Discovery Could Lead To Novel Drugs To Prevent Cancer Metastasis

A Loyola University Chicago Stritch School of Medicine study has revealed details of the complex molecular process involving a protein that enables cancer cells to establish tumors in distant parts of the body.

The finding could lead the way to new drugs to prevent breast cancer and other cancers from spreading to new sites.

The study by Adriano Marchese, PhD, and colleagues is published in the March 16 issue of the Journal of Biological Chemistry.

The study involves a molecule on the surface of cells called CXCR4. There is an abnormal abundance of this molecule in 23 types of cancer, including cancers of the breast, lung, pancreas and thyroid.

What usually kills patients is the spread of cancer from the primary site to other sites. A tumor cell breaks away from the primary site and circulates through the body. A molecule called CXCL12 acts like a beacon to CXCR4, signaling the cancer cell to land and start a new tumor.

The goal of the study was to better understand this complex signaling pathway. (A signaling pathway involves a group of molecules that work together in a cell. After the first molecule in the pathway receives a signal, it activates another molecule, and the process is repeated until the last molecule is activated.)

"We understand the final outcome of this signaling pathway," Marchese said. "What we are trying to do now is understand the molecular details."

In the study, Marchese and colleagues used a line of human cancer cells called HeLa. (The cell line is the subject of the best-selling book "The Immortal Life of Henrietta Lacks".)

Using HeLa cancer cells, the researchers identified a molecule that is a critical link in the signaling pathway. Researchers hope to target this molecule, thereby disabling the signaling pathway and preventing the cancer cell from setting up shop in a new site, Marchese said.

The next step will be to develop a drug that blocks the target molecule. Researchers then would test the drug on an animal model. If the drug worked in animals, it later could be tested in a clinical trial of cancer patients, Marchese said.

"We are laying the groundwork for the development of new drugs to stop cancer from spreading," Marchese said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. Marchese is an associate professor in the Department of Molecular Pharmacology and Therapeutics of Loyola University Chicago Stritch School of Medicine. His co-authors are Rohit Malik, PhD (first author); Unice J.K. Soh, PhD; and JoAnn Trejo, PhD.
The study was supported by a grant from the National Institutes of Health. Malik was supported by a predoctoral fellowship from the American Heart Association. He graduated in December 2011 and is doing postdoctoral training at the University of Michigan.
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HRT With Estrogen Added Raises Breast Cancer Risk

According to a study published March 15 in the Journal of the National Cancer Institute, thoughts about how estrogen alone or estrogen in addition to progestin influence the risk of developing breast cancer has considerably changed in the past 10 years due to results from the Women's Health Initiative (WHI) randomized placebo-controlled hormone therapy trials, and from large prospective cohort studies.

At present, concerns are still being raised regarding hormone therapy-induce breast cancer risk, even though the therapy is used for menopausal symptoms by millions of women. Furthermore, researchers are still not clear on the effects of estrogen in addition to progestin vs estrogen alone on breast cancer.

Rowan T. Chlebowski, M.D., Ph.D., of the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center and Garnet Anderson, Ph.D., at Fred Hutchinson Cancer Research Center, examined data from 2 randomized, placebo-controlled clinical trials carried out in the WHI, in order to examine the effects of estrogen in addition progestin vs estrogen alone on the risk of developing breast cancer.

The first study assessed estrogen alone in post-menopausal women with prior hysterectomy, and the second study assessed estrogen plus progestin in post-menopausal women who had not undergone hysterectomy.

The researchers found that the risk of developing breast cancer was statistically considerably increased by using estrogen in addition to progestin, while the risk was statistically significantly decreased in post-menopausal women with previous hysterectomy who took estrogen alone.

According to the researchers, findings from the randomized human trial and those from the majority of observational studies differ, with the observational studies indicating that both estrogen alone and estrogen plus progestin increase the risk of developing breast cancer.

The researchers explain that:

"An imbalance in the use of mammography with greater screening for hormone users could explain some of the increase in breast cancer incidence with estrogen alone seen in cohort studies because screened populations have more cancers detected than unscreened populations."

Even though the authors do not fully understand the mechanisms underlying the different effects of estrogen alone and estrogen in addition to progestin, they said:

"The findings in the clinic, taken together with preclinical evidence, indicate that many breast cancers in post-menopausal women can survive only a limited range of estrogen exposures."

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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Pancreatic Cancer Action Network, AACR Pathway To Leadership Grants

The Pancreatic Cancer Action Network and the American Association for Cancer Research have awarded Stephanie K. Dougan, Ph.D., postdoctoral fellow at the Whitehead Institute for Biomedical Research, and Oliver G. McDonald, M.D., Ph.D., postdoctoral fellow at Johns Hopkins University, the 2012 Pancreatic Cancer Action Network-AACR Pathway to Leadership Grants.

These five-year grants, each providing $600,000 in research funding, will be formally awarded at the AACR Annual Meeting 2012, held here March 31 - April 4.

"With the partnership of the Pancreatic Cancer Action Network, we are able to provide these grants to encourage gifted, young researchers such as Dr. Dougan and Dr. McDonald to pursue their research endeavors and advance the field," said Margaret Foti, Ph.D., M.D. (h.c.), chief executive officer of the American Association for Cancer Research. "Their projects have the potential to lead to breakthroughs that better prevent, detect and treat pancreatic cancer."

"As the Pancreatic Cancer Action Network works diligently to double the survival rate of pancreatic cancer by 2020, it is critical that we fund the very best science and brightest minds to ensure scientific progress is made. We are honored to welcome Drs. Dougan and McDonald to the team and to our robust community of pancreatic cancer researchers," stated Lynn Matrisian, Ph.D., Pancreatic Cancer Action Network's vice president of scientific and medical affairs. "We look forward to interacting with Drs. Dougan and McDonald and trust that the Pathway to Leadership Grant will accelerate progress toward improved patient outcomes."

The Pathway to Leadership Grant, intended for postdoctoral or clinical research fellows, parallels the highly coveted K99/R00 early-career investigator awards offered by the National Institutes of Health. It provides financial support for two years of mentored research followed by three years of independent research.

The goals of the Pancreatic Cancer Action Network - AACR grants program are to build a robust pancreatic cancer research community; to encourage collaboration, information-sharing and innovation; and to expedite scientific and medical breakthroughs for patient benefit.

Funding decisions for the Pathway to Leadership Grant are made by a stellar committee of experts in pancreatic cancer using a rigorous and transparent process. In addition to receiving research funds, grant recipients are provided with career development opportunities. These include mentorships and connections with senior scientists in the field; invitations to present at scientific sessions, lead conference workshops, and participate in training and educational webinars; involvement with pancreatic cancer survivors and their caregivers; and resources to keep them apprised of emerging developments in the field.

2012 Pathway to Leadership Grant Recipients:

Stephanie K. Dougan, Ph.D.

Dougan's research, "Transnuclear mice: Understanding the T cell response to pancreatic cancer," proposes to generate an innovative mouse model (called TN) of pancreatic cancer with alterations to the immune system. In this TN mouse model, cytotoxic (or killer) T cells of the immune system will be programmed to recognize a protein present in pancreatic cancer cells, mesothelin. The mice will also allow Dougan to investigate the balance between cytotoxic T cells trained to attack pancreatic cancer and regulatory T cells that would otherwise impede the immune response.

Dougan believes that immunotherapy represents a very attractive approach for pancreatic cancer treatment. Through the creation of TN mice, Dougan aims to identify mechanisms to inhibit the immunosuppressive regulatory T cell response, in turn resulting in an increased population of cytotoxic T cells and a heightened immune response generated against the cancer.

"This novel approach will not only generate many lines of useful mouse models, but also identify the specificity of regulatory T cells for the first time, and may help address why these cells home so readily to pancreatic tumors and block the body's innate immune response to the tumor," Dougan said. "Such information will allow us to create targeted therapies to suppress or eliminate regulatory T cells specifically while promoting cytotoxic T cell function."

This research will serve as the foundation of Dougan's independent research program.

Dougan's grant is supported by Celgene Corporation.

Oliver G. McDonald, M.D., Ph.D.

McDonald's research, "Genome-wide epigenetic reprogramming during evolution of pancreatic cancer," will investigate non-sequence related genetic or epigenetic events that induce cellular changes necessary for the onset and eventual metastasis (spread) of human pancreatic cancer.

Previous studies conducted by McDonald and colleagues have mapped the function of various epigenetic modifications that accompany pivotal cellular changes. For example, normal cells of the pancreas would not have the ability to depart the pancreas or survive in the bloodstream, but cancer cells are able to adopt these characteristics. Such modifications represent survival mechanisms exhibited by cancer cells as these epigenetic changes facilitate cell movement necessary for metastasis, as well as chemotherapeutic resistance. By understanding the nature of such modifications and the mechanisms involved in their establishment, McDonald and his colleagues hope to identify key regulators of pancreatic cancer reprogramming, metastasis and resistance to chemotherapy.

"These seminal studies will provide unprecedented insights into epigenetic reprogramming during pancreatic cancer evolution," said McDonald. "The findings will have far-reaching implications, and will pave the way for development of novel diagnostics and therapeutics for pancreatic cancer."

McDonald's research is supported by The Daniel and Janet Mordecai Foundation.

Article adapted by Medical News Today from original press release.
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09.20 | 0 komentar

Obesity Increases The Risk For Colorectal Cancer And Polyps

The American College of Gastroenterology (ACG) and the Campaign to End Obesity (CEO) are joining forces to highlight the potentially deadly link between higher Body Mass Index (BMI) and colorectal cancer. In light of the increasing prevalence of obesity in the United States and the strength of the scientific evidence linking obesity to increased colorectal cancer risk, the two organizations are combining efforts during March Colorectal Cancer Awareness Month. Their goal is to educate the public about obesity as a major risk factor for the second leading cancer killer in the United States and about the importance of colorectal cancer screening in patients with high Body Mass Index.

"Dietary and other modifiable risk factors may account for as many as 90 percent of colorectal cancers, and recent studies suggest that about one-quarter of colorectal cancer cases could be avoided by following a healthy lifestyle," explained ACG President Lawrence R. Schiller, MD, FACG. "Consumers need to understand the link between a higher Body Mass Index and colorectal cancer, take this risk factor seriously, and talk to their doctor about colorectal cancer tests," he added.

"Obesity is the precursor to an array of serious diseases, among them colorectal cancer. With two thirds of adults struggling with being overweight or obese, it is essential people understand their long-term health. Fortunately, we have available many useful and practical tools to help people. Screening is one of the most powerful weapons at-hand for preventing colorectal cancer and obesity. Education around these issues is of utmost importance," said Stephanie Silverman, co-founder of the Campaign to End Obesity.

The association between metabolic syndrome and colorectal cancer mortality, and type 2 diabetes mellitus and colorectal cancer risk, suggests that obesity-induced insulin resistance and hyperinsulinemia may have a role in the development of colorectal cancer. Based on this and other epidemiologic evidence, the American College of Gastroenterology and the Campaign to End Obesity are committed to providing communities, families, educators and policymakers with the latest information, educational tools and resources to empower them to make informed and timely decisions when it comes to healthy body weight and colorectal cancer prevention strategies.

Article adapted by Medical News Today from original press release.
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Surprising Connection Between Breast Cancer Cells And Surrounding Tissue

Rensselaer Polytechnic Institute Biologist Lee Ligon has found a previously unknown connection between breast cancer tumor cells and the surrounding healthy tissue. The results provide new information on the earliest stages of breast cancer metastasis.

The results were published in the journal PLoS One, in a paper titled " Cadherin-23 Mediates Heterotypic Cell-Cell Adhesion between Breast Cancer Epithelial Cells and Fibroblasts." Ligon was joined in the research by Rensselaer doctoral student Maria Apostolopoulou. The research was funded by the American Cancer Society.

The research shows that a specialized type of molecule called Cadherin-23 can be found in and around breast cancer tumors. The molecule, which had never been associated with breast tissue or cancer, helps connect cancerous tumor cells to its neighboring healthy tissue, called the stroma.

"Something happens once cancerous cells enter the stroma and the cancer can very quickly become invasive," Ligon said. "Pathologists studying cancerous tissues have often noted that tumor cells make contact with the cells in the stroma, but they assumed the connections were unimportant."

Ligon and her team sought to uncover exactly what molecules were involved in attaching the tumor cells to the surrounding tissue to determine if those initial points of contact play a role in the progression of cancer through the body.

In the human breast, tumors most often originate in what are known as epithelial tissues. These tissues are made up of a specialized type of cell called epithelial cells. Epithelial cells line the interior of many structures and organs within the human body. In the breast, they line the interior of milk ducts. When epithelial cells start to divide uncontrollably, they eventually break out of the duct and literally spill into the surround tissue or stroma. The stroma is comprised of cells called fibroblasts and extracellular material such as collagen fibers. In many cases, the invading cancerous epithelial cells will glom onto nearby fibroblasts in the stroma.

Ligon and Apostolopoulou worked to pick apart how the epithelial cells attached themselves to the fibroblasts. One of the primary tools the body uses to glue cells together is a family of molecules called cadherins. In the human genome there are over 80 different cadherin family members. In most cases, cadherins stick two cells of the same type together. In the case of the breast cancer tumor cells and fibroblasts, two very different cells were sticking together. Ligon sought to determine which cadherins were involved in this odd interaction.

At first, their findings were not surprising. They found cadherins associated with epithelial cells as well as cadherins associated with fibroblasts. It was the discovery of the highly specialized and unusual cadherin, Cadherin-23, that really surprised them, according to Ligon.

"Cadherin-23 has never before been associated with cancer," Ligon said. "In fact, it has previously only been shown in the sophisticated inner workings of the ear and retina."

It is still largely unknown what happens once the cells have made a connection, but the appearance of Cadherin-23 in elevated levels in cancerous tissues suggests that it might play a real role in the earliest stages of metastasis, according to Ligon. Cadherin-23 is a new and potentially very important new component in the progression of cancer for scientists to investigate, she said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. Ligon is a member of the Center for Biotechnology and Interdisciplinary Studies and the Department of Biology at Rensselaer.
Published March 14, 2012
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12.13 | 0 komentar

New Guidelines For Cervical Cancer Screening

Women ages 21 to 65 should have a Pap smear every three years, according to new guidelines from the United States Preventive Services Task Force (USPSTF). Based on the evidence, women between the ages of 30 and 65 can safely extend the screening interval to once every five years if they undergo the humanpapillomavirus (HPV) test at the same time as the Pap. The guideline is being published early online in Annals of Internal Medicine.
The USPSTF recommends against screening for cervical cancer in women younger than 21, as there is adequate evidence that screening in this population, regardless of sexual history, provides no reduction in cervical cancer incidence and mortality. Women older than 65 who have had adequate prior screening and are not otherwise at high risk also do not need screening.
"This is good news for women because evidence shows that an annual Pap smear is not necessary to prevent deaths from cervical cancer," said Task Force Chair, Virginia Moyer, MD, MPH, Professor of Pediatrics, Baylor Medical College. "Screening every three years starting at age 21 saves the same number of lives as annual screening, but with half the number of colposcopies and fewer false-positive tests."
Since releasing a draft recommendation in October 2011, new evidence became available about the role of HPV testing in cervical cancer screening. The Task Force reviewed the evidence and now recommends HPV screening in combination with the Pap for women aged 30 and 65. If HPV testing is done at the same time as the Pap, women can extend their screening interval to five years. The Task Force does not recommend HPV screening in women under the age of 30, as the infection is prevalent in younger women and often clears up on its own.
According to the Center for Disease Control and Prevention, women aged 30 years old and older who have had a normal Pap result have a very low chance of getting cervical cancer in the next few years. This information supports the wisdom of extended screening intervals for cervical cancer. However, women should not skip regular check-ups.
According to the Task Force guidelines, women who have had a hysterectomy with removal of the cervix and who do not have a history of cervical cancer or a high-grade precancerous lesion do not need to be screened. In this population, there is high certainty that harms of screening outweigh the benefits.
Women over the age of 65 can end screening if they have had three consecutive negative Pap smears or two consecutive negative co-tests within 10 years before cessation of screening, with the last test occurring within five years. Routine screening should continue at least 20 years after spontaneous regression or appropriate management of high-grade precancerous lesion, regardless of the patient's age. Physicians should consider cervical cancer screening in women over the age of 65 who have never been screened.
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cervical cancer / hpv vaccine section for the latest news on this subject. Full text of the guidelines are available free to the public at http://www.annals.org/.
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07.35 | 0 komentar