A Beacon to Guide Cancer Surgery : A modified virus makes cancer cells fluoresce to better identify tumors.

Removing tumors from cancer patients always brings uncertainty. Surgeons fear that cells they don't spot and remove might re-emerge. Researchers have been looking for ways to make cancer cells visible so that none is left behind. Some of these strategies rely on injecting fluorescent probes or nanoparticles like quantum dots that will attach to the surface of cancer cells. Now a company is working on technology that makes cancer cells fluoresce from the inside out. The approach, developed by San Diego-based company AntiCancer, in partnership with scientists at Okayama University in Japan, uses a virus that infects cancer cells to integrate a fluorescence gene into tumors. The result is cancer that permanently glows, which the company hopes would allow surgeons to remove tumors with more precision and to monitor any cancer that re-emerges.

To make cancer cells fluoresce, the researchers used a virus called OBP-401, a modified cold virus that can enter all cells but will only replicate in those that have activated telomerase, an enzyme that is expressed in cancer cells and allows them to divide indefinitely. Normally a cell can only divide a limited number of times before dying, because at every division it loses part of its telomeres, caps of DNA at the ends of chromosomes that keep the genome stable. But cancer cells can keep dividing because telomerase replaces the telomeres every time the cell divides.

The OBP-401 virus had been developed as an anticancer therapy. Here, the researchers modified the virus to carry green fluorescent protein (GFP), a protein derived from jellyfish that fluoresces in blue light. When the virus is injected into an animal, the gene becomes active in cells that express telomerase. Robert Hoffman, president of AntiCancer and a surgeon at the University of California, San Diego, explains that GFP is permanently integrated into the genome of cancer cells, making this technology fundamentally different from approaches that rely on attaching a fluorescent particle to a protein on the surface of cancer cells. Hoffman believes that by creating a genetic marker, the approach "takes advantage of the tumor biology more effectively."

In a recent paper in the Proceedings of the National Academy of Sciences, Hoffman's team used the virus to illuminate tumors in mice that were scattered throughout the body. During surgery to remove the tumors, they could visualize them by exposing tumors to light of the proper wavelength and looking through a filter that picks up GFP fluorescence. "In principle it should pick up any cancer cell," says Hoffman. The team has not yet reached single-cell precision, but they are able to see and remove small cancerous areas that would otherwise be invisible.

Although new cancers that form after the virus is delivered would not be fluorescent, Hoffman says that any of the original cancer that began to grow again should still express GFP, allowing clinicians the opportunity to monitor the results of the surgery over time.

Hisataka Kobayashi, a scientist in the molecular imaging program at the National Cancer Institute, says the advantages of this method are that it very specifically targets cancer cells and makes it possible to monitor the cancer over time. The method also allows for flexibility; for instance, a gene that would cause the cancer cells to kill themselves could be added to the virus along with GFP, pairing imaging with treatment.

Kobayashi says that one of the key questions of the technology is safety. Giving patients a virus carrying a gene for imaging is very similar to giving them a gene to correct a disease, he says, and consequently "all the problems with gene therapy apply to this method." Many gene therapy approaches have been stalled because of immune reactions to the treatment. However, Lily Wu, a scientist at the University of California, Los Angeles, who develops cancer therapies, points out that similar gene therapy treatments for cancer have so far been found safe in clinical trials, whereas safety "is still not determined for other synthetic vectors such as quantum dots." Wu believes that this method offers several advantages over other ways of labeling tumors but says that it will require a more thorough quantitative analysis to demonstrate its effectiveness.

Hoffman says AntiCancer hopes to complete further safety testing that will allow it to bring the technology into clinical trials. Although fluorescence in mice can be visualized throughout the body, in humans the task will be more difficult, because the light scatters easily and doesn't penetrate very far into tissues. For that reason, the researchers envision this technique being used during surgery where the tumor can be seen directly.

Cancer Tracker : Implantable device monitors tumors

Surgical removal of a tissue sample is now the standard for diagnosing cancer. Such procedures, known as biopsies, are accurate but offer only a snapshot of the tumor at a single moment in time. Monitoring a tumor for weeks or months after the biopsy would be much more valuable, says Michael Cima, an MIT professor of materials science and engineering. He has developed the first implantable device that can do just that.

"What this does is basically take the lab and put it in the patient," says Cima, who is also an investigator at the David H. Koch Institute for Integrative Cancer Research at MIT.

The device, which could be implanted at the time of a biopsy, would provide up-to-the-minute information about a tumor--whether it's growing or shrinking, whether chemotherapy drugs have reached it, and whether it has metastasized or is about to do so. In a paper published in the journal Biosensors & Bioelectronics, Cima and his colleagues recently reported that their device successfully tracked for one month a chemical produced by human tumors growing in mice.

The cylindrical, five-­millimeter implant contains magnetic nanoparticles coated with antibodies specific to target molecules such as hormones produced by tumor cells. When target molecules enter the implant through a semipermeable membrane, they bind to the particles and cause them to clump together. Magnetic resonance imaging can detect the clumps--and track whether they're getting bigger or smaller.

Implants that can test for pH levels, which reveal a tumor's metabolism and its response to chemotherapy, could be commercially available in a few years, Cima says. These would be followed by devices that test for complex chemicals such as hormones and drugs.

Unlike biopsies, such technologies could alert doctors that the original tumor has started shedding cancer cells before those cells can form new tumors. "This is one of the tools we're going to need if we're going to turn cancer from a death sentence to a manageable disease," Cima says.

Release link : http://www.technologyreview.com/article/23166/

New treatments offer better survival and fresh challenges in colorectal cancer

Colorectal cancer (CRC) is the second leading cause of cancer-related death in the Western world. Fortunately physicians today have an abundance of drug therapies available to improve survival length for more advanced cancer patients. Now the discovery of genetic biomarkers relevant to CRC means that targeted personalised medication is increasingly common.

CRC affects approximately 150,000 patients and leads to over 52,000 deaths every year in the US alone. In the early stages, CRC can often be cured by surgery. It is in the more advanced, palliative cases that the abundance of drug therapies comes into play, according to Mayo Clinic oncologist Axel Grothey, MD. In his paper Medical treatment of advanced colorectal cancer in 2009 published this week in the journal Therapeutic Advances in Medical Oncology, Grothey details the interplay of therapies currently on offer.

Oncologists now integrate conventional cytotoxic agents oxaliplatin and irinotecan (which directly fight tumour cells) with treatments such as bevacizumab and epidermal growth factor receptor (EGFR) antibodies, cetuximab and panitumumab, as novel targeted agents into standard medical therapy. The result is that median overall survival in metastatic CRC now exceeds two years for the first time.

For decades, standard first-line therapy consisted of the drugs fluorouracil (5-FU) plus leucovorin, which helped just a fifth of patients to survive a median of one year. In the late 1990s and early 2000s, the addition of oxaliplatin and irinotecan to the backbone of 5-FU and leucovorin led to dramatic improvement in median survival to nearly 24 months. Most recently, biologic agents such as bevacizumab, cetuximab, and panitumumab, have yielded even better results for many patients.

"It cannot be overemphasized that these significant improvements in outcome of patients with CRC are closely linked to the number of active drugs available to treat this disease," says Grothey. However, he adds that this treatment abundance also provides oncologists with specific challenges for managing palliative medical therapy in advanced CRC, particularly when they use targeted agents.

One targeted agent is bevacizumab (a monoclonal antibody developed by Genentech under the trade name Avastin), which inhibits vascular endothelial growth factor (VEGF), a natural protein that the tumour uses to grow new blood vessels (angiogenesis). Bevacizumab was the first angiogenesis inhibitor available in the US, and has become established as a standard component of first-line chemotherapy.

To date, no researchers have identified a predictive marker for bevacizumab's activity in metastatic CRC. According to Grothey, key questions surrounding bevacizumab's use in the palliative setting are whether it provides clinical benefit beyond the stage of tumour progression, and which patient group is at higher risk for bevacizumab-related toxicities. Data from a large observational, non-randomised cohort study by Grothey and colleagues in 2008 suggests that patients may benefit from continued use of bevacizumab beyond tumour progression . Randomised phase III clinical trials are currently underway in Europe and the US to determine whether this should become standard practice.

Anti-epidermal growth factor receptor (EGFR) antibodies cetuximab (Erbitux) and panitumumab (Vectibix) are both targeted monoclonal antibody treatments that have demonstrated efficacy both in combination with chemotherapy or, in contrast to bevacizumab, used alone. Trials on unselected patient groups show limited results. But clinical trials and translational studies now indicate that those patients with advanced CRC must have a tumour with specific genetic mutations (wild type KRAS and wild-type BRAF) for EGFR antibodies to be effective. Testing for BRAF and KRAS mutations now excludes about half of patients with CRC from an ineffective, but potentially harmful (and expensive) therapy with cetuximab and panitumumab.

Clinical decisions regarding whether the goal is to rapidly shrink a tumour, whether to attempt curative surgery or to rapidly boost short-term quality of life or survival, or instead aiming for a longer-term quality of life with minimum side effects will determine the physician's choice of approach.

"Although biomarkers will provide some guidance on which agents are potentially useful in a given setting, in particular with regard to the use of EGFR antibodies, the importance of individualizing therapy based on clinical parameters cannot be overemphasized," says Grothey.

Targeted agents have become an integral part of medical therapy for advanced CRC. The next challenge for oncologists is to develop a rationale and biomarker-based treatment algorithm to use all potentially active agents as individualized therapy.

Fine-tuning an anti-cancer drug

Learning from evolution

Cancer remains a deadly threat despite the best efforts of science. New hopes were raised a few years ago with the discovery that the uncontrolled growth of cancer cells could be thwarted by blocking the action of proteasomes. Biochemists at the Technische Universitaet Muenchen (TUM) have illuminated a reaction pathway that does just that, in collaboration with researchers from Nereus Pharmaceuticals, based in San Diego, California. In the current issue of the Journal of Medicinal Chemistry, they report insights that could potentially lead to the development of custom-tailored anti-cancer drugs.

What makes cancer cells so dangerous is that they proliferate much more rapidly than other cells. An important contribution to this capability is made by a particular group of proteins, the so-called kinases. And it's against the kinases that many cancer drugs in development today take aim. Another promising approach came to light a few years ago with the discovery that the proliferation of cancer cells could also be arrested through proteasome inhibition. Yet the first drug to employ this strategy caused a number of severe side-effects. Despite that, the drug is expected to generate revenues of more than a billion U.S. dollars this year.

In the search for alternatives, San Diego-based Nereus Pharmaceuticals homed in on a species of marine bacteria known as Salinispora tropica. These bacteria produce a small molecule that kills affected cells by disabling proteasomes, which serve as their waste processing plants. "In the life cycle of a cell, proteins are always being built up that will need to be demolished after they have done their work," explains TUM Professor Michael Groll, leader of the research team in Munich. "If this breakdown is blocked, the cells choke on their own waste."

After promising preclinical trials, the bacteria-produced Salinosporamide A (NPI-0052; Sal-A) has advanced into human clinical trials. "Over millions of years, the bacteria developed this substance into a perfect weapon," says Dr. Barbara Potts, vice president for chemical and oncological development at Nereus Pharmaceuticals. The ideal cancer drug would kill only cancer cells, while doing the least harm possible to healthy cells. The researchers took a closer look at the pathway for this reaction, in the hope that they might better understand the mechanism and the best approach to future generation analogues.

The research team of Barbara Potts and Michael Groll managed to produce crystals of proteasomes blocked by Salinosporamide A and determined, through X-ray crystallography, the precise arrangement of the atoms. It became clear why the bacterial poison is so effective: The molecule fits an opening in the proteasome like a key, and locks it up. A subsequent reaction transforms the molecule to a complex that can no longer be detached, in effect breaking off the key in the lock. Vital processes come to a halt.

Halogen-hydrocarbons are favored in industrial chemistry, because the halogen atom can be easily separated from other groups. It's just this trick that the Salinispora tropica bacterium employs in the case of Salinosporamide A. It uses a chloride as its so-called "leaving group" to trigger an internal reaction forming a ring-like bond. If the ring is closed, the lock is jammed.

The researchers next produced variants of Salinosporamide A and once again succeeded in crystallizing them and using X-ray techniques for structural analysis. By replacing the chlorine atom with fluorine, they were able to observe the progress of the reaction. After the key had been stuck in the lock for one hour of reaction time, the biochemists were still able to pull it out again. A few hours later, the fluorine was split off, and the lock was blocked.

"After the millions of years that have gone into the evolutionary development of this method in bacteria, it's unlikely that a better way to block the proteasome is even possible," Groll says. "Now that we know how the best possible reaction proceeds, we can alter it in targeted ways with the aim of developing tailored, effective proteasomal drugs that will have improved safety and efficacy."

Reference : http://www.eurekalert.org/pub_releases/2009-08/tum-faa081809.php

New DNA Test Uses Nanotechnology to Find Early Signs of Cancer

Using tiny crystals called quantum dots, Johns Hopkins researchers have developed a highly sensitive test to look for DNA attachments that often are early warning signs of cancer. This test, which detects both the presence and the quantity of certain DNA changes, could alert people who are at risk of developing the disease and could tell doctors how well a particular cancer treatment is working.

The new test was reported in a paper called “MS-qFRET: a quantum dot-based method for analysis of DNA methylation,” published in the August issue of the journal Genome Research. The work also was presented at a conference of the American Association of Cancer Research.

“If it leads to early detection of cancer, this test could have huge clinical implications,” said Jeff Tza-Huei Wang, an associate professor of mechanical engineering whose lab team played a leading role in developing the technique. “Doctors usually have the greatest success in fighting cancer if they can treat it in its early stage.”

Wang and his students developed the test over the past three years with colleagues at the Johns Hopkins Kimmel Cancer Center. Stephen B. Baylin, deputy director of the center and a co-author of the Genome Research study, said the test represents “a very promising platform” to help doctors detect cancer at an early stage and to predict which patients are most likely to benefit from a particular therapy.

The recent study, which included the detection of DNA markers in the sputum from lung cancer patients, was designed to show that the technology was sound. Compared to current methods, the test appeared to be more sensitive and delivered results more quickly, the researchers said. “The technique looks terrific, but it still needs to be tested in many real-world scenarios,” Baylin said. “Some of these studies are already under way here. If we continue to see exciting progress, this testing method could easily be in wide use within the next five years.”

The target of this test is a biochemical change called DNA methylation, which occurs when a chemical group called methyl attaches itself to cytosine, one of the four nucleotides or base building blocks of DNA. When methylation occurs at critical gene locations, it can halt the release of proteins that suppress tumors. When this occurs, it is easier for cancer cells to form and

multiply. As a result, a person whose DNA has this abnormal gene DNA methylation may have a higher risk of developing cancer. Furthermore, these methylation changes appear to be an early event that precedes the appearance of genetic mutations, another precursor to cancer.

To detect this DNA methylation, the Johns Hopkins team found a way to single out the troublesome DNA strands that have a methyl group attached to them. Through a chemical process called bisulfite conversion, all segments that lack a methyl group are transformed into another nucleotide.

Then, another lab process is used to make additional copies of the remaining target DNA strands that are linked to cancer. During this process, two molecules are attached to opposite ends of each DNA strand. One of these molecules is a protein called biotin. The other is a fluorescent dye. These partner molecules are attached to help researchers detect and count the DNA strands that are associated with cancer.

To do this, these customized DNA strands are mixed with quantum dots, which are crystals of semiconductor material whose sizes are in the range of only few nanometers across. (A nanometer is one-billionth of a meter, far too small to see with the naked eye.).These dots are usually employed in electronic circuitry, but they have recently proved to be helpful in biological applications as well. Quantum dots are useful because they possess an important property: They easily transfer energy. When light shines on a quantum dot, the dot quickly passes this energy along to a nearby molecule, which can use the energy to emit a fluorescent glow. This behavior makes the cancer-related DNA strands light up and identify themselves.

In the Johns Hopkins cancer test, the quantum dots have been coated with a chemical that is attracted to biotin–one of the two molecules that were attached to the DNA strands. As a result, up to 60 of the targeted DNA strands can stick themselves to a single quantum dot, like arms extending from an octopus. Then, an ultraviolet light or a blue laser is aimed at the sample. The quantum dots grab this energy and immediately transfer it to the fluorescent dyes that were attached earlier to the targeted DNA strands. These dye molecules use the energy to light up.

These signals, also called fluorescence, can be detected by a machine called a spectrophotometer. By analyzing these signals, the researchers can discover not only whether the sample contains the cancer-linked DNA but how much of the DNA methylation is present. Larger amounts can be associated with a higher cancer risk.

“This kind of information could allow a patient with positive methylation to undergo more frequent cancer screening tests. This method could replace the traditionally more invasive ways for obtaining patient samples with a simple blood test,” said Vasudev J. Bailey, a biomedical engineering doctoral student from Bangalore, India, who was one of the two lead authors on the Genome Research paper. “It’s also important because these test results could possibly help a doctor determine whether a particular cancer treatment is working. It could pave the way for personalized chemotherapy.”

In addition, because different types of cancer exhibit distinctive genetic markers, the researchers say the test should be able to identify which specific cancer a patient may be at risk of developing. Markers for lung cancer, for example, are different from markers for leukemia.
The other lead author of the Genome Research paper was Hariharan Easwaran, a cancer biology research fellow in the Johns Hopkins School of Medicine. Along with Wang and Baylin, the other co-authors were Yi Zhang, a biomedical engineering doctoral student at Johns Hopkins; Elizabeth Griffiths, an oncology clinical fellow in the School of Medicine; Steven A. Belinsky, of the Lovelace Respiratory Research Institute in Albuquerque, N.M.; James G. Herman, a professor of cancer biology in the School of Medicine; and Hetty E. Carraway, an assistant professor of oncology in the School of Medicine.

Johns Hopkins Technology Transfer staff members have applied for international patent protection covering the testing technique and are in talks with a biotechnology company that has expressed interest in licensing the application.

The research was supported by grants from the National Cancer Institute, the National Science Foundation, the Hodson Foundation and the Flight Attendant Medical Research Institute.

Reference :

http://releases.jhu.edu/2009/08/17/new-dna-test-uses-nanotechnology-to-find-early-signs-of-cancer/

Neutralize tumor growth in embryonic stem cell therapy

Researchers at the Hebrew University of Jerusalem have discovered a method to potentially eliminate the tumor-risk factor in utilizing human embryonic stem cells. Their work paves the way for further progress in the promising field of stem cell therapy.

Human embryonic stem cells are theoretically capable of differentiation to all cells of the mature human body (and are hence defined as "pluripotent"). This ability, along with the ability to remain undifferentiated indefinitely in culture, make regenerative medicine using human embryonic stem cells a potentially unprecedented tool for the treatment of various diseases, including diabetes, Parkinson’s disease and heart failure.

A major drawback to the use of stem cells, however, remains the demonstrated tendency of such cells to grow into a specific kind of tumor, called teratoma, when they are implanted in laboratory experiments into mice. It is assumed that this tumorigenic feature will be manifested upon transplantation to human patients as well. The development of tumors from embryonic stem cells is especially puzzling given that these cells start out as completely normal cells.

A team of researchers at the Stem Cell Unit in the Department of Genetics at the Silberman Institute of Life Sciences at the Hebrew University has been working on various approaches to deal with this problem.

In their latest project, the researchers analyzed the genetic basis of tumor formation from human embryonic stem cells and identified a key gene that is involved in this unique tumorigenicity. This gene, called survivin, is expressed in most cancers and in early stage embryos, but it is almost completely absent from mature normal tissues.

The survivin gene is especially highly expressed in undifferentiated human embryonic stem cells and in their derived tumors. By neutralizing the activity of survivin in the undifferentiated cells as well as in the tumors, the researchers were able to initiate programmed cell death (apoptosis) in those cells.

This inhibition of this gene just before or after transplantation of the cells could minimize the chances of tumor formation, but the researchers caution that a combination of strategies may be needed to address the major safety concerns regarding tumor formation by human embryonic stem cells.

A report on this latest project of the Hebrew University stem cell researchers appeared in the online edition of Nature Biotechnology. The researchers are headed by Nissim Benvenisty, who is the Herbert Cohn Professor of Cancer Research, and Ph.D. student Barak Blum. Others working on the project are Ph.D. student Ori Bar-Nur and laboratory technician Tamar Golan-Lev.

Release link :

http://hunews.huji.ac.il/articles.asp?cat=6&artID=975

I think what i beleive

Cancer is a dangerous and harmful dieseas in the world.One will understand what the impact of cancer in ones family and his/her personal life.Now a days cancer is becoming a easy treated in European /American countries.But In Bangladesh or in the Asia cancer is becomes most dangerous.

I feel what the thinking of cancer patients.My mother is a cancer patient.She thinks in her way that me spend all the money for her!!! But alas ! she is my mother .I cant think without her.I cant believe myself with out my mother.I love her.I do not think that she is not with me and I am expending my money in some bars/clubs.

I always try to feel her pain.When I took her in the hospital for chemotherapy,I don't leave her then.I sit beside her and try to keep pace with her as it is my pain.

I will try to give you all the updated research,news of cancer through this blog.

Tumor mutations can predict chemo success

Genetic profiling of tumors could have 'immediate impact' on treating cancer, study shows:

New work by MIT cancer biologists shows that the interplay between two key genes that are often defective in tumors determines how cancer cells respond to chemotherapy.

The findings should have an immediate impact on cancer treatment, say Michael Hemann and Michael Yaffe, the two MIT biology professors who led the study. The work could help doctors predict what types of chemotherapy will be effective in a particular tumor, which would help tailor treatments to each patient.

"This isn't something that's going to take five years to do," says Yaffe, who, along with Hemann is a member of the David H. Koch Institute for Integrative Cancer Research at MIT. "You could begin doing this tomorrow."

The work could also guide the development of new chemotherapy drugs targeted to tumors with specific genetic mutations.

Hemann, Yaffe, and their colleagues report their results in the Aug. 15 issue of the journal Genes and Development. Koch Institute postdoctoral associates Hai Jiang and H. Christian Reinhardt are lead authors of the study, which the researchers say is one of the first examples of how genetic profiling of tumors can translate to improvements in patient treatment.

"There's a huge amount of genetic information available, but it hasn't made its way into clinical practice yet," says Hemann.

Genetic mystery

The research team focused on two proteins often involved in cancer, p53 and ATM. One of the first tumor suppressor genes discovered, p53 serves a watchdog function over a cell's genome, activating repair systems when DNA is damaged and initiating cell death if the damage is irreparable.

ATM is also involved in controlling the cell's response to DNA damage and is known to help regulate p53.

Mutations in p53, ATM or both are often seen in tumor cells. (ATM mutations occur in about 15 percent of cancers, and p53 is mutated in about 30 percent.)

Scientists have long tried to pin down a relationship between mutations in these genes and the effectiveness of DNA-damaging chemotherapy agents, but published studies have produced conflicting reports.

"It's been unclear whether the loss of p53 made tumors easier to treat or harder to treat. You could find examples of either case in the clinical literature," says Yaffe, adding that the same holds true for ATM.

The new study, conducted with human cancer cells, shows that tumors in which both p53 and ATM are defective are highly susceptible to chemotherapy agents that damage DNA. The double mutation prevents tumor cells from being able to repair DNA, and the cells commit suicide.

However, in cells where p53 is mutated but ATM is not, that type of chemotherapy is less effective. Remarkably, tumors where ATM is mutated but p53 is not turn out to be highly resistant to those types of chemotherapy.

With this new information, doctors could choose chemotherapy treatments based on the status of the p53 and ATM genes in a patient's tumor. Traditional DNA-damaging chemotherapy would be a good option for patients with both p53 and ATM mutations, but not for those with normal p53 and mutated ATM.

For patients who have normal ATM and mutated p53, other options might be better: New drugs that inhibit ATM, now in clinical trials, could improve tumors' susceptibility to chemotherapy in those patients.

The study shows the importance of studying cancer genes as a network, rather than trying to predict outcomes based on the status of single genes such as p53, says Robert Abraham, director of the cancer drug discovery program at Wyeth Pharmaceuticals.

Once ATM inhibitors are approved, "understanding the combined status of ATM and p53 should allow physicians to identify patients who should be treated with ATM inhibitors and chemotherapy and those for whom such a therapy could potentially be harmful," Abraham says.

In patients with normal p53 and mutated ATM, doctors could use drugs that target alternative DNA repair pathways. In their Genes and Development paper, the MIT researchers showed that treating such tumors with a drug that targets DNA-PK, another protein involved in DNA repair, renders them vulnerable to chemotherapy.

The MIT researchers collaborated with scientists from the Centre for Genotoxic Stress Research in Denmark, Helsinki University Central Hospital in Finland, and Uppsala University Hospital in Sweden.

The research was funded by the National Institutes of Health, the David H. Koch Fund, the Deutsche Forschungsgemeinschaft, the Deutsche Nierenstiftung, the Danish Cancer Society, the European Community, the Czech Ministry of Education and the Helsinki University Central Hospital Research Fund.

About the researcher :

1. Michael T. Hemann

• Latham Family Career Development Assistant Professor of Biology
• Ph.D. 2001, Johns Hopkins Univ.
• Room E17-128B
• Phone: 617-324-1964
• Email: hemann@mit.edu
• 
  
• Assistant: Ryan Hayman,
• (617) 253-0796,
• rhayman@mit.edu

2. Michael B. Yaffe

• Associate Professor, Biology
• Ph.D. 1987, Case Western Reserve University
• M.D. 1989, Case Western Reserve University
• Room E18-580
• Phone: (617) 452-2442
• Email: myaffe@mit.edu
• Assistant: Elena Garza
• (617) 452-2103
• ecgarza@mit.edu

Reference : http://web.mit.edu/newsoffice/2009/cancer-personal-0806.html