell and me via email, he's helping himself stay on top of things. Having a patient who is fully aware of what's going on has kept us on our toes and helped us develop and coordinate a more fool-proof system.”Still, as a single, stubbornly independent man, Alston needed help and support. Luckily, his mother, Barbara Alston, a retired medical professional from Concord, is by his side.Both are staying at SECU Family House, the 40-bedroom hospital hospitality house minutes from UNC Hospitals for seriously ill adult patients and their family member caregivers.The Alstons will stay at Family House during the nine weeks total that David is expected to be hospitalized. He will join her between transplants and for post-transplant monitoring.”It's a comfort being here at Family House,” Barbara Alston said. “If we need something, it's taken care of, both here and at the hospital. I'm assured David's getting the care he needs. I'm helping him whenever and wherever I can.”SECU Family House will play an even larger role in Alston's recovery post-transplant, both Rathmell and Armistead agreed.”This treatment is intense, and David will be more in the hospital than out,” Rathmell said. “He will need a solid support system, and he has that with his mother. It's a fragile time, and she has his best interest at heart.”"Post-transplant David will need to be monitored closely because his immune system will be very weak,” Armistead said. “His mother's medical background is a bonus. The Family House folks are used to immune-suppressed patients and can get them to the hospital quickly if needed.”Alston has kept himself swimming in information to minimize the fear and mystery. Barbara has been the great translator when his own efforts didn't yield the level of detail he needed.”The constant learning gives it all a degree of routine that took some of the scariness away,” Alston said. “But you can't be too independent or too brainy when you have cancer.”Cancer blows you out of the water, but it leaves you with valuable insight,” he said. “How you deal with cancer is self-guided and you learn things about yourself and your personality that you never knew. It's the ultimate in snatching the silver lining from a cloud.”

Elizabeth Swaringen wrote this article for UNC Health Care.

See the rest here:
Carrboro man to get stem cell transplant

Cancer Stem Cell Research Drives Growth in RBCC’s Target Market

Stem Cell Medical Center | Posted by admin
Feb 22 2012

NOKOMIS, Fla.–(BUSINESS WIRE)–

Research into Cancer Stem Cells (CSC) is on the rise, fueling industry growth that Rainbow Coral Corp. (OTCBB: RBCC.OB – News) expects to translate into demand for n3D cell growth technologies.

RBCC is finalizing an equity funding agreement with n3D Biosciences, the maker of a revolutionary new system that allows scientists to grow three-dimensional cell cultures more easily than ever before. The device, called the Bio-Assembler, could have an extraordinary impact on cell research worldwide, and RBCC expects to find a strong market for the device once its funding agreement with n3D is finalized.

Many cancers, including breast, prostate, pancreatic, colon, brain, and lung cancers, contain a subset of stem-like cells understood to play a critical role in the development and progression of the disease. Research suggests that these cells, called Cancer Stem Cells, are able to “seed” new tumor formation and drive metastasis.

Because these cells are believed to be at the root of the development and spread of cancer, they’re quickly becoming the center of cancer diagnostics and biomarkers. CSCs are resistant to a number of chemotherapy drugs and radiotherapy, and approximately 20 different strategies are currently being pursued in the hope of selectively targeting CSCs. This creates a huge opening for new companies and technologies dedicated to streamlining cellular research.

RBCC believes that the Bio-Assembler could allow researchers to dramatically shorten the development timeline for new CSC drugs and treatments, potentially proving very lucrative to the company.

For more information on Rainbow BioSciences, please visit www.rainbowbiosciences.com/investors.

Rainbow BioSciences will develop new medical and research technology innovations to compete alongside companies such as Celgene Corp. (NASDAQ: CELG), Cardinal Health, Inc. (NYSE: CAH), Abbott Laboratories (NYSE: ABT) and Affymax, Inc. (NASDAQ: AFFY).

Follow us on Twitter at www.twitter.com/RBCCinfo.

About Rainbow BioSciences

Rainbow BioSciences is a division of Rainbow Coral Corp. (OTCBB: RBCC). The company continually seeks out new partnerships with biotechnology developers to deliver profitable new medical technologies and innovations. For more information on our growth-oriented business initiatives, please visit our website at [www.rainbowbiosciences.com]. For investment information and performance data on the company, please visit www.RainbowBioSciences.com/investors.

Notice Regarding Forward-Looking Statements

Safe Harbor Statement under the Private Securities Litigation Reform Act of 1995: This news release contains forward-looking information within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, including statements that include the words “believes,” “expects,” “anticipate” or similar expressions. Such forward-looking statements involve known and unknown risks, uncertainties and other factors that may cause the actual results, performance or achievements of the company to differ materially from those expressed or implied by such forward-looking statements. In addition, description of anyone's past success, either financial or strategic, is no guarantee of future success. This news release speaks as of the date first set forth above and the company assumes no responsibility to update the information included herein for events occurring after the date hereof.

Read more:
Cancer Stem Cell Research Drives Growth in RBCC’s Target Market

Stem cell implants boost monkeys with Parkinson's

Stem Cell Treatment | Posted by admin
Feb 22 2012

Monkeys suffering from Parkinson's disease show a marked improvement when human embryonic stem cells are implanted in their brains, in what a Japanese researcher said Wednesday was a world first.

A team of scientists transplanted the stem cells into four primates that were suffering from the debilitating disease.

The monkeys all had violent shaking in their limbs — a classic symptom of Parkinson's disease — and were unable to control their bodies, but began to show improvements in their motor control after about three months, Kyoto University associate professor Jun Takahashi told AFP.

About six months after the transplant, the creatures were able to walk around their cages, he said.

“Clear improvements were confirmed in their movement,” he said.

Parkinson's disease is a progressive neurological illness linked to a decrease in dopamine production in the brain. There is currently no medical solution to this drop off in a key neurotransmitter.

The condition, which generally affects older people, gained wider public recognition when Hollywood actor Michael J. Fox revealed he was a sufferer.

Takahashi said at the time of the implant about 35 percent of the stem cells had already grown into dopamine neuron cells, with around 10 percent still alive after a year.

He said he wants to improve the effectiveness of the treatment by increasing the survival rate of dopamine neuron cells to 70 percent.

“The challenge before applying it to a clinical study is to raise the number of dopamine neuron cells and to prevent the development of tumours,” he said.

“I would like to make this operation more effective and safe” before clinical trials, Takahashi said.

Takahashi said so far he had used embryonic stem cells, which are harvested from foetuses, but would likely switch to so-called Induced Pluripotent Stem (iPS) cells, which are created from human skin, for the clinical trial.

His team, which has also transplanted iPS cells into monkeys, are now looking to see if the primates with Parkinson's disease show similar improvements in their motor control.

Scientists say the use of human embryonic stem cells as a treatment for cancer and other diseases holds great promise, but the process has drawn fire from religious conservatives, among others.

Opponents say harvesting the cells, which have the potential to become any cell in the human body, is unethical because it involves the destruction of an embryo.

The Japanese government currently has no guidelines on the use of human stem cells in clinical research.

In October last year, the Court of Justice of the European Union banned the patenting of stem cells when their extraction causes the destruction of a human embryo, a ruling that could have repercussions on medical research.

Scientists warned that the ruling would damage stem cell research in Europe, while the Catholic church hailed it as a victory for the protection of human life.

Excerpt from:
Stem cell implants boost monkeys with Parkinson's

Editor’s move sparks backlash

Stem Cell Medical Center | Posted by admin
Feb 22 2012

Bioethicist Glenn McGee’s new job raised questions of conflict of interest at the journal he founded.

J. WILSON/KRT/NEWSCOM

The field of bioethics is embroiled in a period of soul-searching, sparked by a startling career move by one of its biggest names.

Glenn McGee is the editor-in-chief of the American Journal of Bioethics (AJOB), the most cited bioethics journal, which he founded in 1999. Since December 2011, he has also been president for ethics and strategic initiatives at CellTex Therapeutics in Houston, Texas, a controversial company involved in providing customers with unproven stem-cell therapies. A CellTex press release says that “Dr McGee’s responsibilities will include ensuring that all of the firm’s work, centered on adult stem cells, will meet the highest ethical standards of the medical and scientific communities.”

Although McGee has said he will leave the journal on 1 March, many bioethicists have criticized him, the journal’s editorial board and its publisher, London-based Taylor and Francis. They argue that in holding both posts, McGee has a conflict of interest between his responsibilities to the journal and his new employer’s desire to promote the clinical application of stem-cell treatments that are not approved by the US Food and Drug Administration.

“Imagine if the Editor of the New England Journal of Medicine took a job as Vice President at Merck, and the Mass Medical Society asked him to stay on as Editor, opining that the conflicts of interest would be manageable. One might rightly wonder, ‘What are these people smoking?’,” says John Lantos, director of the Children’s Mercy Bioethics Center in Kansas City, Missouri, and a past president of the American Society for Bioethics and Humanities.

More broadly, bioethicists are questioning whether it can ever be acceptable to work for companies, which, they argue, may be using the appointment to present a veneer of ethical probity. The episode brings to a head concerns that have emerged among bioethicists over the past decade, says Insoo Hyun, a stem-cell bioethicist at Case Western Reserve University in Cleveland, Ohio. “It’s a perfect storm,” he says.

McGee is a leading voice on one side of the debate, arguing that bioethics must have practical relevance. For the past three years he has been chair of bioethics at the non-profit Center for Practical Bioethics in Kansas City, where he ran a course for those who might go on to chair hospital ethics committees or serve as ethical advisers to corporations.

But during McGee’s tenure as editor-in-chief of the AJOB, four editors are known to have resigned from the editorial board because of differences in opinion over how the journal handles conflicts of interest. Two left this month, including Lantos, who wrote on his blog that he will no longer work with the journal because of McGee’s simultaneous employment at the AJOB and CellTex, and frustration over the lack of a clear conflict-of-interest policy at the AJOB. In response to Nature’s questions about the situation, Taylor and Francis responded that it “is grateful for Dr McGee’s editorship of AJOB” and “supportive of Glenn’s decision to step down”.

On 17 February, McGee announced that he is merely acting in an advisory capacity at the journal until 1 March, when its new editors-in-chief take over. They are David Magnus, director of the Center for Biomedical Ethics at Stanford University, California, and Summer Johnson McGee, director of graduate studies at the Center for Practical Bioethics and the journal’s current executive editor. She is also Glenn McGee’s wife.

“Mainstream bioethics is no longer speaking truth to power.”

Responding to questions from Nature, Summer Johnson McGee says that the journal has a conflict-of-interest policy that requires editors to withdraw from reviewing a manuscript if they perceive a conflict. She calls allegations that her appointment results from her relationship with her husband “baseless and sexist”. “David Magnus and I were hired by our publisher, not by my husband.” Magnus says that at least a dozen editorial board members have supported his and Summer Johnson McGee’s appointments. Two even indicated that Glenn McGee should have been able to retain an advisory or editorial role.

Other bioethicists’ blogs and Twitter feeds about the episode have expressed concerns, however. Leigh Turner of the University of Minnesota, Minneapolis, called on the entire editorial board of the AJOB to resign for allowing the situation to persist. And many say that McGee’s move illustrates a broader problem. “Mainstream bioethics is no longer speaking truth to power,” complains Jan Helge Solbakk at the University of Oslo. “Instead it has become the handmaiden of the medico-industrial complex, and of bioscience and technology.”

So how should companies get their advice on bioethics? Magnus never takes cash from industry for advising or speaking — “I’m a hardass about that” — but he believes that bioethicists can work for industry as long as they give up their academic positions, including posts on journal editorial boards.

Working for a respected company may be acceptable to some bioethicists, but McGee’s new employer comes with a great deal of baggage. CellTex, which was founded last year and as yet has no website, licenses stem-cell technology from Seoul-based RNL Bio. The South Korean company has made a business out of taking fat cells from people, processing them in a way that they say increases the number of mesenchymal stem cells, and then reinjecting them in an effort to treat conditions such as spinal cord injury.

McGee already had a connection with RNL Bio. In 2010, two patients died following injections of RNL’s cells. McGee, working for stem-cell lobby group the International Cellular Medicine Society, based in Salem, Oregon, helped to conduct an investigation into the company. This concluded that only one of the two cases was likely to be related to the injections, and because the patient understood the risk the company was not culpable.

Jin Han Hong, the then president of RNL’s US subsidiary, admitted in 2010 that there was no clinical-trial evidence proving that these treatments are effective (Nature 468, 485; 2010). As treatment with RNL’s stem cells is not approved in the United States or South Korea, for the procedures the company sends patients to China or Japan, where regulations are less strictly enforced. Using RNL’s methods, CellTex is banking stem cells that have gone on to be used in a number of patients, including Rick Perry, governor of Texas (Nature 477, 377–378; 2011). CellTex says that it does not conduct medical procedures itself.

When Nature contacted McGee to put the criticisms to him, he directed us to previous statements indicating that he wants to put CellTex on firmer ethical ground by having it conduct clinical trials that meet standards set by the International Society for Stem Cell Research, based in Deerfield, Illinois, which represents most mainstream stem-cell researchers around the world.

Hyun warns that working directly for business can be fraught with danger, however good a bioethicist’s intentions. In 2005, he helped to craft the informed consent procedure for egg donations used in a cloning procedure by disgraced Korean stem-cell scientist Woo Suk Hwang. Following Hwang’s claim, later proved fraudulent, that he had cloned human embryos and harvested stem cells from them, it emerged that he had ignored the consent procedure for egg donations (Nature 438, 536–537; 2005), leading to embarrassment for Hyun.

“I know first hand how difficult it is to separate conflict of interest — to maintain the role of bioethicist,” says Hyun. “I know you need to not be too chummy with enterprises trying to speed ahead in stem cells.”

Read this article:
Editor’s move sparks backlash

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

Cell Medicine | Posted by admin
Feb 22 2012

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

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

A breakthrough in understanding the biology and treatment of ovarian cancer

Cell Medicine | Posted by admin
Feb 22 2012

Public release date: 21-Feb-2012
[ | E-mail | Share ]

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.”

###

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/.

[ | E-mail | Share ]

 

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

See the original post here:
A breakthrough in understanding the biology and treatment of ovarian cancer

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

Cell Medicine | Posted by admin
Feb 22 2012

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.

The rest is here:
Biocept to Present at the Molecular Medicine Tri-Conference on Circulating Tumor Cell (CTC) Technologies

Cell energy sensor mechanism discovered

Cell Medicine | Posted by admin
Feb 22 2012

ScienceDaily (Feb. 21, 2012) — Johns Hopkins and National Taiwan University researchers have discovered more details about how an energy sensing “thermostat” protein determines whether cells will store or use their energy reserves.

In a report in the Feb. 9 edition of Nature, the researchers showed that a chemical modification on the thermostat protein changes how it's controlled. Without the modification, cells use stored energy, and with it, they default to stockpiling resources. When cells don't properly allocate their energy supply, they can die off or become cancerous. The Johns Hopkins team focused especially on enzymes that add or remove so-called acetyl groups from protein molecules.

“Understanding how cells are affected by adding acetyl groups to proteins, particularly those involved in energy use, is important because there is increasing use of drugs that block acetyl-removing enzymes for treatment of cancer and neurodegenerative diseases,” says Jef Boeke, Ph.D., professor of molecular biology, genetics and oncology, and director of the High Throughput Biology Center at the Johns Hopkins University School of Medicine. “Blocking acetyl-removing enzymes turns on anticancer genes that help fight cancer; however, it is not known what other genes and cellular processes may also be affected by these treatments.”

To determine which enzymes remove acetyl chemical groups from which proteins, the researchers engineered human cells with reduced levels of each of 12 enzymes known to remove acetyl chemical groups. In each of these cell lines, they then turned down each of about 20,000 genes and used a DNA “chip” to identify which genes were affected by reduced levels of the acetyl-removing enzymes. The DNA chip highlighted a specific interaction between the thermostat protein, AMP-activated protein kinase (AMPK), and one of the acetyl-removing enzymes, HDAC1.

With less HDAC, AMPK was turned “off,” presumably because it retains its acetyl group, the researchers concluded. AMPK acts like an energy thermostat because when energy levels are low in the cell, AMPK kick-starts processes that use the cell's energy reserves and cuts off reactions that store energy. On the other hand, when the cell has plenty of energy, AMPK turns off, causing energy in the form of sugar and fats being stored for later use.

Because the HDAC1 protein turned on AMPK, the researchers presumed there would be a corresponding acetyl-adding enzyme to specifically turn off AMPK. To find this enzyme, they extracted AMPK protein from eight different cell lines, each with reduced levels of a type of acetyl-adding enzyme. They found that AMPK in cells with reduced levels of this acetyl-adding enzyme, called p300, was less acetylated than in cells containing normal amounts of p300.

To confirm the idea that adding or removing acetyl groups directly affects how AMPK controls the way the cell uses energy, they measured the cell's energy stores with the help of a dye that accumulates in the fat globules of a cell. The dye let them estimate the size of fat globules that store energy. The cells unable to add acetyl to AMPK contained less of the dye and therefore smaller fat globules compared to normal human cells. Conversely, the cells unable to remove acetyl groups from AMPK contained more of the dye, indicating bigger fat globules. The research team concluded that when AMPK contains acetyl groups the cell uses less of its energy reserves than when AMPK does not contain acetyl groups.

Boeke says the work on human cells followed similar studies on yeast energy proteins done earlier in his laboratory.

Additional authors of the study include Yu-yi Lin, Shang-Yun Liu and Yi-hsuan Chou of the National Taiwan University; Jin-ying Lu of the National Taiwan University Hospital; Chin Ni Khnor and Chi-Long Lin of Academia Sinica, Taipei, Taiwan; Samara Kiihl and Rafael Irizarry of the Johns Hopkins University Bloomberg School of Public Health; and Yasir Suhail, Zheng Kuang and Joel Bader of the Johns Hopkins University School of Medicine.

The study was supported by funds from National Science Council grants, National Taiwan University Frontier and Innovative Research, National Taiwan University Excellent Translational Medicine Research Project, a National Health Research Institutes Career Development grant, the Liver Disease Prevention and Treatment Research Foundation and a National Institutes of Health Common Fund grant.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Johns Hopkins Medicine, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Yu-yi Lin, Samara Kiihl, Yasir Suhail, Shang-Yun Liu, Yi-hsuan Chou, Zheng Kuang, Jin-ying Lu, Chin Ni Khor, Chi-Long Lin, Joel S. Bader, Rafael Irizarry, Jef D. Boeke. Functional dissection of lysine deacetylases reveals that HDAC1 and p300 regulate AMPK. Nature, 2012; 482 (7384): 251 DOI: 10.1038/nature10804

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Follow this link:
Cell energy sensor mechanism discovered

Energy network within cells may be new target for cancer therapy

Cell Therapy | Posted by admin
Feb 22 2012

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

Read more here:
Energy network within cells may be new target for cancer therapy

VistaGen Therapeutics Engages MissionIR as Its Investor Relations Advisor

Cell Therapy | Posted by admin
Feb 22 2012

ATLANTA, GA–(Marketwire -02/21/12)- VistaGen Therapeutics, Inc. (OTC.BB: VSTA.OB – News) (OTCQB: VSTA.OB – News), a biotechnology company applying stem cell technology for drug rescue and cell therapy, has retained MissionIR, a national investor relations consulting firm, to develop and implement a strategic investor relations campaign. Through a network of investor-oriented online websites and full suite of investor awareness services, MissionIR broadens the influence of publicly traded companies and enhances their ability to attract growth capital and improve shareholder value.

“VistaGen's work with human stem cell technology is groundbreaking,” said Sherri Snyder, Director of Marketing at MissionIR. “The company's versatile platform, Human Clinical Trials in a Test Tube™, provides clinically relevant predictions of potential heart toxicity of new drug candidates long before they are ever tested on humans. Guided by a management team with decades of experience, VistaGen's stem cell technology can potentially save billions of dollars in the healthcare industry while recapturing prior R&D investment in once-promising new drug candidates.”

“We are pleased to bring MissionIR on board as our external investor relations partner,” said Shawn Singh, VistaGen's Chief Executive Officer. “The crucial work our company is doing can fundamentally change the way medicine is developed. Paired with MissionIR's global presence and sound investor relations programs, we can further grow our shareholder base and accelerate internal initiatives already in place to bring our stem cell technology platform to the forefront of drug development.”

About MissionIR

MissionIR is committed to connecting the investment community with companies that have great potential and a strong dedication to building shareholder value. Through a full suite of investor relations and consultancy services, we help public companies develop and execute a strategic investor awareness plan as we've done for hundreds of others. Whether it's capital raising, increasing awareness among the financial community, or enhancing corporate communications, we offer a variety of solutions to meet the objectives of our clients.

For more information, visit www.MissionIR.com

About VistaGen Therapeutics

VistaGen is a biotechnology company applying human pluripotent stem cell technology for drug rescue and cell therapy. VistaGen's drug rescue activities combine its human pluripotent stem cell technology platform, Human Clinical Trials in a Test Tube™, with modern medicinal chemistry to generate new chemical variants of once-promising small-molecule drug candidates. These are once-promising drug candidates discontinued by pharmaceutical companies during development due to heart toxicity, despite positive efficacy data demonstrating their potential therapeutic and commercial benefits. VistaGen uses its pluripotent stem cell technology to generate early indications, or predictions, of how humans will ultimately respond to new drug candidates before they are ever tested in humans.

Additionally, VistaGen's small molecule drug candidate, AV-101, is in Phase 1b development for treatment of neuropathic pain. Neuropathic pain, a serious and chronic condition causing pain after an injury or disease of the peripheral or central nervous system, affects approximately 1.8 million people in the U.S. alone. VistaGen plans to initiate Phase 2 clinical development of AV-101 in the fourth quarter of 2012. VistaGen is also exploring opportunities to leverage its current Phase 1 clinical program to enable additional Phase 2 clinical studies of AV-101 for epilepsy, Parkinson's disease and depression. To date, VistaGen has been awarded over $8.5 million from the NIH for development of AV-101.

Visit VistaGen at http://www.VistaGen.com, follow VistaGen at http://www.twitter.com/VistaGen or view VistaGen's Facebook page at http://www.facebook.com/VistaGen.

Continue reading here:
VistaGen Therapeutics Engages MissionIR as Its Investor Relations Advisor







Personalized Gene Medicine | Mesenchymal Stem Cells | Stem Cell Treatment for Multiple Sclerosis | Stem Cell Treatments | Board Certified Stem Cell Doctors | Stem Cell Medicine | Personalized Stem Cells Therapy | Stem Cell Therapy TV | Individual Stem Cell Therapy | Stem Cell Therapy Updates | MD Supervised Stem Cell Therapy | IPS Stem Cell Org | IPS Stem Cell Net | Genetic Medicine | Gene Medicine | Longevity Medicine | Immortality Medicine | Nano Medicine | Gene Therapy MD | Individual Gene Therapy | Affordable Stem Cell Therapy | Affordable Stem Cells | Stem Cells Research | Stem Cell Breaking Research