Cancer blog page

February 18, 2010, 9:50 PM CT

Natural Compound that Inhibits Cancer Cell Migration

Investigators at Sanford-Burnham Medical Research Institute (Sanford-Burnham, formerly Burnham Institute for Medical Research) led by Kristiina Vuori, M.D., Ph.D., have discovered that the natural compound sceptrin, which is found in marine sponges, reduces cancer cell motility (movement) and has very low toxicity. Metastasis is one of the deadliest aspects of cancer, so restricting aberrant cell movement is an important step towards advancing therapys. The research was published online in ACS Chemical Biology, in collaboration with Phil S. Baran, Ph.D., of The Scripps Research Institute.

The team tested sceptrin in multiple tumor cell types, including cervical, breast and lung cancers. Sceptrin restricted motility in all cell lines. Further tests showed the compound works by limiting the cells' ability to contract, a critical function for cell motility. The scientists also observed that sceptrin synthesized in the laboratory was just as effective at combating motility as the naturally-derived compound.

"Given the recently achieved synthesis of sceptrin in multi-gram quantities by the Baran laboratory, sceptrin could prove to be an attractive lead molecule for further preclinical testing and development for therapeutic purposes," said Dr. Vuori. "It may also prove to be a useful research tool in order to elucidate the mechanisms involved in cell motility"......... Posted by: Jesmi24      Read more         Source

February 10, 2010, 8:04 AM CT

How to kill pediatric brain tumors

Scientists at Washington University School of Medicine in St. Louis have shown once again that "ready, fire, aim," nonsensical though it may sound, can be an essential approach to research.

The researchers robotically "fired" 2,000 compounds into culture plates containing tumor cells to see if the compounds had any effect. When the robotic screener found one substance had scored a hit by inhibiting growth of the tumor cells in its plate, scientists analyzed what that compound acted against. Follow-up studies showed that the drug slowed tumor growth in mice by inhibiting the function of a protein called STAT3.

As a result, scientists now have a previously unrecognized target, STAT3, at which they can "aim" new drugs for the therapy of cancer in neurofibromatosis-1 (NF1), a genetic condition that causes increased risk of non-malignant and cancerous brain tumors.

"We were excited to find that the slowed tumor growth we observed following therapy resulted from increased tumor cell death - an effect we hadn't seen before when we blocked other NF1 growth control molecules," says senior author David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology. "Now we can identify the genes that STAT3 influences to fine-tune our therapys and ensure that we kill cancer cells with minimal harm to normal cells"......... Posted by: Jesmi24      Read more         Source

February 3, 2010, 7:58 AM CT

Community Hospitals as Safe Surgical Option

Low-risk patients who require certain cancer surgeries can have the procedures performed with low operative mortality rates at community hospitals, as per a newly released study.

The research showed that for 13 different kinds of cancer surgeries such as gastric and colon, younger patients with few pre-existing illnesses survived operations at community hospitals at a similar rate as at cancer centers.

But patients who are considered high risk or who need complicated cancer surgeries have a higher survival rate at specialized cancer centers. Patients with pancreatic and esophageal cancer, among the most complex cancer surgeries, are twice as likely to survive an operation at a specialized cancer center. The study defined these centers as those designated as Comprehensive Cancer Centers by the National Cancer Institute and those that have the highest volume of specific cancer surgeries.

The study from Northwestern's Feinberg School of Medicine and the American College of Surgeons will be published in a future issue of the Annals of Surgery and is accessible via its Web site. The study measured the death rates (known according toioperative mortality) after surgery.

Main author Karl Bilimoria, M.D., surgery resident at the Feinberg School and a research fellow at the American College of Surgeons, noted that the study does not look at long-term survival after surgery or factors that affect long-term outcomes, such as whether surgery removed all of the cancer......... Posted by: Jesmi24      Read more         Source

February 1, 2010, 8:09 AM CT

Quality radiation therapy

The American Association of Physicists in Medicine (AAPM) has issued a statement today in the wake of several recent articles in the New York Times yesterday and earlier in the week that discuss many rare but tragic events in the last decade involving people undergoing radiation treatment.

While it does not specifically comment on the details of these events, the statement acknowledges their gravity. It reads in part: "The AAPM and its members deeply regret that these events have occurred, and we continue to work hard to reduce the likelihood of similar events in the future." The full statement appears at: http://www.aapm.org/publicgeneral/QualityRadiationTherapy.asp.

Today's statement also seeks to reassure the public on the safety of radiation treatment, which is safely and effectively used to treat hundreds of thousands of people with cancer and other diseases every year in the United States. Medical physicists in hospitals and clinics across the United States are board-certified professionals who play a key role in assuring quality during these therapys because they are directly responsible for overseeing the complex technical equipment used.

"The primary day-to-day responsibility of our members is to safeguard the welfare of people undergoing radiation treatment," says AAPM President Michael G. Herman, Ph.D. FAAPM, FACMP. "While adverse events during such therapys are very rare, the recent articles serve as a poignant reminder that they still occur, and like all medical professionals, we are deeply saddened by the stories of human tragedy when they do"......... Posted by: Jesmi24      Read more         Source

February 1, 2010, 7:39 AM CT

Assessing risks associated with low-dose radiation

There remains a lack of consensus amongst the medical and scientific communities about any cancer risk from low level radiation, especially low-dose radiation delivered from computed tomography (CT) scans. However, the study of epigenetics may play a role in determining whether or not future trends of diseases can in fact be associated with utilization of CT, as per an article in the recent issue of the Journal of the American College of Radiology (JACR).

The term epigenetics refers to changes in the phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying DNA sequence. These changes may remain through cell divisions for the remainder of the cell's life and may also last for multiple generations.

"Radiation safety is, without a doubt, a large concern for practicing radiologists today," said Shella Farooki, MD, author of the article and radiologist and director of research for Columbus Radiology Corp in Columbus, OH. "However, the current focus does not account for the possibility of harm to future generations from radiation delivered today. I think that it is equally, if not more important, to consider potential harm to the patient's offspring and their offspring's offspring," she said.

"The effects of ionizing radiation have been demonstrated in neighboring cells (non-targeted radiation), known as the bystander effect. In addition, ionizing radiation effects have been shown to span generations, resulting in heritable defects in mice. However, we need to bridge the gap between understanding the epigenome functionality and radiation exposure before assuming anything," said Farooki......... Posted by: Jesmi24      Read more         Source

January 28, 2010, 7:54 AM CT

Targeting stem cells to fight ovarian cancer

Eliminating cancer stem cells (CSCs) within a tumor could hold the key to successful therapys for ovary cancer, which has been notoriously difficult to detect and treat, as per new findings published this week in the journal Oncogene by Yale School of Medicine researchers.

"We observed that stopping the expression of two genesLin28 and Oct4reduces ovary cancer cell growth and survival," said Yingqun Huang, M.D., assistant professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine.

Ovary cancer has been challenging to treat because it tends to recur frequently and develop resistance to therapy. The poor outcome for women with ovary cancer has been linked to subtle and nonspecific symptomsearning it the moniker the "disease that whispers."

"This recurrence and drug resistance appears to be due to the presence of CSCs within the tumors that have the capacity to reproduce and to differentiate into non-CSC tumor cells that repopulate the tumor mass," said Huang, who is a member of Yale Stem Cell Center and Yale Cancer Center. "Eliminating these CSCs appears to be key to successful therapys".

While in the process of studying the functions of stem cell proteins in human embryonic stem cells, Huang and her colleagues unexpectedly discovered that a sub-population of ovary cancer cells express stem cell proteins Lin28 and Oct4. They also observed that the two proteins appear to act together in ovary cancer tissue cells to produce more advanced tumors. Inhibiting their combined expression led to a significant decrease in the growth and survival of cancer cells. A larger-scale ovary cancer study is currently underway to confirm the significance of the findings......... Posted by: Jesmi24      Read more         Source

January 25, 2010, 8:11 AM CT

Reversing Cancer Cell Metabolism And Tumor Growth

A team of researchers led by Professor Adrian Krainer, Ph.D., of Cold Spring Harbor Laboratory has discovered molecular factors in cancer cells that boost the production of an enzyme that helps alter the cells' glucose metabolism. The altered metabolic state, called the Warburg effect, promotes extremely rapid cell proliferation and tumor growth.

Discovered eighty years ago by Nobel Prize-winning scientist Otto Warburg, this altered metabolism in cancer cells is most critically mediated by a protein called PK-M2 (pyruvate kinase M2). This is one of two versions - or isoforms - of the enzyme pyruvate kinase, whose other isoform, PK-M1, is harmless.

As per a research findings published online ahead of print in the Proceedings of the National Academy of Sciences, Krainer and his colleagues report their discovery of three factors that contribute to high levels of PK-M2 in cancer cells, in part by suppressing production of PK-M1.

"These findings suggest a new way in which cancer's altered glucose metabolism might be targeted for therapeutic benefit," explains Krainer. "Drugs that inhibit these factors and reverse the Warburg effect might work as anti-cancer agents." The study waccording toformed in collaboration with Professor Lewis Cantley, Ph.D., and colleagues at Harvard Medical School and The Broad Institute, in Cambridge, Mass......... Posted by: Jesmi24      Read more         Source

April 27, 2009, 5:22 AM CT

Improved detection of bladder tumors

Making tumors inside the bladder fluoresce red under blue light allows physicians to more easily find and remove them, substantially reducing the rate at which these cancers come back, says a Mayo Clinic doctor who is presenting results of a large, multicenter international clinical trial.

VIDEO ALERT: Additional audio and video resources, including excerpts from an interview with Dr. Lance Mynderse describing the research, are available on the Mayo Clinic News Blog (http://newsblog.mayoclinic.org/)Mayo Clinic News Blog. These materials are also subject to embargo, but appears to be accessed in advance by journalists for incorporation into stories. The password for the post is hvxaua1.

The findings, which are being reported at the annual meeting of the American Urological Association, show that this new diagnostic technique found more of the most common bladder tumors than the traditional white-light detection method in almost 17 percent of the patients, and demonstrated a 22 percent relative reduction in the recurrence rate within nine months of the procedure.

"This is the first demonstration that photodynamic diagnosis (PDD) cystoscopy along with the study drug (hexaminolevulinate) improves immediate detection, but more importantly reduces tumor recurrence rates of papillary bladder tumors; this is a significant improvement in therapy for our patients," says urologist Lance Mynderse, M.D., (http://www.mayoclinic.org/bio/10475311.html), who practices at Mayo Clinic's campus in Rochester, Minn. The 766-patient phase III study was conducted in 28 U.S. and European centers, and its principal investigator is Barton Grossman, M.D., of The University of Texas M.D. Anderson Cancer Center. Dr. Mynderse is presenting study results as spokesman for the lead enrolling site in North America......... Posted by: Jesmi24      Read more         Source

April 27, 2009, 5:17 AM CT

Robotic surgery for kidney cancer

Fox Chase Cancer Center scientists find that outcomes of robotic assisted kidney cancer surgery, when performed by experienced surgeons at high volume centers, prove more beneficial to patients when in comparison to open surgery. The study, authored by Fox Chase robotic surgeon Rosalia Viterbo, MD, was presented today at the American Urological Association's Annual Meeting, .

The standard therapy for kidney cancer is to surgically remove the entire or a portion of the kidney. This is known as nephron-sparing surgery, or partial nephrectomy, and is usually performed using traditional open surgery. Recently, there has been interest in applying a laparoscopic approach for this procedure, however it has proven to be technically challenging to a number of surgeons.

Experienced laparoscopic surgeons at high volume centers, such as Fox Chase, are now using the da Vinci robot assisted surgical system for patients with kidney cancer, or renal cell carcinoma. The advanced technology has enabled faster and greater technical proficiency allowing for completion of complex surgical procedures, facilitating a minimally invasive approach for partial nephrectomy.

"Our patients have experienced a number of benefits from the robot assisted approach, including shorter hospital stays (average 3 days), preserved kidney function (reduced need for dialysis), smaller scars with optimal cosmetic results, lower blood loss and easier and earlier return to normal activity," says Viterbo......... Posted by: Jesmi24      Read more         Source

April 13, 2009, 1:32 PM CT

SIRT1 takes down tumors

Yuan et al. have identified another anti-cancer effect of the "longevity" protein SIRT1. By speeding the destruction of the tumor promoter c-Myc, SIRT1 curbs cell division. The study will be published online April 13 (www.jcb.org) and will appear in the April 20 print issue of the Journal of Cell Biology

The yeast and nematode equivalents of SIRT1 are fountains of youth that stretch lifespan. Whether SIRT1 slows aging in mammals isn't certain, but it's beneficial in other ways. The protein tunes up metabolism, reducing blood levels of glucose and insulin, and might forestall neurodegenerative illnesses such as Alzheimer's disease and ALS. Given its pro-life credentials, you might expect SIRT1 to inhibit cancer. And several studies suggest that it does. But other work indicates that the protein aids tumors. For example, SIRT1 chops off acetyl groups, which can inactivate the tumor suppressor p53.

Yuan et al. determined SIRT1's effect on the transcription factor c-Myc, whose expression surges in a number of breast, colon, and liver cancers. The two proteins are tangled in a regulatory loop, the team found. c-Myc latched onto SIRT1's promoter, spurring cells to manufacture more SIRT1. In turn, SIRT1 detached acetyl groups from c-Myc, hastening its breakdown. To test SIRT1's effects on tumor growth, the scientists implanted malignant cells expressing c-Myc into nude mice that lack immune defenses. Boosting production of SIRT1 blocked tumor formation......... Posted by: Jesmi24      Read more         Source

December 24, 2008, 5:11 AM CT

How radiation therapy causes chronic inflammation of bowels

The use of radiation treatment to treat cancer inevitably involves exposure of normal tissues. Eventhough the benefits of this therapy have been well established, many patients experience distressing complications as a result injury to normal tissue These side effects correlation to inflammatory process cause discomfort and decreases the therapeutic benefit by increasing the overall therapy time.

A research article would be published on December 14, 2008 in the World Journal of Gastroenterology addresses the question. The research led by Dr. Christine Linard and her colleagues from the Institute for Radioprotection and Nuclear safety (IRSN) in France used experimentally a fractionated colorectal irradiation model to demonstrate an immune imbalance during the radiotherapy protocol and persisting in long term.

They observed that without causing histological damage, fractionated radiation induced elevated expression of IL-1beta, TNF alpha, MCP-1, and iNOS in distal colonic mucosa during the early post-irradiation phase. At that time, a Th2 profile was confirmed by expression of both the Th2-specific transcription factor GATA-3 and the chemokine receptor CCR4 and by suppression of the Th1 cytokine IFN gamma/IP-10 throughout the irradiation protocol. After 6 mo, despite the 2-fold reduction of iNOS and MCP-1 levels, the Th2 profile persisted, as shown by a 50% reduction in the expression of the Th1 transcription factor T-bet, the chemokine receptor CCXCR3, and the IFNgamma /STAT1 pathway. At the same time-point, the immunosuppressive IL-10/STAT3 pathway, known to regulate the Th1/Th2 balance, was expressed, in irradiated rats, at approximately half its level as in comparison to controls. This suppression was linked to an overexpression of SOCS3, which inhibits the feedback of the Th1 polarization and regulates IL-10 production......... Posted by: Jesmi24      Read more         Source

December 9, 2008, 10:29 PM CT

New therapy prevents dangerous side effect for lymphoma patients

Patients respond well to a new three-drug combination for indolent B cell lymphoma that also spares them prolonged, potentially lethal, suppression of blood production in the bone marrow, scientists at The University of Texas M. D. Anderson Cancer Center report today at the 50th annual meeting of the American Society of Hematology.

Pentostatin, cyclophosphamide and rituximab together are providing the same remission rate as other combinations but with minimal long-term bone marrow suppression, said study presenter Felipe Samaniego, M.D., associate professor in M. D. Anderson's Department of Lymphoma and Melanoma.

Myelosuppression leads to production of fewer red blood cells, white blood cells and platelets. When prolonged, it can lead to myelodysplastic syndrome, which comprises several conditions that cause potentially lethal insufficient blood production.

"The worst outcome of long-term myelosuppression for indolent B cell lymphoma patients is myelodysplastic syndrome," Samaniego said. "In this study, out of 80 patients, none developed MDS".

And 77 of 80 (96 percent) experienced either complete remission or unconfirmed complete remission. Some did have low blood counts, but all were short-term. Overall, the combination is well-tolerated, the research team reported......... Posted by: Jesmi24      Read more         Source

November 19, 2008, 8:09 PM CT

New platinum-phosphate compounds kill ovarian cancer

A new class of compounds called phosphaplatins can effectively kill ovarian, testicular, head and neck cancer cells with potentially less toxicity than conventional drugs, as per a new study published this week in the journal Proceedings of the National Academy of Sciences.

The compounds could be less harmful than current cancer therapys on the market such as cisplatin and carboplatin because they don't penetrate the cell nucleus and attach to DNA, said lead author Rathindra Bose. Conventional drugs can interfere with the functions of the cell's enzymes, which lead to side effects such as hearing and hair loss and kidney dysfunction.

Though researchers don't fully understand the mechanism by which the phosphaplatins kill cancer cells, they suspect that the compounds bind to the cell surface membrane proteins and transmit a "death signal" to the interior of the cell, Bose said. The compounds are created by attaching platinum to a phosphate ligand, which can readily anchor to the cell membrane. Future studies will focus on identifying the exact process.

"The findings suggest a paradigm shift in potential molecular targets for platinum anticancer drugs and in their strategic development," said Bose, a professor of biomedical sciences and chemistry and vice president for research at Ohio University who conducted the work while at Northern Illinois University......... Posted by: Jesmi24      Read more         Source

July 1, 2008, 10:01 PM CT

Death, Division or Cancer?

Each day, a staggering number of cells perform a feat that still amazes scientists with its complexity: they divide to produce perfect replicas of each other. The process is called mitosis, and an inability to control it is one of the hallmarks of cancer.

Little is known about the biochemical processes that control mitosis, but now scientists from Fox Chase Cancer Center and Technion-Israel Institute of Technology in Haifa, Israel, have discovered a novel activity, called the mitotic checkpoint factor 2 (MCF2). This appears to be integral in preventing cells that are unable to equally separate their chromosomes from dividing. The identities of the proteins involved in MCF2 remain to be determined, however, their findings offer insight into a fundamental question of biology, which may also help to increase the efficiency of cancer drugs that disrupt DNA replication, like gemcitabine, or drugs that prevent mitosis, like paclitaxel.

They publish their findings today online in the Early Edition of the Proceedings of the National Academy of Sciences.

"At any given moment, 250 million cells in your body are undergoing mitosis in order to replenish cells that die as a result of normal turnover," says Tim J. Yen, Ph.D., senior member at Fox Chase. "The mitotic checkpoint is a complex series of quality control systems, just like in a factory assembly line, that ensures that each new cell gets their proper share of DNA." (Click here for illustration)......... Posted by: Jesmi24      Read more         Source

May 19, 2008, 6:40 PM CT

Predicting prostate cancer treatment failure

Dynamic contrast-enhanced MRI (DCE-MRI) plus diffusion weighted imaging (DWI) can accurately diagnose residual or recurrent prostate cancer in patients treated with high-intensity focused ultrasonic ablation, a new study shows.

The study included 27 patients who had increased levels of prostate specific antigen after being treated with high-intensity focused ultrasonic (HIFU) ablation; 18 of these patients had local tumor progression seen at biopsy. DCE-MRI and DWI had about a 72% accuracy rate in determining which patients needed additional therapy because they had residual or recurrent cancer, said Chan Kyo Kim, MD, lead author of the study. The study observed that DWI had fewer false positives than DCE-MRI, but DCE-MRI had fewer false negatives.

After HIFU ablation, the normal anatomy of the prostate gland is completely lost or deformed making it difficult to distinguish non-malignant tissue from cancer, said Dr. Kim. The two imaging studies together, which can be done in about seven minutes, can overcome that challenge, he said.

HIFU is becoming more common as a prostate cancer therapy option, especially for those persons who cant or dont want to undergo a radical prostatectomy, said Dr. Kim......... Posted by: Jesmi24      Read more         Source

May 18, 2008, 9:45 PM CT

Drug fends off kidney cancer progression

New data from an international, multicenter Phase III clinical trial has observed that the experimental targeted treatment everolimus (RAD001) significantly delays cancer progression in patients with metastatic kidney cancer whose disease had worsened on other therapys. The study was led by Robert Motzer, MD, an attending doctor at Memorial Sloan-Kettering Cancer Center (MSKCC), who will present the findings on May 31 at the annual meeting of the American Society for Clinical Oncology.

This study has given us a new and clearly useful tool for treating renal cell tumors, and everolimus is an important step forward in terms of disease management and quality of life for patients living with this disease, said Dr. Motzer.

Kidney cancer is among the ten most common cancers in both men and women. The American Cancer Society estimates that there will be about 54,390 new cases of kidney cancer diagnosed in the US in 2008, and that about 13,010 people will die from the disease.

Everolimus, a once-daily oral treatment, targets the mTOR protein, which acts as a central regulator of tumor cell division, cell metabolism, and blood vessel growth. It is currently being reviewed for the therapy of several other cancers including lymphoma and neuroendocrine tumors......... Posted by: Jesmi24      Read more         Source

March 9, 2008, 6:09 PM CT

Researchers control growth rate of blood vessels

Scientists have discovered a way to control the growth rate of replacement tissue and the formation of new blood vessels, which solves one of the vexing problems of growing replacement tissue to treat injuries and trauma in humans.

The procedure could be used in bone grafts, tissue replacement, dental procedures or for diabetics or elderly patients who experience wound healing problems, said William Giannobile, professor at the University of Michigan School of Dentistry and College of Engineering, and corresponding author of the paper. Peter Ma, U-M professor with appointments in engineering and dentistry, is co-author and principal investigator on the National Institutes of Health project.

"If you have such a large defect that your body can't completely heal, this is a way to augment and dose a natural wound healing protein," Giannobile said.

Scientists put platelet-derived growth factor into nanoparticles and then attached them to a lattice-like, biodegradable scaffold. In experiments, the growth factor recruited cells that stimulate the body's own machinery responsible for healing, said Ma, whose lab developed the scaffold and the nanoparticles.

As the tissue grows, it crawls into the scaffold, which eventually dissolves.

"Growth factor is typically dumped in and releases over a period of hours," said Giannobile, who also directs the Michigan Center for Oral Health Research. "With certain wounds you might want a lot (of growth factor) in the beginning, and with others you might want a little released over a longer period of time. We've basically found a way to dial up or dial down the release rate of these growth factors"......... Posted by: Jesmi24      Read more         Source

March 4, 2008, 6:03 PM CT

Cancer risk higher for women in discontinued hormone treatment trial

A follow up study of participants in the Womens Health Initiative (WHI) clinical trial led by a University of North Carolina at Chapel Hill researcher has observed that women who were taking the combined hormone treatment of estrogen plus progestin may have an increased risk of cancer since the intervention was stopped, in comparison to participants in the trials placebo group.

However, the increased risks of heart disease, stroke and blood clots which had been seen in women taking the treatment as part of the WHI trial have diminished in the three years since scientists stopped it, as per a research studyreported in the March 5 issue of the Journal of the American Medical Association.

The studys lead author is Dr. Gerardo Heiss, a Kenan professor of epidemiology in the UNC School of Public Health.

The WHI trial of estrogen plus progestin which included 16,608 healthy postmenopausal women was originally designed to study what effect the hormone therapy would have on cardiovascular disease, cancer risks and bone fractures.

The trial was stopped in July 2002 after participants had been on the treatment for an average of 5.6 years because scientists saw an increased risk of breast cancer and cardiovascular disease in women randomly assigned to hormone treatment, compared with those who received a placebo......... Posted by: Jesmi24      Read more         Source

February 14, 2008, 10:17 PM CT

Oncoproteins destroy vital tumor-suppressor

Two previously unconnected cancer-promoting proteins team up to ambush a critical tumor suppressor by evicting it from the cell's nucleus and then marking it for death by a protein-shredding mechanism, a team led by researchers at The University of Texas M. D. Anderson Cancer Center reports in the Feb. 10 issue of Nature Cell Biology.

The paper is the first to illuminate a mechanism of attack on FOXO3a, a member of the forkhead family of tumor-suppressing proteins, notes senior author Mien-Chie Hung, Ph.D., chair of M. D. Anderson's Department of Molecular and Cellular Oncology.

"We know that FOXO3a is inactivated in about 80 percent of breast tumors, and that it's likely to be inactivated in other solid tumors because three major oncogenic pathways separately target it," Hung said. "The implication is that forkhead activation will be a great therapeutic target because it would be a powerful tumor-suppressor".

Hung and his colleagues focused on the effect of the RAS-ERK signaling pathway, which is known to promote tumor growth and proliferation. FOXO3a and its other forkhead cousins have a specific structure - the forkhead box - that allows them to connect with DNA. They are transcription factors, activating or repressing target genes involved in tumor suppression and DNA damage repair......... Posted by: Jesmi24      Read more         Source

February 4, 2008, 9:24 PM CT

Lnk between cancer, Down syndrome

Theres new hope for breast cancer research, and its coming from a very unlikely place. Scientists at the Texas A&M University College of Veterinary Medicine & Biomedical Sciences recently published articles in the journals Molecular and Cellular Biology and Carcinogenesis indicating that a protein long suspected to play a role in Down Syndrome may also contribute to treating this devastating disease.

It has long been known that Down Syndrome is caused when an individual has an extra copy of the 21st chromosome, giving them a total of three instead of the normal chromosome pair. With improved medical care, people with Down Syndrome are now living longer, healthier lives. With this advance came the observation that individuals with Down Syndrome have a significant decrease in risk for several types of tumors. Most striking is the observation that women with Down Syndrome are 10-25 times less likely to develop breast cancer.

This effect is believed to be due to the presence of one or more tumor suppressor genes on chromosome 21. However, the identity of such genes has not been known, until now.

Years of research into the genetics of Down Syndrome have helped us to discover a very important gene on chromosome 21, said Dr. Weston Porter, associate professor in the Veterinary Integrative Biosciences Department. This gene, called Single-minded 2 or SIM2 is thought to play an important role in Down Syndrome by regulating neuron growth in the developing brain. Based on its developmental role, we hypothesized that SIM2 may also be involved in breast cancer, which is essentially a disease of uncontrolled growth......... Posted by: Jesmi24      Read more         Source

November 12, 2007, 10:08 PM CT

How to switch off cancer cell genes

A new study led by scientists at the University of Southern California (USC) identifies how genes are silenced in cancer cells through distinct changes in the density of nucleosomes within the cells.

The findings, reported in the Nov. 13 issue of the journal Cancer Cell, will enable scientists to explore new therapies to switch the genes back on and may lead to novel therapys for human cancers, says study lead author Peter A. Jones, Ph.D., D.Sc., director of the USC/Norris Comprehensive Cancer Center and Distinguished Professor at the Keck School of Medicine of USC.

"The study shows for the first time exactly how genes get shut down in cancer cells," Jones says. "It identifies what the target looks like so that new therapies can be designed to turn them back on".

The study showed that silencing of transcription start sites in some cancer cells involves distinct changes in nucleosomal occupancy'or the density of nucleosomes'in the cell. Scientists observed that three nucleosomes, almost completely absent from the start site in normal cells, are present in the methylated and silenced promoter, suggesting that epigenetic silencing may be accomplished by the stable placement of nucleosomes into previously vacant positions.

DNA cytosine methylation'the addition of a group of specific chemicals to a stretch of DNA that can lock or silence a gene'may ultimately lead to silencing by enabling the stable presence of nucleosomes at the start sites of cancer-related genes, the study suggests......... Posted by: Jesmi24      Read more         Source

October 2, 2007, 10:28 PM CT

New strategies with greater antitumorous efficacy

One of the biggest problems in the current therapy of cancer is that the agents that are efficacious in the destruction of tumorous cells are, at the same time, extremely toxic for the rest of the healthy cells and tissues of the patient. To address the problem the University of the Basque Country (UPV/EHU) is seeking more specific therapys and studying the differences between tumorous cells and healthy ones.

A research team from the Faculty of Medicine and Odontology is working on identifying pharmacological agents that increase the therapeutic benefit of combinations of chemo-, immune and radiotherapy agents in the therapy of cancer ailments.

The aim of the research team was to identify compounds that act on the metabolic pathways and processes that take place differently depending whether a diseased tissue of a patient or healthy tissue is involved; in this way selective action can be undertaken, increasing the sensitivity of therapys for diseased tissues without damaging healthy cells or tissues at the same time.

With this general goal the scientists tested various biomodulators on many different tumorous modules such as melanoma, sarcoma and cancer of the colon. On the one hand, they studied agents that modulated levels of glutathione (GSH) - key element in the biological processes of cells, both healthy and tumorous. Tumorous cells with high GSH levels have a greater growth and metastatic capacity and a lower sensitivity to antitumorous agents. Conversely, one of the features of tumorous cells is that they lose their normal level of differentiation and, instead of exercising a determined function, they start to proliferate and generate a greater quantity of tumorous cells. This is why the scientists have also used agents that induce differentiation, such as are retinoids......... Posted by: Jesmi24      Read more         Source

August 8, 2007, 8:44 PM CT

Light-activated Molecules To Kill Cancer Cells

A key challenge facing doctors as they treat patients suffering from cancer or other diseases resulting from genetic mutations is that the drugs at their disposal often dont discriminate between healthy cells and dangerous ones -- think of the brute-force approach of chemotherapy, for instance. To address this challenge, Florida State University scientists are investigating techniques for using certain molecules that, when exposed to light, will kill only the harmful cells.

Igor V. Alabugin is an associate professor of chemistry and biochemistry at FSU. He specializes in a branch of chemistry known as photochemistry, in which the interactions between atoms, small molecules and light are analyzed.

When one of the two strands of our cellular DNA is broken, intricate cell machinery is mobilized to repair the damage, he said. Only because this process is efficient can humans function in an environment full of ultraviolet irradiation, heavy metals and other factors that constantly damage our cells.

However, a cell that sustains so much damage that both DNA strands are broken at the same time eventually will commit suicide -- a process known as apoptosis.

In our research, were working on ways to induce apoptosis in cancer cells -- or any cells that have harmful genetic mutations -- by damaging both of their DNA strands, Alabugin said. We have observed that a group of cancer-killing molecules known as lysine conjugates can identify a damaged spot, or cleavage, in a single strand of DNA and then induce cleavage on the DNA strand opposite the damage site. This double cleavage of the DNA is very difficult for the cell to repair and typically leads to apoptosis......... Posted by: Jesmi24      Read more         Source

July 19, 2007, 10:04 PM CT

Nonsmall cell lung cancer: chemotherapy before surgery

Combining pre-operative chemotherapy and surgery increases the average chance of survival at five years by approximately 6% compared with surgery alone.

This conclusion was drawn by a team of Cochrane Researchers from the MRC Clinical Trials Unit in London after they identified 12 eligible randomised controlled trials. Data from seven of these trials were available from trial reports and were combined in a meta-analysis. The seven trials involved a total of 988 patients.

This is currently the best estimate of the effectiveness of this therapy, but is based on a relatively small number of trials and patients, says lead researcher Sarah Burdett.

There was, however, insufficient data to break the patients down into sub-groups and see whether the effectiveness varies for different types of patients or stages of the disease.

This research is important because around the world more than a million new cases of lung cancer are diagnosed each year, around 80% of which are non-small cell lung cancer. In addition, many patients are only diagnosed after the disease has progressed, so survival rates across all stages of disease tend to be fairly low at around 14%, with only a quarter of patients being suitable for surgery.

The Cochrane Systematic Review found that using chemotherapy before surgery can reduce the size of tumours making the surgery simpler, and increasing the number of patients who may be candidates for surgery. The worry is, however, that having a course of chemotherapy delays the operation, and could therefore leave patients at risk of allowing the tumour to spread......... Posted by: Jesmi24      Read more         Source