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Old 06-28-2009, 08:40 AM
gdpawel gdpawel is offline
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Default Controversial Cancer Stem Cells Offer New Direction For Treatment

In a review in Science, a University of Rochester Medical Center researcher sorts out the controversy and promise around a dangerous subtype of cancer cells, known as cancer stem cells, which seem capable of resisting many modern treatments.

The article proposes that this subpopulation of malignant cells may one day provide an important avenue for controlling cancer, especially if new treatments that target the cancer stem cell are developed and combined with traditional chemotherapy and/or radiation.

"The fact that these concepts are steadily making their way into the clinic is exciting, and suggests that the recent interest in cancer stem cells may yield beneficial outcomes in potentially unexpected ways," wrote co-authors Craig T. Jordan, Ph.D., professor of Medicine at URMC and director of the James P. Wilmot Cancer Center Translational Research for Hematologic Malignancies program; and Jeffrey Rosen, Ph.D., the C.C. Bell Professor of Molecular and Cellular Biology and Medicine at Baylor College of Medicine.

Cancer stem cells (CSCs) are a hot topic in the scientific community. First identified in 1994 in relation to acute myeloid leukemia, CSCs have now been identified in several solid tumors in mice as well. Scientists who study CSCs believe they have distinct properties from other cancer cells, and may be the first cells to undergo mutations.

Research from the past 10 years suggests that because CSCs may be the root of cancer, they also might provide a new opportunity for a treatment. Jordan and a group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukemia CSCs to self destruct.

Another new approach, the authors said, is the use of chemical screens to search drug libraries for already approved agents that may target CSCs, or make resistant tumor cells more sensitive to chemotherapy and radiation.

Cancer stem cell biologists hypothesize that any treatment that targets the source of origin rather than simply killing all cells, healthy and malignant, would be an improvement over most conventional therapies.

Some scientists, however, are uncertain if CSCs have unique biological properties or any relevance to treatment, the authors noted. What is more likely to fuel cancer, other studies have found, are unfavorable factors in the neighboring cells surrounding the tumor, such as mutated genes, proteins that encourage cell growth, and a poor immune system, for instance.

The most challenging issue facing CSC biologists is that the number and type of cancer stem cells can vary from patient to patient. In some tumor samples, for example, CSCs are rare while in others they constitute a large portion of the tumor mass, the authors said.

To understand why CSCs are so variable, investigators are trying to determine what genes and pathways are responsible for activating cancers that have a poor prognosis, and whether these cancers also have a higher frequency of CSCs.

"Whether the cancer stem cell model is relevant to all cancers or not," they wrote, "it is clear that we need new approaches to target tumor cells that are resistant to current therapies and give rise to recurrence and treatment failure."

An unexpected benefit of so much attention on normal stem cells is that it has stimulated research in areas not previously the focus of cancer therapies, Jordan and Rosen said.

For example, pathways known to be important for normal stem cell self-renewal, such as the Wnt, Notch and Hedgehog(Hh) pathways, are now of increased interest due to their potential role in CSCs. The first clinical trial using an agent to block the Notch pathway in combination with chemotherapy for breast cancer has begun.

The authors conclude by spotlighting the pressing need for preclinical models to test appropriate doses and combinations of CSC therapies before they can move into human clinical trials.

Source: University of Rochester Medical Center
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Old 06-28-2009, 07:24 PM
gdpawel gdpawel is offline
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Default Are Stem Cells the root of the problem?

Stem cells have that infinite ability to renew themselves and produce the many different cell types that make up a human. Cancer's hallmark is its ability to grow infinitely, multiplying into various cells that make up a tumor. Is cancer the result of a normal stem cell turned bad or an ordinary cell that somehow acquires a stem cell's immortality and versatility?

A recent finding that Temodar (temozolomide) increased the number of cancer cells with stem-like characteristics sounds eerily similar to the increase in the number of metabolic activity of mitochondria of the surviving cells from taxane (Taxol) therapy, even in cases where the majority of the cells are being killed by taxanes. It may indeed give clinical response (tumor shrinkage), however, these are mostly short-lived and relapses after a reponse to taxanes are often dramatic.

In stem cell research, anti-cancer treatments often effectively shrink the size of tumors, but some might have the opposite effect, actually expanding the small population of cancer stem cells that then are capable of metastasizing. Using the CellSearch System technique that quantifies circulating tumor cells, scientists had shown that chemotherapy with Taxol causes a massive release of cells into the circulation, while at the same time reducing the size of the tumor, explaining that complete pathologic responses do not correlate well with improvements in survival.

Circulating tumor cells (CTCs) are cancer cells that have detached from solid tumors and entered the blood stream. This can begin the process of metastasis, the most life-threatening aspect of cancer. To metastasize, or spread cancer to other sites in the body, CTCs travel through the blood and can take root in another tissue or organ.

Even before the advent of the CellSearch technique, it had been observed in Cell Function Analysis that there was an increase in the number of metabolic activity of mitochondria of the surviving cells from Taxol therapy, even in cases where the majority of the cells were being killed by Taxol.

This new research hightens the faults of gene amplificaton/mutation studies. Genetic profiling assumes that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can genetic profiling tell anything about drug combinations.

Are you sure that you’ve identified every single protein that might influence sensitivity or resistance to drugs? The "cell" is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems' response to drug treatments, not theoretical predispositions.

Cancer is a complex disease and needs to be attacked on many fronts. Cellular profiling holds the key to solving some of the problems confronting the critical task of matching individual patients with the treatments most likely to benefit them.

The fact that cancer stem cells (CSCs) may have unique biological properties more likely to fuel cancer, or unfavorable factors in the neighboring cells surrounding the tumor, such as mutated genes, proteins that encourage cell growth, it is important to look at the "forest" and not just the "trees." There are many pathways to altered cellular (forest) function (hence all the different "trees" which correlate in different situations). Cell functional analysis measures what happens at the end (the effects on the forest), rather than the status of the individual trees.
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Old 04-22-2011, 10:02 AM
gdpawel gdpawel is offline
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Default Embryonic Stem Cell Research in Cancer

According to Robert Weinberg, Ph.D., Professor for Cancer Research at the Massachusetts Institute of Technology (MIT), the "epithelial-mesenchymal transition" (EMT) is a cell-biological behavioral program that operates during the development of normal embryos and is responsible for interconverting one type of cell to another type of cell, more specifically a cell with epithelial properties to one with mesenchymal properties.

An epithelial cell typically sits still and surrounds itself with other epithelial neighbors; without this surrounding company, a typical epithelial cell will quickly die. Epithelial cells line the cavities of all of our organs, including the mouth, lungs, stomach, GI tract, liver, pancreas, prostate, breast milk ducts and so forth.

Mesenchymal cells are, in contrast, typically mobile cells that do not establish stable long-term relationships with their neighbors and are quite resistant to cell death. When a cell passes through an EMT, typically a carcinoma cell that arises from a normal epithelial tissue will acquire mesenchymal traits that confer on it the ability to invade and even to metastasize to distant sites in the body.

Hence by resurrecting a normal cell-biological program, carcinoma cells can acquire an entire suite of traits and ability that make them truly malignant and life-threatening.

Scientists from the University of Manchester, England studied cancer cell movement by using embryonic stem cells to investigate how some tumors are able to migrate to other parts of the body, thereby making cancer treatments more difficult.

Researchers studied a crucial change what makes cancer cells able to start moving and spread into other tissues. That crucial change - known as the epithelial-mesenchymal transition - was observed in the early embryo. It is theorized that embryonic stem cells might undergo a similar process.

They have shown that embryonic stem cells spontaneously change in a manner that is remarkably similar to the epithelial-mesenchymal transition They lose the proteins that cells use to bind to each other and have other protein alterations that are characteristic of spreading cancer cells.

By studying such cells, researchers have identified a novel component of the transition process and expect to identify other factors involved in cancer cell spread, hopefully leading to new cancer therapies.

The findings were published in the journal Molecular Biology of the Cell.

Embryonic Stem Cell Protein Inhibits Melanoma/Breast Cancer

A study by researchers at Northwestern University in Chicage sayd a protein called Lefty that regulates development of human embryonic stem cells can inhibit the growth and spread of deadly melanomas and aggressive breast cancers.

The findings, published in an issue of the Proceedings of the National Academy of Sciences, add to the team's previous efforts to identify the genes and cellular pathways involved in cancer metastasis, and may help lead to new kinds of cancer treatments.

Lefty is secreted only in human embryonic stem cells (hESCs) and not in any other types of stem cells, including those isolated from amniotic fluid, umbilical cord blood or adult bone marrow.

In an earlier study, the Northwestern team found that aggressive melanoma and breast cancer produce a protein called Nodal, which may serve as a marker of aggressive behavior in human cancers.

In this new study, the researchers exposed metastatic melanoma and breast cancer cells to hESCs containing Lefty and noted a dramatic reduction in Nodal production in the cancer cells, along with decreased growth and an increase in programmed cell death (apoptosis).

"The remarkable similarity of the responses of the two tumor types is likely attributable to the commonality of plasticity (for example, the aberrant and unregulated expression of Nodal) that indiscriminately unifies highly aggressive cancer cells, regardless of their tissue of origin.

Further, the tumor suppressive effects of the hESC microenvironment, by neutralizing the expression of Nodal in aggressive tumor cells, provide previously unexplored novel therapeutic modalities for cancer treatment.

Source: Northwestern University
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Old 04-22-2011, 10:05 AM
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Default Three-dimensional (3D) system in laboratory culture

University of Pittsburgh researchers have devised a three-dimensional system in laboratory culture that mimics the growth patterns of colon cancer stem cells in patients. Their findings were presented at the American Association for Cancer Research special conference on Colorectal Cancer: Biology to Therapy, held Oct. 27-30, 2010.

The assay, which uses green fluorescent "reporter" proteins to watch the process of stem cell differentiation, is designed to understand how these cancer stem cells behave, and to identify and test therapies that could halt production of the endless generations of new cancer stem cells that continually revive a tumor.

"Colon cancer stem cells are thought to be the root of therapy resistance, metastases and recurrence in colon cancer, so our approach is to find a way to remove the ability of these stem cells to self-renew," said the study's lead investigator, Julie Chandler, a graduate student in pathology.

"While many labs have investigated notch inhibitors and others have investigated cancer stem cells, our unique approach combines both in a three-dimensional culture that mimics what happens in patients," she said. Animal models, which are immunodeficient and use human xenografs, may not provide accurate information about colon cancer stem cell behavior, Chandler added.

Colon cancer stem cells have the ability to repopulate a tumor after treatment, using stem cells that are resistant to treatment. Such treatment forces a response in these cells, which are genetically unstable, forcing the cells to adapt and pass on resistance to daughter stem cells.

In the same way that adult intestinal stem cells self-renew, colon stem cells give rise to different kinds of cells, including daughter stem cells and fully differentiated cells, such as the goblet epithelial cells that line the colon. Researchers would like to force cancer stem cells to differentiate and behave like goblet cells because these cells do not self renew. Chandler said the notch pathway that controls differentiation in stem cells is inactivated in goblet cells. One way to possibly do that is to use agents that shut down the notch pathway, such as gamma secretase inhibitors, she said. Cancer treatment may then be able to destroy tumors that are now populated by fully differentiated goblet cells.

In their new assay, Chandler used a three-dimensional culture matrix in which she could watch a single cancer stem cell divide and produce progeny, which is called an "independent organoid."

To see the kind of cells a colon cancer stem cell produces, they labeled a protein that is specific only to goblet cells. To date, the researchers have found that some colon cancer stem cells produce many differentiated cells, such as goblets and others, while others produce more primitive, self-renewing cells.

In this way, the researchers can test the ability of notch pathway inhibitors to force progeny cancer stem cells to differentiate into harmless goblet cells.

"Green goblet cells are no longer capable of promoting cancer growth," Chandler said. "It may be that a certain notch inhibitor or similar drug is all that is needed to prevent cancer recurrence and metastasis that so often follows an initial response to treatment. This new tool will help us determine if that is so."

Source: American Association for Cancer Research
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Old 04-22-2011, 10:07 AM
gdpawel gdpawel is offline
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Default To Evade Chemotherapy, Some Cancer Cells Mimic Stem Cells

Anti-cancer treatments often effectively shrink the size of tumors, but some might have an opposite effect, actually expanding the small population of cancer stem cells believed to drive the disease, according to findings presented today in Atlanta, Georgia at the American Association for Cancer Research's second International Conference on Molecular Diagnostics in Cancer Therapeutic Development.

"Our experiments suggest that some treatments could be producing more cancer stem cells that then are capable of metastasizing, because these cells are trying to find a way to survive the therapy," said one of the study's investigators, Vasyl Vasko, M.D. Ph.D., a pathologist at the Uniformed Services University of the Health Sciences in Bethesda, Md.

"This may help explain why the expression of stem cell markers has been associated with resistance to chemotherapy and radiation treatments and poor outcome for patients with cancers including prostate, breast and lung cancers," Dr. Vasko said. "That tells us that understanding how to target these markers and these cells could prove useful in treating these cancers."

The cancer stem cell markers include Nanog and BMI1, both of which contribute to stem cells' defining ability to renew themselves and differentiate into different cell types, Dr. Vasko said. These same molecules are found in embryonic stem cells.

Researchers have recently debated the notion that some therapies are not capable of eradicating cancer because they do not target the cancer stem cells responsible for tumor development. To test this hypothesis, Dr. Vasko, along with scientists from the CRTRC Institute for Drug Development in San Antonio and from the Johns Hopkins University, set out to measure both stem cells markers and tumor volume before and after treatment in a mouse model.

They selected a rare form of cancer, mesenchymal chondrosarcoma (MCS), which has not been well described and for which there is no effective treatment. The researchers first determined that Nanog and BMI1 stem cell markers were more highly expressed in metastatic tumors compared to primary tumors. "This suggests that expression of the marker plays some role in development of metastasis," Dr. Vasko said.

They then applied various therapies - from VEGF inhibitors such as Avastin to the proteasome inhibitor Velcade - in mice implanted with human MSC, and analyzed the effects on tumors. Some of the treatments seemed to work, because they led to a dramatic decrease in the size of the tumors, Dr. Vasko said. But analysis of stem cell expression before and after treatment revealed that even as some anti-cancer treatments shrank tumors, they increased expression of Nanog and BMI1. "These treatments were not enough to completely inhibit tumor growth, and the cancer stem cell markers were still present," Dr. Vasko said.

Use of the agents Velcade and Docetaxel led to the most significant increase in stem cell markers within the treated tumor, while ifosfamide and Avastin inhibited expression of the markers in this cancer subtype.

"We hypothesize that the tumor escapes from chemotherapy by induction of stem cell marker expression," he said. "The small number of cells that survive the treatment could then generate another tumor that metastasizes."

Dr. Vasko doesn't know how this happens, but theorizes that "dying cells could secrete a lot of factors that induce expression of stem cell markers in other cancer cells. I think they are trying to survive and they use a mechanism from their experience of embryonic life."

If scientists understood the pathways cancer stem cells use to survive treatment or increase their ranks, then therapeutic targets could be developed, Dr. Vasko said. Some novel therapies are already being tested against cancer stem cells, he added.

Source: American Association for Cancer Research
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Old 04-22-2011, 10:15 AM
gdpawel gdpawel is offline
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Default human cancer cell capable of initiating tumor growth in immunodeficient mice

The idea of cancer stem cells is a theory that cancer evolves from normal stem cells that have been mutated and grow out of control. The opposite theory for this is that a normal, differentiated cell has undifferentiated (i.e. lost markers for its differentiated state) and become more stem-cell-like.

This loss of differentiation is termed Epithelium to Mesenchymal Transition (EMT) when it happens in epithelium cells. Again both theories, cancer stem cells and EMT, are being debated but I think it will turn out that both theories may happen to be right under certain situations.

Is the cancer stem cell a mutated stem epithelial cell or a fibroblast stem cell or other? According to a Toronto researchers study, the cancer stem cell is an endothelial stem cell since it had the CD133 marker.

Nature 445, 106-110 (4 January 2007) | doi:10.1038/nature05372

A human colon cancer cell capable of initiating tumour growth in immunodeficient mice

Catherine A. O'Brien (1), Aaron Pollett (2), Steven Gallinger (3) & John E. Dick(1),(4)

1. Division of Cell and Molecular Biology, University Health Network, Toronto, Ontario, M5G 1L7, Canada
2. Department of Pathology and Laboratory Medicine,
3. Center for Cancer Genetics-Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, M5G 1X5, Canada
4. Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario, M5S 1A8, Canada
Correspondence to: John E. Dick1,4 Correspondence and requests for materials should be addressed to J.E.D.

Colon cancer is one of the best-understood neoplasms from a genetic perspective, yet it remains the second most common cause of cancer-related death, indicating that some of its cancer cells are not eradicated by current therapies. What has yet to be established is whether every colon cancer cell possesses the potential to initiate and sustain tumour growth, or whether the tumour is hierarchically organized so that only a subset of cells—cancer stem cells—possess such potential. Here we use renal capsule transplantation in immunodeficient NOD/SCID mice to identify a human colon cancer-initiating cell (CC-IC). Purification experiments established that all CC-ICs were CD133+; the CD133- cells that comprised the majority of the tumour were unable to initiate tumour growth. We calculated by limiting dilution analysis that there was one CC-IC in 5.7 104 unfractionated tumour cells, whereas there was one CC-IC in 262 CD133+ cells, representing >200-fold enrichment. CC-ICs within the CD133+ population were able to maintain themselves as well as differentiate and re-establish tumour heterogeneity upon serial transplantation. The identification of colon cancer stem cells that are distinct from the bulk tumour cells provides strong support for the hierarchical organization of human colon cancer, and their existence suggests that for therapeutic strategies to be effective, they must target the cancer stem cells.

Therapy involving attack of CD133 would have to probably wait since it targets a natural marker. The therapeutic window will probably be small if at all and would no doubt kill your natural adult stem cells unless an antibody could recognize a difference in CD133 between cancerous stem cells and normal stem cells. CD133 as a marker is already being studied to isolate stem cells for transplants in leukemia.

CD133 is the name of the epitope the antibody uses to identify the protein. The protein identified by CD133 is called Prominin-1. Its biological function is not clear as of yet. But it has been implicated in macular degeneration.

Int J Biochem Cell Biol. 2005 Apr;37(4):715-9.

AC133/CD133/Prominin-1.

Shmelkov SV, St Clair R, Lyden D, Rafii S.

Weill Medical College of Cornell University, Department of Genetic Medicine, 1300 York Avenue, New York, NY 10021, USA.

Abstract

Prominin-1, originally found on neuroepithelial stem cells in mice, is a five transmembrane domain cell-surface glycoprotein that localizes to membrane protrusions. Its homologue human Prominin-1 was first isolated from hematopoietic stem cells by a monoclonal antibody recognizing a specific epitope designated as AC133 (CD133). Transcription of Prominin-1 is driven by five tissue-specific alternative promoters resulting in the formation of differentially spliced mRNA isoforms. Prominin-1 is expressed on different types of stem cells, but it is not known if it plays a significant role in key stem cell functional features. Although the biological function of Prominin-1 is not well understood, the AC133 epitope currently serves as a useful marker for the isolation of hematopoietic and endothelial progenitor cells.

PMID:15694831

[url]http://www.nature.com/nature/journal/v445/n7123/abs/nature05372.html
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Old 04-22-2011, 10:20 AM
gdpawel gdpawel is offline
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Default The Debate About Cancer Metastasis

A team of scientists, led by researchers at the University of California, San Diego School of Medicine, has shown for the first time how cancer cells control the ON/OFF switch of a program used by developing embryos to effectively metastasize in vivo, breaking free and spreading to other parts of the body, where they can proliferate and grow into secondary tumors.

The findings are published in the December 11, 2012 issue of the journal Cancer Cell.

In 90 percent of cancer deaths, it is the spreading of cancer, known as metastasis, which ultimately kills the patient by impacting ever-more tissues and functions until the body fails. Ten years ago, a French cancer researcher named Jean Paul Thiery hypothesized that tumor cells metastasized by exploiting a developmental process known as epithelial-to-mesenchymal transition or EMT.

EMT is seen in developing embryos whose cells transform from stationary epithelial cells into more mobile mesenchymal cells, the latter able to migrate to new locations and create new types of tissue and organs. Thiery proposed that cancer cells also switch "ON" EMT, temporarily changing attributes so that they can detach from primary tumors, enter the bloodstream and seed new tumors elsewhere. After arriving at a new location, the cancer cells then turn "OFF" the EMT program and grow into carcinoma metastases or tumors.

Thiery's hypothesis was controversial because researchers haven't been able to find supporting evidential proof in vivo. "Although this model was proposed in 2002, there have been no experiments done to attest to it in a spontaneous tumor model," said Jing Yang, PhD, associate professor of pharmacology and pediatrics and senior author of the Cancer Cell paper. "Our new study provides an in vivo demonstration of the reversible EMT in metastasis and helps to resolve the controversy on this leading theory in metastasis."

Using a mouse squamous cell carcinoma model, Jeff Tsai, PhD, a postdoctoral fellow in Yang's lab and first author of the study, with help from collaborators at the Whitehead Institute for Biomedical Research in Cambridge, MA and The Sanford-Burnham Medical Research Institute in La Jolla, showed that activation of an EMT-inducing gene called Twist1 is sufficient to turn "ON" the EMT switch and promote carcinoma cells to disseminate into blood circulation. Equally importantly, the researchers found that turning "OFF" the EMT switch at distant sites is essential for disseminated tumor cells to proliferate and form metastases. Their findings indicate that reversible EMT likely represents a key driving force in human carcinoma metastasis.

"There are many similarities between developmental EMT and EMT in metastasis," Yang said. "Both processes seem to use the same cellular machineries and signaling pathways to activate the EMT program. During embryogenesis, the EMT program tends to be more permanent and epithelial cells commit to a mesenchymal fate. Our study shows that carcinoma cells need a reversible EMT to achieve efficient metastasis. It suggests that EMT reversion could be a critical step to wake up tumor cells from dormancy, a phenomenon in which cancer patients develop metastasis years after the initial primary tumor diagnosis and removal."

It's not entirely known how Twist1 becomes active in primary tumors, though previous studies have pointed to factors like hypoxia and inflammation in the tumor microenvironment. Researchers do not know exactly how Twist1 is "turned off at distant organs." Yang said these are subjects of current experiments.

More broadly, the published findings suggest that more research is needed to determine how to target EMT to combat cancer metastasis. Several pharmaceuticals and research institutes are already pursuing EMT inhibitors as possible cancer treatments.

"Since reversion of EMT promotes colonization and growth of metastases, this study actually cautions that therapies inhibiting EMT could be counterproductive in preventing distant metastases when patients already present circulating tumor cells. Instead, blocking EMT reversion may prevent dormant tumor cells from establishing metastases."
References:

Co-authors of the paper include Sandra Chau, Department of Pharmacology, UCSD School of Medicine; Joana Liu Donaher, Whitehead Institute for Biomedical Research; and Danielle A. Murphy, The Sanford-Burnham Medical Research Institute.

Funding came, in part, from the American Cancer Society, the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, California Breast Cancer Research program, University of California Cancer Research Coordinating Committee, UCSD Cancer Center Training Program in Drug Development and UCSD Cancer Center Specialized Support Grant.

University of California - San Diego. "The Debate About Cancer Metastasis: Study Helps Resolve The Dilemma." Medical News Today. MediLexicon, Intl., 2 Dec. 2012.
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Last edited by gdpawel : 12-03-2012 at 12:42 AM. Reason: spelling errors
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