Cancer blog page

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

July 19, 2007, 10:01 PM CT

Impact of False-positive Cancer Tests

According to a new study in Value in Health, women coping with the strain of being mistakenly diagnosed with breast cancer have not been adequately studied in the past. The focus of the study is a new survey that accurately assesses the negative effects of false diagnosis and provides useful information to health care practitioners and researchers.

"We know that having a false alarm at a breast cancer screening causes significant negative psychological harm," says Dr. John Brodersen, co-author of the study. "Unfortunately, previous studies of the long-term psychological consequences of these false alarms have used inadequate measures".

The survey, developed by Brodersen and his colleagues, focuses on six psychosocial dimensions; anxiety, behavioral impact, sense of dejection, impact on sleep, breast examination and sexuality. The survey showed that women who had an abnormal screening mammography later confirmed to be false-positive were negatively influenced in all six categories.

"This is an urgent issue to be addressed, because one-in-four women following the European Union-recommended biannual breast cancer screening program over a 20-year period will experience a false-positive screening mammogram," says Brodersen. "Thousands of women experience false-positive screening results. Therefore, women should be better informed both before breast cancer screening and during the screening process. This should include a discussion about the implications of a false-positive result, as well as the benefits of early detection of breast cancer"......... Posted by: Jesmi24      Read more         Source

Fri, 22 Jun 2007 03:04:18 GMT

"Tarts" cancer jab will "ruin lives"

"Gardasil is almost 100% effective against Human Papilloma Virus, the main cause of cervical cancer, which can be fatal, and genital warts. It is now being prescribed in Britain , with calls for the 'wonder drug' to be administered wholesale to school-girls. Cervical cancer charity Jo's Trust has called for a nation-wide programme of vaccination in secondary schools to be launched by the end of the year, even though no tests have been done on girls of that age and long-term side-effects are as yet unknown.

The use of the vaccine which prevents cervical cancer has been condemned by a Christian prayer and lobby group."
Stephen Green, National Director of Christian Voice, said today:

'The best way of not getting cervical cancer and genital warts is to stay a virgin and marry a virgin. Why don't these officials want young people to do that? Why don't we raise their expectations and ours and treat them with some respect?' (Christian Voice)Madness.

I saw Alice, a sixteen year old girl, this morning. She is not a tart. She is a schoolgirl. She has not been able to have a Gardasil immuisation because of prudery and government delay (Patricia saving pennies again) and now she cannot even get contraception.

Yesterday afternoon, after school, Alice had intercourse with her boyfriend. The condom split.

This has not happened to her before. She went to the local chemist to get the "morning after pill". The well known high street chemist that she visited charges £25 to provide one levonorgestrel pill. (Levonelle 1500)

Alice is a school girl. She is hard up. She did not have £25 and nor did her boyfriend. Together, they could only raise £11.

Alice's parents do not know she is sexually active. In fact, they think she is not. She was nervous about coming to the family doctor because I know her parents. And her sister. However, she is a sensible girl, and realised that it was essential that she got the morning after pill so she set off to school very early this morning and was waiting at the door of the surgery when I arrived.

In 2006 there were approximately 194,000 abortions in the UK, nearly five percent more than the previous year.

Contraception is supposed to be free in the UK. Chemists are allowed to sell the morning after pill without prescription to make it easier for young girls like Alice to get help.

And it is easier.

If they can afford it.

Utter madness.Labels: gardasil, morning after contraception Posted by: Dr John Crippen      Read more     Source

June 15, 2007, 12:24 AM CT

Target tumor microenvironment to stop cancer growth

Cold Spring Harbor Laboratory (CSHL) researchers led by Daniel Nolan and Assistant Professor Vivek Mittal have found that bone marrow (BM) derived endothelial progenitor cells (EPCs) play a critical role in the early stages of tumor progression and that eliminating EPCs stops cancer growth. Using sophisticated high-resolution microscopy and flow cytometry, they zeroed in on the earliest stages of cancer progression and identified the role of EPCs in generating blood vessels that allow cancers to grow. If we selectively blocked the EPCs, tumors were unable to make blood vessels and could not sustain their own growth, said Vivek Mittal, CSHL Assistant Professor.

The findings open an entirely new field of research on how vascular progenitor cells control tumor growth and underscore their potential for cancer therapeutics. Published on June 15, 2007 in Genes & Development, the CSHL study settles a dispute in the field of angiogenesis that has resulted from years of inconsistent findings about the existence of EPCs in cancer tumors. Until now, this field of research that focuses on new blood vessel development has been split between researchers who have suggested the existence of EPCs and those who have vehemently disputed their presence.

The CSHL research posits that those who did not find evidence of EPCs in tumors were probably looking for them in later stages of tumor progression when EPCs are diluted by host endothelial cells. The new results show that EPCs are only present in the earliest stages of tumor progression, before the formation of blood vessels. We found that the role of EPCs is to direct the formation and organization of the vascular structure that ultimately feeds the tumor as it grows, said CSHL researcher Daniel Nolan......... Posted by: Jesmi24      Read more         Source

June 13, 2007, 1:24 PM CT

Prostate cancer risk in BRCA2 carriers

Carriers of a BRCA2 variation specific to Iceland are more likely to develop aggressive and lethal prostate cancer than noncarriers, as per a research studypublished online June 12 in the Journal of the National Cancer Institute

Mutations in the BRCA2 gene are linked to increased prostate cancer risk, but it has been unclear whether they are correlation to progression of the disease.

Laufey Tryggvadttir of the Icelandic Cancer Registry and his colleagues compared survival and disease progression in patients with prostate cancer with the Icelandic BRCA2 999del5 founder mutation and those without the mutation. Using a pool of male relatives of women with breast cancer, scientists identified patients with prostate cancer diagnosed in Iceland between 1955 and 2004. The mutation was present in 30 patients (5.7%).

The mutations carriers were younger at the time of diagnosis and had more advanced staged cancer, higher-grade tumors, and shorter median survival time (2.1 years vs. 12.4 years) compared with noncarriers.

The authors conclude that it is of great importance to study whether these results can be confirmed for carriers of mutations at other locations within the BRCA2 gene. Finally, the results indicate that in the search for new methods to predict prostate cancer progression, it may be fruitful to look for gene or protein expression patterns in prostate cancers resembling the patterns seen in BRCA2 mutation carriers......... Posted by: Jesmi24      Read more         Source

May 22, 2007, 9:51 PM CT

Stem cells provide clues to cancer spread

Scientists have made a breakthrough in understanding how cancers spread in what could lead to new ways of beating the disease.

The University of Manchester study used embryonic stem (ES) cells to investigate how some tumours are able to migrate to other parts of the body, which makes the treatment of cancer much more difficult.

Dr Chris Ward, in the Universitys Faculty of Medical and Human Sciences, studied a crucial change that makes cancer cells able to start moving and spread into other tissues.

Normal cells, as well as early cancer cells, are called epithelial cells because they bind tightly to each other forming stable layers of tissue. However, as a tumour becomes more advanced, some of the cells change to become mesenchymal.

Mesenchymal cells do not bind to each other, forming more disorganised tissues in which the cells can move around. Since this crucial change known as the epithelial-mesenchymal transition, was first observed in the early embryo, Dr Ward theorised that embryonic stem cells might undergo a similar process.

Dr Ward, whose findings are reported in the journal Molecular Biology of the Cell, said: "We have shown that ES 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......... Posted by: Jesmi24      Read more         Source

May 21, 2007, 12:30 AM CT

Role of age, gender, race and weight on cancer risk

While cancer has been studied extensively to determine the major contributing factors for risk and ultimate outcome, a number of variables still remain and doctors are puzzled by new cases that do not fit "old" protocol. Research presented today at Digestive Disease Week 2007 (DDW) demonstrates improved results in determining these risks, including the relative "weight" of being heavy on risk for colon cancer; possible risk of cancer surgery among elderly individuals; and how race determines incidence as well as therapy decisions. DDW is the largest international gathering of physicians and scientists in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery.

"Drilling down into clinical trials data for different types of patients can lead to varying and important conclusions," said Marcia R. Cruz-Correa, M.D., Ph.D., Associate Professor of Medicine and Biochemistry, University of Puerto Rico Comprehensive Cancer Center. "In these instances, management of risk factors for colon cancer and therapy decisions for a particular sub-group of patients can be influenced by these analyses".



Racial and Geographic Disparities in the Utilization of Surgical Therapy for Hepatocellular Carcinoma (Abstract #276)

Hepatocellular carcinoma (HCC), a cancer of cells in the liver, is on the rise in part due to the high prevalence of chronic hepatitis C infection, which increases the risk for the disease. Surgery is the only potential curative therapy for HCC and this study sought to determine the patterns of use for this therapy......... Posted by: Jesmi24      Read more         Source

May 6, 2007, 5:50 PM CT

MR imaging helps predict recurrence

MR images taken of patients with prostate cancer previous to therapy that show that the cancer has spread outside the prostate gland capsule help predict whether the cancer will return, as per a recent study conducted by radiologists at the University of California-San Francisco.

The study consisted of 74 men with biopsy-proven prostate cancer who underwent endorectal MR imaging of the prostate, said Antonio Westphalen, MD, lead author of the study. Tumor size, stage and extracapsular extension (cancer spread outside the prostate gland capsule) were all recorded.

"The study focused on patients who were treated with radiation treatment, more specifically, external beam radiation treatment, which is the therapy of choice of about one-third of patients with newly diagnosed prostate cancer," said Dr. Westphalen.

After a follow-up of an average 42 months, four patients developed metastases all four had extracapsular extension seen on MR imaging before therapy, Dr. Westphalen said. Three of them had more than 5mm of extracapsular extension at MR imaging, he said.

"The main goal of our study was to identify features on our imaging that would predict therapy failure, perhaps allowing for a more conscientious decision ahead of time. We observed that a subset of patients who presented with imaging signs of extracapsular extension previous to radiation were more likely to develop metastases in the future," said Dr. Westphalen......... Posted by: Jesmi24      Read more         Source

April 30, 2007, 6:54 PM CT

The Tungsten Nevada Leukemia Link

Tungsten began increasing in trees in Fallon, Nev. several years before the town's rise in childhood leukemia cases, according to a new research report.

The amount of tungsten in tree rings from Fallon quadrupled between 1990 and 2002, whereas the amount in tree rings from nearby towns remained the same, according to a research team led by Paul R. Sheppard of The University of Arizona's Laboratory of Tree-Ring Research.

This is the first study that has examined changes in levels of heavy metals in Fallon over time.

"Trees take up metals from the environment and those metals show up in the tree rings. By analyzing chemicals in tree rings, we can look back in time years, and even decades," said Sheppard, a UA assistant professor of dendrochronology.

"Tree ring values for the early 1990s for tungsten are roughly equivalent to nearby towns, but go up in Fallon in the mid-1990s while staying the same in other towns," he said.

Tungsten levels in Fallon trees began increasing in 1994, while levels in neighboring towns remained the same. Since 1997, 17 cases of childhood leukemia have been diagnosed in children who lived in the Fallon area for some time prior to diagnosis. Fallon's high incidence of leukemia has been acknowledged as a leukemia cluster by the Nevada State Health Division......... Posted by: Jesmi24      Read more         Source

April 25, 2007, 9:35 PM CT

Short chromosomes put cancer cells in forced rest

A Johns Hopkins team has stopped in its tracks a form of blood cancer in mice by engineering and inactivating an enzyme, telomerase, thereby shortening the ends of chromosomes, called telomeres.

"Normally, when telomeres get critically short, the cell commits suicide as a means of protecting the body," says Carol Greider, Ph.D., the Daniel Nathans chair of molecular biology and genetics at Johns Hopkins. Her study, appearing online this month at Cancer Cell, uncovers an alternate response where cells simply - and permanently - stop growing, a process known as senescence.

In an unusual set of experiments, the research team first mated mice with nonoperating telomerase to mice carrying a mutation that predisposed them to Burkitts lymphoma, a rare but aggressive cancer of white blood cells. Telomerase helps maintain the caps or ends of chromosomes called telomeres, which shrink each time a cell divides and eventually - when the chromosomes get too short - force the cell to essentially commit suicide. Such cell death is natural, and when it fails to happen, the result may be unbridled cell growth, or cancer.

The first generation pups born to these mice contained no telomerase and very long telomeres. These mice all developed lymphomas by the time they were 7 months old. The researchers then continued breeding the mice to see what would happen in later generations. By the fifth generation, the researchers discovered that the mice had short telomeres and stopped developing lymphomas......... Posted by: Jesmi24      Read more         Source

April 23, 2007, 10:06 PM CT

Antioxidant is selective killer of leukemia cells

A naturally occurring compound found in many fruits and vegetables as well as red wine, selectively kills leukemia cells in culture while showing no discernible toxicity against healthy cells, according to a study by researchers at the University of Pittsburgh School of Medicine. These findings, which were published online March 20 in the Journal of Biological Chemistry and will be in press on May 4, offer hope for a more selective, less toxic therapy for leukemia.

Current treatments for leukemia, such as chemotherapy and radiation, often damage healthy cells and tissues and can produce unwanted side effects for many years afterward. So, there is an intensive search for more targeted therapies for leukemia worldwide, said corresponding author Xiao-Ming Yin, M.D., Ph.D., associate professor of pathology, University of Pittsburgh School of Medicine.

Leukemia is not a single disease but a number of related cancers that start in the blood-forming cells of the bone marrow. Meaning literally white blood in Greek, leukemia occurs when there is an excess of abnormal white blood cells. There are both acute and chronic forms of leukemia, each with many subtypes that vary in their response to treatment. According to the National Cancer Institute, about 44,000 new leukemia cases will be diagnosed in the United States in 2007, and there will be about 22,000 leukemia-related deaths......... Posted by: Jesmi24      Read more         Source