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December 15, 2005, 8:13 PM CT

Cancers Use "Cellular Bookmarks"

Cancers Use
Howard Hughes Medical Institute scientists and their colleagues have discovered that non-cancerous bone marrow cells establish "cellular bookmarks" in target organs that guide the spread of cancer cells to their predetermined destination.

The scientists said their findings could have a major impact on how oncologists assess the likeliness of metastasis to specific organs. Their discovery may also help identify subsets of high risk cancer patients who are prone to distant metastases. Those patients would likely benefit from a more aggressive adjuvant treatment to prevent cancer relapse.

Ultimately, understanding how cellular bookmarking works at the molecular level could lead to new information that may help thwart metastasis, a major cause of death among cancer patients, said one of the study's senior authors, Shahin Rafii, a Howard Hughes Medical Institute investigator at Weill Medical College of Cornell University.

The researchers, led by David Lyden and Rafii, published their findings in the December 8, 2005, issue of the journal Nature. Lyden and colleagues are at Memorial Sloan-Kettering Cancer Center and the Weill Medical College.

Rafii and Lyden's group had established that a specific subset of bone marrow derived cells (BMDCs ) - which are comprised of hematopoietic progenitor cells capable of dividing and forming colonies- are recruited by tumors to aid in the growth of new blood vessels. The generation of new blood vessels occurs through a process called angiogenesis. In prior studies, the scientists had shown that co-recruitment of hematopoietic BMDCs expressing the angiogenic factor receptor, VEGFR1, along with the vascular cells accelerated the assembly of newly formed blood vessels and tumor growth.

"In the current paper, we set forth another novel concept by demonstrating that a non-cancerous cluster of VEGFR1-positive hematopoietic BMDCs were recruited to a pre-metastatic niche, thereby establishing a permissive docking site previous to the arrival of the circulating tumor cells, " said Rafii. Biologists use the term "niche" to describe a specialized cellular microenvironment that provides support to specific types of cells. A "pre-metastatic niche" is a cellular microenvironment that is specialized for the development of metastatic tumor cells.........

Daniel      Permalink

December 15, 2005, 7:32 PM CT

Radiotherapy after lumpectomy saves lives

Radiotherapy after lumpectomy saves lives
Following a lumpectomy for breast cancer, radiotherapy to the breast reduces the risk of eventually dying from the disease - according to research published in today's (Friday's) The Lancet*.

An international team of scientists found that a woman's five-year risk of the cancer returning in or near the breast after a lumpectomy dropped from 26 percent to seven percent if she also received radiotherapy, and the 15-year risk of dying from the disease dropped from 36 percent to 31 percent.

They carried out a worldwide overview of trials of radiotherapy and of different types of surgery, involving 40,000 women with early breast cancer, and found that for every four breast cancer recurrences avoided by radiotherapy, one death is prevented.

The findings from this Cancer Research UK and Medical Research Council funded study will help doctors and patients decide on the most appropriate therapy.

Present UK guidelines on improving outcomes in breast cancer already state that radiotherapy should be regarded as standard therapy after a lumpectomy. But, as with any procedure, the therapy given depends on discussions between doctors and patients about the benefits and side effects, and may, in a minority of cases, result in non-standard therapy being offered.

The study also shows similar benefits from radiotherapy for women who had their entire breast removed but whose cancer had already spread to the armpit. The chances of the cancer coming back in or near the breast or armpit dropped from 23 percent to six percent, and the risk of dying from breast cancer dropped from 60 percent to 55 percent.

However, for women who had a breast removed, but whose cancer had not spread to the armpit, radiotherapy was found not to be appropriate; any benefits were slight and were outweighed by the side effects of radiotherapy. These can include permanent swelling of the arm, permanent limitation of shoulder movement and, occasionally, life-threatening diseases such as heart attack or a new cancer in the lung or opposite breast.........

Emily      Permalink

December 15, 2005, 7:3 PM CT

Mechanisms of Tumor Growth

Mechanisms of Tumor Growth
Scientists at Columbia University Medical Center have identified an inherent feature of stem and progenitor cells that may promote initiation and progression of malignant tumors.

As per a research findings published in the recent issue of Cancer Cell, the team showed that stem and progenitor cells are susceptible to a specific error during cell division that can result in severe chromosomal defects. This susceptibility may explain how a tumor-initiating cell, also known as a cancer stem cell, arises from a normal cell. It may also explain how a cancer stem cell acquires additional mutations that increase tumor malignancy.

According to Timothy Bestor, Ph.D., and Marc Damelin, Ph.D., of Columbia University College of Physicians and Surgeons, understanding the nature of cancer stem cells could result in new therapies that specifically target those cells, which are thought to be the driving force of tumor progression.

The process of cell division is closely monitored by the cell, because a mistake can result in a cancer-causing chromosome abnormalities. Typically during cell division, cells monitor quality control with a series of checkpoints. One such checkpoint confirms that the cell's chromosomes have been disentangled before they are to be pulled apart in mitosis, to ensure that the chromosomes will be separated appropriately.

The Columbia scientists found, however, that stem and progenitor cells are deficient in this checkpoint and will divide even if the chromosomes are entangled. All three cell types tested by the scientists - mouse embryonic stem cells, mouse neural progenitor cells, and human bone marrow progenitor cells - attempted cell division with entangled chromosomes. The scientists think it likely that cancer stem cells, which closely resemble normal stem cells, have the same deficiency.........

Daniel      Permalink

December 14, 2005, 9:43 PM CT

New Therapy For Advanced-Stage Lymphoma

New Therapy For Advanced-Stage Lymphoma Follicular lymphoma
Oncologists have been stymied by how to treat some patients with lymphoma who do not respond to new, targeted therapies. A study by researchers at the University of Rochester Medical Center and other institutions shows there might be a new drug that combats indolent non-Hodgkin's lymphoma when others fail.

Bendamustine, an agent that attacks cancer cells' DNA forcing them to self-destruct and disrupting the cell-division cycle, was given to 77 patients, most of whom had advanced follicular lymphoma, who did not respond to rituximab, considered the wonder-drug for lymphomas, and 74 percent of them responded, including 35 percent who were brought into remission.

"This is very exciting because it's the first study of chemotherapy for a class of patients who didn't respond to rituximab and it provides an effective alternative for them," said Jonathan Friedberg, M.D., of the James P. Wilmot Cancer Center at the University of Rochester Medical Center. He presented results of the international study today at the American Society of Hematology's annual meeting in Atlanta.

"It's unusual to see this kind of response in patients so far along in the course of their disease, particularly since they previously did not response to other alkylators and were relapsed from rituximab," said Friedberg, associate director of lymphoma clinical research at Wilmot.

About half of follicular lymphoma patients respond to rituximab as a single agent, and a standard therapy is with a chemotherapy combination called CHOP. Doctors have struggled with how to treat people who don't respond, or stop responding to that treatment. It's common for patients with follicular lymphoma to relapse multiple times during the typically 10-year natural progression of the disease.........

Daniel      Permalink

December 14, 2005 7:11 PM CT

Comprehensive Effort to Explore Cancer Genomics

Comprehensive Effort to Explore Cancer Genomics
The National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), both part of the National Institutes of Health (NIH), today launched a comprehensive effort to accelerate our understanding of the molecular basis of cancer through the application of genome analysis technologies, particularly large-scale genome sequencing. The overall effort, called The Cancer Genome Atlas (TCGA), will begin with a pilot project to determine the feasibility of a full-scale effort to systematically explore the universe of genomic changes involved in all types of human cancer.

"Now is the time to move forward with this pioneering initiative. Thanks to the tools and technologies developed by the Human Genome Project and recent advances in using genetic information to improve cancer diagnosis and therapy, it is now possible to envision a systematic effort to map the changes in the human genetic blueprint associated with all known forms of cancer," said NIH Director Elias A. Zerhouni, M.D. "This atlas of genomic changes will provide new insights into the biological basis of cancer, which in turn will lead to new tests to detect cancer in its early, most treatable stages; new therapies to target cancer at its most vulnerable points; and, ultimately, new strategies to prevent cancer."

NCI and NHGRI announced today at a news conference in Washington, D.C., that they have each committed $50 million over three years to the TCGA Pilot Project. The project will develop and test the complex science and technology framework needed to systematically identify and characterize the genetic mutations and other genomic changes associated with cancer. The pilot will involve a few types of cancer that will be chosen for their value in helping to determine the feasibility of a possible larger-scale project. The process for determining the types of cancers to be studied is currently underway.........

Daniel      Permalink

December 14, 2005

Pancreatic Cancer Linked to Insulin Resistance

Pancreatic Cancer Linked to Insulin Resistance
A new study led by scientists at the National Cancer Institute (NCI), part of the National Institutes of Health, shows for the first time that male smokers with the highest insulin levels are twice as likely to develop pancreas cancer as men with the lowest levels. Similarly, men with glucose levels in the range of clinical diabetes were twice as likely to develop the cancer as men with normal glucose levels. This study examined data from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study* of 29,000 male smokers in Finland and appears in the December 14, 2005, issue of the Journal of the American Medical Association.

Study investigators drew blood from enrollees when they joined the ATBC Study in the mid-1980s. This allowed the scientists to determine participants' overnight fasting insulin and glucose levels a number of years ahead of when they might be diagnosed with cancer. Over the course of 17 years, 169 men in the study developed pancreas cancer.

Study results show a two-fold increase in risk of pancreas cancer in the quartile of men with the highest fasting serum insulin levels (greater than 6.1 microinternational units per milliliter) compared to those in the lowest quartile (less than 2.75 microinternational units per milliliter). Increasing concentrations of glucose, insulin, and insulin resistance were also associated with pancreas cancer. Moreover, the risk for pancreas cancer increased with longer follow-up time.

"Some men were in the highest quartile of insulin or had abnormal glucose levels more than a decade before the cancer appeared," noted lead researcher Rachael Stolzenberg-Solomon, Ph.D., of NCI's Division of Cancer Epidemiology and Genetics. "It is important to note, however, that this study was only done in male smokers and that any assumptions about risk in the general population or whether one can determine their own pancreas cancer risk specifically based on insulin levels is premature."........

Daniel      Permalink

December 14, 2005

Amn107 In Leukemia Resistant To Gleevec

Amn107 In Leukemia Resistant To Gleevec
The targeted agent AMN107 can produce dramatic benefits in patients with some forms of leukemia that are resistant to Gleevec, the standard treatment for these cancers, say scientists at The University of Texas M. D. Anderson Cancer Center (meeting abstract #37).

At the 47th Annual Meeting of the American Society of Hematology (ASH), the investigators reported marked improvement in outcome in all three phases of chronic myeloid leukemia (CML) as well as benefit in treating a form of acute lymphocytic leukemia (ALL) that shares the same genetic abnormality as CML, the Philadelphia chromosome.

"This drug is very promising and appears at this point to offer an effective option for patients who do not achieve an optimal response to Gleevec treatment," says Hagop Kantarjian, M.D., professor and chair of the Department of Leukemia.

If additional studies continue to show such results, Kantarjian says, he believes AMN107, which is taken in pill form, "will either replace Gleevec as the standard of care in the future or will be used in combination with it.".

Both CML and Philadelphia-positive ALL is caused by the swapping of genetic material in bone marrow stem cells between two chromosomes, which produces an abnormality called the Philadelphia chromosome. This new gene then produces a novel tyrosine kinase (Bcr-Abl) that signals the abnormal cell growth that leads to development of leukemia.

While both Gleevec and AMN107 shut down the activity of Bcr-Abl, laboratory experiments with AMN107 show it is up to 50 times more potent because it binds more efficiently to the enzyme than does Gleevec.

In the phase I clinical trial being reported, 119 patients who were resistant to Gleevec were given AMN107, and in some cases the dose was increased up to twelve fold. The scientists found that the range of response varied, depending on the form of the cancer and the presence of genetic mutations. For example, hematologic response from the drug (defined as control of white blood cell counts) ranged from 44 percent to 100 percent in different subgroups of CML patients, and the more enduring cytogenetic response (elimination of cells with the cancer-causing defect) ranged from 22 percent to 100 percent. There was less overall response in ALL patients (ranging from 10 percent to 33 percent, depending on extent of disease).........

Daniel      Permalink

December 14, 2005

Immune Responses To Cancer

Immune Responses To Cancer
There is growing evidence for a link between the immune system and the control of cancer. Support for this link comes from observations that the immune system can protect against the development of spontaneous and chemically-induced tumors in laboratory systems. Further, a large number of targets for immune recognition of human cancer have been identified and characterized.

Results of a large study published in Proceedings of the National Academy of Sciences, Early Edition provide further evidence for the role of the immune system in controlling cancer.

The international research team, led by investigators from Roswell Park Cancer Institute (RPCI) and part of the global Cancer Vaccine Collaborative, examined the precise location of subpopulations of immune cells [tumor infiltrating lymphocytes (TILs)] in 117 RPCI patients with epithelial ovary cancer (EOC) to determine the interrelationship between subpopulations of TILs and overall survival.

Results of the detailed immunohistochemical analysis of TILs in EOC indicated that eventhough most subtypes correlated with each other, intraepithelial CD8+ was the only subtype associated with a favorable prognosis. Further, high CD8+/CD4+ and CD8+/regulatory T cell (Tregs) ratios were associated with a favorable prognosis in EOC; the latter corresponding to an almost 70 percent reduction in the risk of death.

"This work represents a major step forward in documenting evidence for immune responses to cancer," according to Kunle Odunsi, MD, PhD, departments of Gynecologic Oncology and Immunology at RPCI and corresponding author of this study. "Further, it implies that a critical balance must be achieved in the ratio of CD8+ T cells to Tregs in immune therapies, and that manipulation of Tregs could be a powerful method to enhance the efficacy of such therapies."........

Daniel      Permalink

December 13, 2005

Treat Leukemia With Green Tea Extract

Treat Leukemia With Green Tea  Extract
A new case study by Mayo Clinic scientists provides preliminary evidence to suggest a component of green tea may lead to clinical improvement in patients with chronic lymphocytic leukemia (CLL). Findings are published online in Leukemia Research.

In the small case study, the scientists report on four patients who appeared to have an improvement in the clinical state of their disease after starting over-the-counter products containing epigallocatechin gallate (EGCG), an extract of green tea. Three of the four patients met the standard criteria used to define a response therapy for clinical trials. These same investigators had previously shown that EGCG kills leukemia cells from patients with CLL in the test tube by interrupting the communication signals they need to survive. That study was published in Blood in 2004.

"The experience of these individuals provides some suggestion that our previously published laboratory findings may actually translate into clinical effects for patients with this disease," says Tait Shanafelt, M.D., Mayo Clinic hematologist and lead author of the article. Despite these encouraging preliminary findings, he urges caution. "We do not know how a number of patients were taking similar products and failed to have any benefit. We also do still not know the optimal dose that should be used, the frequency with which patients should take the medication, and what side effects will be observed with long-term administration."

Dr. Shanafelt and colleagues say more studies are needed to determine these things before they would recommend widespread use by patients. Dr. Shanafelt is also the lead investigator in an ongoing clinical trial sponsored by the National Cancer Institute studying pharmacologic doses of EGCG in pill form for patients with CLL.........

Daniel      Permalink

December 13, 2005

Aspirin May Cut Risk of Esophageal Cancer

Aspirin May Cut Risk of Esophageal Cancer
Aspirin and other nonsteroidal anti-inflammatory drugs, such as ibuprofen, may significantly reduce the risk of esophageal cancer among people with Barrett's esophagus, a premalignant condition associated with chronic heartburn that affects an estimated 1 million to 2 million Americans.

These findings, by Thomas L. Vaughan, M.D., M.P.H., and his colleagues at Fred Hutchinson Cancer Research Center, will appear Nov. 8 in the online edition of The Lancet Oncology. Scientists at Virginia Mason Medical Center in Seattle and The Brigham and Women's Hospital and Harvard Medical School in Boston also collaborated on the study, which was funded by the National Institutes of Health.

In the largest and longest observational study of its kind, lead author Vaughan and his colleagues studied the impact of nonsteroidal anti-inflammatory drugs, or NSAIDs, on changes in the lining of the esophagus that signal the advancement toward cancer.

"We found that people with Barrett's esophagus who regularly took NSAIDs like aspirin or ibuprofen did not go on to get cancer as frequently or as soon as people who did not take these medications regularly," said Vaughan, head of the Epidemiology Program and member of the Hutchinson Center's Public Health Sciences Division. "Current users of NSAIDs had one-third the risk of getting esophageal adenocarcinoma as compared to never users," he said.

Five years after joining the study, the incidence of esophageal cancer was 14.4 percent among never users, 9.7 percent among former users (those who had used NSAIDs regularly for a year or more previous to joining the study) and 6.6 percent among current users (those who took NSAIDs at least once a week).

Because this was a long-term observational study and not a clinical trial, the investigators cannot recommend NSAIDs for people with Barrett's esophagus and they advise anyone who considers taking these medications for this condition should do so under the direction of a physician.........

Sue      Permalink

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