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Fayetteville, NC, February 24, 2017 --( The project, which began in late August 2016, required demolition of the existing space. Renovations to the facility include new acoustical ceiling tiles and grids, new wall coatings, wall protection, doorframes, floor tile and epoxy flooring, updated fire protection, as well as upgrades to the facility’s electrical and plumbing systems. The renovations to the CFVH Lung Nodule Clinic and Oncology Center will improve patient care by enabling the hospital to determine whether a patient’s lung nodule is benign or malignant in a more efficient manner. These diagnoses allow the hospital staff to properly treat lung cancer, giving the hospital an upper hand and another asset in the fight against cancer. Located within the Cape Fear Valley Health System in Fayetteville, the CFVH Lung and Nodule Clinic and Oncology Center will be staffed by pulmonologists, respiratory therapists and nurses. Known for completing projects on time and on budget, Riley Contracting Group has extensive experience with medical and laboratory construction projects in the Triangle, including projects for Duke University Health Systems and WakeMed Health and Hospitals. Most recently, Riley Contracting completed a $1.3M interior fit up for Duke Primary Care Oxford to relocate the family medical clinic to a more convenient location for the community. Quotes: “We’re proud to have been given the opportunity to work with Cape Fear Valley Health, an exceptional hospital serving the Fayetteville and Fort Bragg communities, on this project and other upcoming projects as well,” said Calin Riley, president of Riley Contracting. “The updated facilities will aid Cape Fear Valley’s premiere staff deliver patient-centered care and save lives of those suffering from cancer.” New Media Content: Riley Contracting Group Facebook page: https://www.facebook.com/rileycontgroup Riley Contracting Group Twitter account: https://twitter.com/rileycontgroup Riley Contracting Group LinkedIn page: https://www.linkedin.com/company/riley-contracting-group-inc- About Riley Contracting Group: Riley Contracting Group, Inc. is a team-oriented general contractor that has been building relationships throughout central North Carolina for more than 25 years. Founded in 1987 by Michael G. Riley, the firm specializes in commercial construction for industries including assisted living, biotech and pharmaceutical, retail, healthcare, education, industrial and municipal. Riley Contracting Group serves both the North Carolina and South Carolina markets. Fayetteville, NC, February 24, 2017 --( PR.com )-- Riley Contracting Group, a family-owned, local general contractor serving North Carolina for over 25 years, has completed renovations to the Cape Fear Valley Health (CFVH) Lung Nodule Clinic and Oncology Center, increasing the scope of patient care available at the facility.The project, which began in late August 2016, required demolition of the existing space. Renovations to the facility include new acoustical ceiling tiles and grids, new wall coatings, wall protection, doorframes, floor tile and epoxy flooring, updated fire protection, as well as upgrades to the facility’s electrical and plumbing systems.The renovations to the CFVH Lung Nodule Clinic and Oncology Center will improve patient care by enabling the hospital to determine whether a patient’s lung nodule is benign or malignant in a more efficient manner. These diagnoses allow the hospital staff to properly treat lung cancer, giving the hospital an upper hand and another asset in the fight against cancer.Located within the Cape Fear Valley Health System in Fayetteville, the CFVH Lung and Nodule Clinic and Oncology Center will be staffed by pulmonologists, respiratory therapists and nurses.Known for completing projects on time and on budget, Riley Contracting Group has extensive experience with medical and laboratory construction projects in the Triangle, including projects for Duke University Health Systems and WakeMed Health and Hospitals. Most recently, Riley Contracting completed a $1.3M interior fit up for Duke Primary Care Oxford to relocate the family medical clinic to a more convenient location for the community.Quotes:“We’re proud to have been given the opportunity to work with Cape Fear Valley Health, an exceptional hospital serving the Fayetteville and Fort Bragg communities, on this project and other upcoming projects as well,” said Calin Riley, president of Riley Contracting. “The updated facilities will aid Cape Fear Valley’s premiere staff deliver patient-centered care and save lives of those suffering from cancer.”New Media Content:Riley Contracting Group Facebook page:https://www.facebook.com/rileycontgroupRiley Contracting Group Twitter account:https://twitter.com/rileycontgroupRiley Contracting Group LinkedIn page:https://www.linkedin.com/company/riley-contracting-group-inc-About Riley Contracting Group:Riley Contracting Group, Inc. is a team-oriented general contractor that has been building relationships throughout central North Carolina for more than 25 years. Founded in 1987 by Michael G. Riley, the firm specializes in commercial construction for industries including assisted living, biotech and pharmaceutical, retail, healthcare, education, industrial and municipal. Riley Contracting Group serves both the North Carolina and South Carolina markets. Click here to view the list of recent Press Releases from Riley Contracting


CRANBURY, N.J.--(BUSINESS WIRE)--During his 18 years at FDA, Richard Pazdur, MD, has worked to balance the needs of patients anxious for new cancer cures with the agency’s standards that protect them from harm. In January, Pazdur took on a new role—director of the new Oncology Center of Excellence (OCE), which was borne of the National Cancer Moonshot’s call for greater collaboration among those charged with speeding the arrival of new cancer-fighting products. Pazdur outlines how OCE will function—and how it bring a stronger patient voice to FDA’s decisions—in a special issue of Evidence-Based Oncology,™ (EBO™); the issue features coverage from the spring 2017 Oncology Stakeholders’ Summit, which focused on regulatory issues. “This new center leverages the combined skills of regulatory scientists and reviewers with oncology clinical expertise across the FDA, emulating the multidisciplinary organizational model of academia and cancer care centers and building on the integrative approach to medical product development that the agency’s broader oncology community has embraced over the past decade,” Pazdur writes. Since 2005, when he became director of the Office of Hematology and Oncology Products (OHOP) within FDA, Pazdur has overseen the arrival of faster pathways to approval, which tracked the rise of new treatment methods, including immunotherapy. As he explains, OCE builds on that record but with some key additions. “An important aim of the OCE is to facilitate incorporation of the patient view into regulatory decision-making,” he writes. A key feature of the OCE calls for new submissions to head to a clinical review team that draws from three medical product centers. The team will make recommendations, which will head to Pazdur for review and sign-off. Other aspects of FDA review remain with their traditional centers, he explains. The OCE will embrace new trial designs, with the goal of making research simpler and requiring fewer data points. “These initiatives will allow us to expedite drug development and approval of truly novel agents that will have a major impact on our patients, while allowing us to make thoughtful decisions regarding the risk-benefit of oncology drugs,” Pazdur writes. Pazdur remains the acting director of OHOP while taking on his new role. The American Journal of Managed Care® (AJMC®) is a peer-reviewed, MEDLINE-indexed journal that keeps readers on the forefront of health policy by publishing research relevant to industry decision makers as they work to promote the efficient delivery of high-quality care. AJMC.com is the essential website for managed care professionals, distributing industry updates daily to leading stakeholders. Other titles in the AJMC® family include The American Journal of Accountable Care® and two evidence-based series, Evidence-Based Oncology™ and Evidence-Based Diabetes Management™. These comprehensive offerings bring together stakeholder views from payers, providers, policymakers and other industry leaders in managed care. To order reprints of articles appearing in AJMC® publications, please contact Dr. Jeff Prescott at (609) 716-7777, x331.


LONDON, UK / ACCESSWIRE / May 25, 2017 / Active Wall St. blog coverage looks at the headline from Merck & Co., Inc. (NASDAQ: MRK) as the Company announced that the US Food and Drug Administration (FDA) has granted accelerated approval to a treatment for patients whose cancers have a specific genetic feature (biomarker). This is the first time the agency has approved a cancer treatment based on a common biomarker rather than the location in the body where the tumor originated. Register with us now for your free membership and blog access at: One of Merck & Co.'s competitors within the Drug Manufacturers - Major space, Retrophin, Inc. (NASDAQ: RTRX), posted on May 04, 2017, its financial results for Q1 2017 and also provided a corporate update. AWS will be initiating a research report on Retrophin in the coming days. Today, AWS is promoting its blog coverage on MRK; touching on RTRX. Get all of our free blog coverage and more by clicking on the link below: Keytruda (pembrolizumab) is indicated for the treatment of adult and pediatric patients with unresectable or metastatic solid tumors that have been identified as having a biomarker referred to as microsatellite instability-high (MSI-H), or mismatch repair deficient (dMMR). This indication covers patients with solid tumors that have progressed following prior treatment and who have no satisfactory alternative treatment options and patients with colorectal cancer that has progressed following treatment with certain chemotherapy drugs. Keytruda works by targeting the cellular pathway known as PD-1/PD-L1. By blocking this pathway, Keytruda may help the body's immune system fight the cancer cells. The FDA previously approved Keytruda for the treatment of certain patients with metastatic melanoma, metastatic non-small cell lung cancer, recurrent or metastatic head and neck cancer, refractory classical Hodgkin lymphoma, and urothelial carcinoma. "This is an important first for the cancer community," said Richard Pazdur, M.D., acting director of the Office of Hematology and Oncology Products in the FDA's Center for Drug Evaluation and Research and director of the FDA's Oncology Center of Excellence, "Until now, the FDA has approved cancer treatments based on where in the body the cancer started - for example, lung or breast cancers. We have now approved a drug based on a tumor's biomarker without regard to the tumor's original location." The safety and efficacy of Keytruda for this indication were studied in patients with MSI-H or dMMR solid tumors enrolled in one of five uncontrolled, single-arm clinical trials. In some trials, patients were required to have MSI-H or dMMR cancers, while in other trials, a subgroup of patients were identified as having MSI-H or dMMR cancers by testing tumor samples after treatment began. The review of Keytruda for this indication was based on the percentage of patients who experienced complete or partial shrinkage of their tumors (overall response rate) and for how long (durability of response). Of the 149 patients who received Keytruda in the trials, 39.6% had a complete or partial response. For 78% of those patients, the response lasted for six months or more. The FDA granted this application Priority Review designation, under which the FDA's goal is to take action on an application within six months where the agency determines that the drug, if approved, would significantly improve the safety or effectiveness of treating, diagnosing or preventing a serious condition. Merck also announced that its Board of Directors has declared a quarterly dividend of $0.47 per share of the Company's common stock for Q3 2017. Payment will be made on July 10, 2017, to shareholders of record at the close of business on June 15, 2017. On Wednesday, May 24, 2017, the stock closed the trading session at $64.93, slightly up by 0.59% from its previous closing price of $64.55 with a total volume of 7.04 million shares traded. Merck's stock price surged 4.22% in the last month, 4.22% in the past six months, and 16.78% in the previous twelve months. Furthermore, since the start of the year, shares of the Company have gained 10.29%. The Company's shares are trading at a PE ratio of 41.60 and have a dividend yield of 2.90%. At Wednesday's closing price, the stock's net capitalization stands at $177.90 billion. 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News Article | May 26, 2017
Site: www.chromatographytechniques.com

A team led by Johns Hopkins researchers has discovered a biochemical signaling process that causes densely packed cancer cells to break away from a tumor and spread the disease elsewhere in the body. In their study, published online May 26 in Nature Communications, the team also reported that the combined use of two existing drugs disrupts this process and appears to significantly slow cancer's tendency to travel, a behavior called metastasis. The new findings are important, the researchers said, because 90 percent of cancer deaths are caused by metastasis, and anything that derails this activity could improve the prognosis for patients. The crucial new signaling process turned up when the team took a closer look at cellular events that promote metastasis. "We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor," said lead author Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins' Physical Sciences-Oncology Center. "At a fundamental level, we found that cell density is very important in triggering metastasis. It's like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere." Jayatilaka and her colleagues found a medication mix that kept this microscopic message from being delivered. The team members cautioned that this treatment was tested in animal models, but not yet on human cancer patients. Nevertheless, they said the discovery contributes to a promising new focus for cancer research: disrupting the biochemical activity that prods cancer cells to spread through the body. One of the study's senior authors, Denis Wirtz, who is Johns Hopkins University's vice provost for research and director of its Physical Sciences-Oncology Center, said no commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates. "The pharmaceutical companies view metastasis as a by-product of tumor growth," said Wirtz, who also holds Johns Hopkins faculty appointments in chemical and biomolecular engineering, in pathology and at the Johns Hopkins Kimmel Cancer Center. "Our study looked more closely at the steps that actually initiate metastasis. By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor. This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes." The two key drivers of metastasis, Wirtz said, are cancer cells' tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body. By studying tumor cells in a three-dimensional environment that resembles human tissue, the researchers were able to determine how these activities begin. The team discovered that as two types of cancer cells reproduced and created more crowded conditions in the test site, these cells secreted certain proteins that encouraged migration. The researchers identified these proteins as Interleukin 6 (IL-6) and Interleukin 8 (IL-8). "IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor," said lead author Jayatilaka, who recently earned her doctorate in chemical and biomolecular engineering as a member of Wirtz's lab team and earlier received her undergraduate degree from Johns Hopkins' Whiting School of Engineering. In the team's animal studies, the researchers found that applying two existing drugs--Tocilizumab and Reparaxin--blocked the receptors that enable cancer cells to get their relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer cases. Reparaxin is being evaluated as a possible treatment for breast cancer. "In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased," Jayatilaka said. "We discovered a new signaling pathway that, when blocked, could potentially curb cancer's ability to metastasize."


News Article | May 26, 2017
Site: www.eurekalert.org

A team led by Johns Hopkins researchers has discovered a biochemical signaling process that causes densely packed cancer cells to break away from a tumor and spread the disease elsewhere in the body. In their study, published online May 26 in Nature Communications, the team also reported that the combined use of two existing drugs disrupts this process and appears to significantly slow cancer's tendency to travel, a behavior called metastasis. The new findings are important, the researchers said, because 90 percent of cancer deaths are caused by metastasis, and anything that derails this activity could improve the prognosis for patients. The crucial new signaling process turned up when the team took a closer look at cellular events that promote metastasis. "We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor," said lead author Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins' Physical Sciences-Oncology Center. "At a fundamental level, we found that cell density is very important in triggering metastasis. It's like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere." Jayatilaka and her colleagues found a medication mix that kept this microscopic message from being delivered. The team members cautioned that this treatment was tested in animal models, but not yet on human cancer patients. Nevertheless, they said the discovery contributes to a promising new focus for cancer research: disrupting the biochemical activity that prods cancer cells to spread through the body. One of the study's senior authors, Denis Wirtz, who is Johns Hopkins University's vice provost for research and director of its Physical Sciences-Oncology Center, said no commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates. "The pharmaceutical companies view metastasis as a by-product of tumor growth," said Wirtz, who also holds Johns Hopkins faculty appointments in chemical and biomolecular engineering, in pathology and at the Johns Hopkins Kimmel Cancer Center. "Our study looked more closely at the steps that actually initiate metastasis. By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor. This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes." The two key drivers of metastasis, Wirtz said, are cancer cells' tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body. By studying tumor cells in a three-dimensional environment that resembles human tissue, the researchers were able to determine how these activities begin. The team discovered that as two types of cancer cells reproduced and created more crowded conditions in the test site, these cells secreted certain proteins that encouraged migration. The researchers identified these proteins as Interleukin 6 (IL-6) and Interleukin 8 (IL-8). "IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor," said lead author Jayatilaka, who recently earned her doctorate in chemical and biomolecular engineering as a member of Wirtz's lab team and earlier received her undergraduate degree from Johns Hopkins' Whiting School of Engineering. In the team's animal studies, the researchers found that applying two existing drugs--Tocilizumab and Reparaxin--blocked the receptors that enable cancer cells to get their relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer cases. Reparaxin is being evaluated as a possible treatment for breast cancer. "In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased," Jayatilaka said. "We discovered a new signaling pathway that, when blocked, could potentially curb cancer's ability to metastasize." The other senior authors of the Nature Communications paper were Daniele M. Gilkes of the Oncology and Pathology departments in the Johns Hopkins University School of Medicine and Rong Fan of the Department of Biomedical Engineering at Yale University. Other Johns Hopkins University co-authors were Pranay Tyle, Julia Ju, Hyun Ji Kim and Pei-Hsun Wu. Other co-authors from Yale were Jonathan J. Chen and Minsuk Kwak. Jerry S. H. Lee of the Johns Hopkins Department of Chemical and Biomolecular Engineering and the Center for Strategic Scientific Initiatives at the National Cancer Institute, was also a co-author. This research was supported by National Cancer Institute grants 1U54CA210173-01 and R01CA174388. The Physical Sciences-Oncology Center at Johns Hopkins is based within the university's Institute for NanoBioTechnology.


News Article | May 26, 2017
Site: www.sciencedaily.com

A team led by Johns Hopkins researchers has discovered a biochemical signaling process that causes densely packed cancer cells to break away from a tumor and spread the disease elsewhere in the body. In their study, published online May 26 in Nature Communications, the team also reported that the combined use of two existing drugs disrupts this process and appears to significantly slow cancer's tendency to travel, a behavior called metastasis. The new findings are important, the researchers said, because 90 percent of cancer deaths are caused by metastasis, and anything that derails this activity could improve the prognosis for patients. The crucial new signaling process turned up when the team took a closer look at cellular events that promote metastasis. "We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor," said lead author Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins' Physical Sciences-Oncology Center. "At a fundamental level, we found that cell density is very important in triggering metastasis. It's like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere." Jayatilaka and her colleagues found a medication mix that kept this microscopic message from being delivered. The team members cautioned that this treatment was tested in animal models, but not yet on human cancer patients. Nevertheless, they said the discovery contributes to a promising new focus for cancer research: disrupting the biochemical activity that prods cancer cells to spread through the body. One of the study's senior authors, Denis Wirtz, who is Johns Hopkins University's vice provost for research and director of its Physical Sciences-Oncology Center, said no commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates. "The pharmaceutical companies view metastasis as a by-product of tumor growth," said Wirtz, who also holds Johns Hopkins faculty appointments in chemical and biomolecular engineering, in pathology and at the Johns Hopkins Kimmel Cancer Center. "Our study looked more closely at the steps that actually initiate metastasis. By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor. This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes." The two key drivers of metastasis, Wirtz said, are cancer cells' tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body. By studying tumor cells in a three-dimensional environment that resembles human tissue, the researchers were able to determine how these activities begin. The team discovered that as two types of cancer cells reproduced and created more crowded conditions in the test site, these cells secreted certain proteins that encouraged migration. The researchers identified these proteins as Interleukin 6 (IL-6) and Interleukin 8 (IL-8). "IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor," said lead author Jayatilaka, who recently earned her doctorate in chemical and biomolecular engineering as a member of Wirtz's lab team and earlier received her undergraduate degree from Johns Hopkins' Whiting School of Engineering. In the team's animal studies, the researchers found that applying two existing drugs -- Tocilizumab and Reparaxin -- blocked the receptors that enable cancer cells to get their relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer cases. Reparaxin is being evaluated as a possible treatment for breast cancer. "In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased," Jayatilaka said. "We discovered a new signaling pathway that, when blocked, could potentially curb cancer's ability to metastasize."


News Article | May 26, 2017
Site: www.futurity.org

Scientists now know the biochemical signal that tells crowded cancer cells to break away from tumors and start the deadly migration called metastasis. They also discovered that two existing drugs used in combination can disrupt the process and appear to significantly slow cancer cells’ tendency to travel. The findings are important, researchers say, because metastasis causes 90 percent of cancer deaths, and anything that derails this activity could improve patient outcomes. “We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor,” says Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins University’s Physical Sciences-Oncology Center. “At a fundamental level, we found that cell density is very important in triggering metastasis. It’s like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere,” says Jayatilaka, lead author of the study in the journal Nature Communications. The two key drivers of metastasis are cancer cells’ tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body. Studying tumor cells in a 3D environment that resembles human tissue, the researchers were able to determine how the cancer migration begins. As two types of cancer cells reproduced and created more crowded conditions in the test site, they secreted proteins identified as Interleukin 6 and Interleukin 8. “IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor,” says Jayatilaka, who recently earned her doctorate at Johns Hopkins in chemical and biomolecular engineering. No commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates, says senior author Denis Wirtz, professor of chemical and biomolecular engineering, materials science, pathology and oncology and director of the Physical Sciences-Oncology Center. “The pharmaceutical companies view metastasis as a by-product of tumor growth. Our study looked more closely at the steps that actually initiate metastasis.” Animal studies show that combining two existing drugs—Tocilizumab and Reparaxin—blocks the receptors where cancer cells get their chemical relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer. Reparaxin is being evaluated as a possible treatment for breast cancer. “In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased,” Jayatilaka says. “We discovered a new signaling pathway that, when blocked, could potentially curb cancer’s ability to metastasize.” The researchers caution that the treatment was tested in animal models and appears promising, but has not yet been tried on human cancer patients. Other members of the team were from Johns Hopkins, Yale University, and the National Cancer Institute. Funding came from the NCI.


News Article | May 26, 2017
Site: www.chromatographytechniques.com

A team led by Johns Hopkins researchers has discovered a biochemical signaling process that causes densely packed cancer cells to break away from a tumor and spread the disease elsewhere in the body. In their study, published online May 26 in Nature Communications, the team also reported that the combined use of two existing drugs disrupts this process and appears to significantly slow cancer's tendency to travel, a behavior called metastasis. The new findings are important, the researchers said, because 90 percent of cancer deaths are caused by metastasis, and anything that derails this activity could improve the prognosis for patients. The crucial new signaling process turned up when the team took a closer look at cellular events that promote metastasis. "We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor," said lead author Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins' Physical Sciences-Oncology Center. "At a fundamental level, we found that cell density is very important in triggering metastasis. It's like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere." Jayatilaka and her colleagues found a medication mix that kept this microscopic message from being delivered. The team members cautioned that this treatment was tested in animal models, but not yet on human cancer patients. Nevertheless, they said the discovery contributes to a promising new focus for cancer research: disrupting the biochemical activity that prods cancer cells to spread through the body. One of the study's senior authors, Denis Wirtz, who is Johns Hopkins University's vice provost for research and director of its Physical Sciences-Oncology Center, said no commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates. "The pharmaceutical companies view metastasis as a by-product of tumor growth," said Wirtz, who also holds Johns Hopkins faculty appointments in chemical and biomolecular engineering, in pathology and at the Johns Hopkins Kimmel Cancer Center. "Our study looked more closely at the steps that actually initiate metastasis. By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor. This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes." The two key drivers of metastasis, Wirtz said, are cancer cells' tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body. By studying tumor cells in a three-dimensional environment that resembles human tissue, the researchers were able to determine how these activities begin. The team discovered that as two types of cancer cells reproduced and created more crowded conditions in the test site, these cells secreted certain proteins that encouraged migration. The researchers identified these proteins as Interleukin 6 (IL-6) and Interleukin 8 (IL-8). "IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor," said lead author Jayatilaka, who recently earned her doctorate in chemical and biomolecular engineering as a member of Wirtz's lab team and earlier received her undergraduate degree from Johns Hopkins' Whiting School of Engineering. In the team's animal studies, the researchers found that applying two existing drugs--Tocilizumab and Reparaxin--blocked the receptors that enable cancer cells to get their relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer cases. Reparaxin is being evaluated as a possible treatment for breast cancer. "In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased," Jayatilaka said. "We discovered a new signaling pathway that, when blocked, could potentially curb cancer's ability to metastasize."


"This is an important first for the cancer community," said Richard Pazdur, M.D., acting director of the Office of Hematology and Oncology Products in the FDA's Center for Drug Evaluation and Research and director of the FDA's Oncology Center of Excellence. "Until now, the FDA has approved cancer treatments based on where in the body the cancer started—for example, lung or breast cancers. We have now approved a drug based on a tumor's biomarker without regard to the tumor's original location." MSI-H and dMMR tumors contain abnormalities that affect the proper repair of DNA inside the cell. Tumors with these biomarkers are most commonly found in colorectal, endometrial and gastrointestinal cancers, but also less commonly appear in cancers arising in the breast, prostate, bladder, thyroid gland and other places. Approximately 5 percent of patients with metastatic colorectal cancer have MSI-H or dMMR tumors. Keytruda works by targeting the cellular pathway known as PD-1/PD-L1 (proteins found on the body's immune cells and some cancer cells). By blocking this pathway, Keytruda may help the body's immune system fight the cancer cells. The FDA previously approved Keytruda for the treatment of certain patients with metastatic melanoma, metastatic non-small cell lung cancer, recurrent or metastatic head and neck cancer, refractory classical Hodgkin lymphoma, and urothelial carcinoma. Keytruda was approved for this new indication using the Accelerated Approval pathway, under which the FDA may approve drugs for serious conditions where there is unmet medical need and a drug is shown to have certain effects that are reasonably likely to predict a clinical benefit to patients. Further study is required to verify and describe anticipated clinical benefits of Keytruda, and the sponsor is currently conducting these studies in additional patients with MSI-H or dMMR tumors. The safety and efficacy of Keytruda for this indication were studied in patients with MSI-H or dMMR solid tumors enrolled in one of five uncontrolled, single-arm clinical trials. In some trials, patients were required to have MSI-H or dMMR cancers, while in other trials, a subgroup of patients were identified as having MSI-H or dMMR cancers by testing tumor samples after treatment began. A total of 15 cancer types were identified among 149 patients enrolled across these five clinical trials. The most common cancers were colorectal, endometrial and other gastrointestinal cancers. The review of Keytruda for this indication was based on the percentage of patients who experienced complete or partial shrinkage of their tumors (overall response rate) and for how long (durability of response). Of the 149 patients who received Keytruda in the trials, 39.6 percent had a complete or partial response. For 78 percent of those patients, the response lasted for six months or more. Common side effects of Keytruda include fatigue, itchy skin (pruritus), diarrhea, decreased appetite, rash, fever (pyrexia), cough, difficulty breathing (dyspnea), musculoskeletal pain, constipation and nausea. Keytruda can cause serious conditions known as immune-mediated side effects, including inflammation of healthy organs such as the lungs (pneumonitis), colon (colitis), liver (hepatitis), endocrine glands (endocrinopathies) and kidneys (nephritis). Complications or death related to allogeneic hematopoietic stem cell transplantation after using Keytruda has occurred. Patients who experience severe or life-threatening infusion-related reactions should stop taking Keytruda. Women who are pregnant or breastfeeding should not take Keytruda because it may cause harm to a developing fetus or newborn baby. The safety and effectiveness of Keytruda in pediatric patients with MSI-H central nervous system cancers have not been established. The FDA granted this application Priority Review designation, under which the FDA's goal is to take action on an application within six months where the agency determines that the drug, if approved, would significantly improve the safety or effectiveness of treating, diagnosing or preventing a serious condition. The FDA granted accelerated approval of Keytruda to Merck & Co. For more information: FDA: Office of Hematology and Oncology Products  FDA: Approved Drugs: Questions and Answers  FDA: Fast Track, Breakthrough Therapy, Accelerated Approval, Priority Review The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation's food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/fda-approves-first-cancer-treatment-for-any-solid-tumor-with-a-specific-genetic-feature-300462731.html


News Article | February 21, 2017
Site: www.eurekalert.org

In order for cancer to spread, malignant cells must break away from a tumor and through the tough netting of extracellular matrix, or ECM, that surrounds it. To fit through the holes in this net, those cancerous cells must elongate into a torpedo-like shape. Researchers from the University of Pennsylvania and The Wistar Institute have now found that physical forces exerted between these cells and the ECM are enough to drive this shape change. Those forces converge on an optimal stiffness that allows cancer cells to spread. The findings, published in the Proceedings of the National Academy of Sciences, suggest that drugs that target the stiffness of the ECM could potentially be used to prevent metastasis. he study was led by Vivek Shenoy, professor in the Department of Materials Science and Engineering in Penn's School of Engineering and Applied Science, and Hossein Ahmadzadeh, a graduate student in his lab, with contributions from Ashani Weeraratna, the Ira Brind Associate Professor and program leader of the Tumor Microenvironment and Metastasis Program at Wistar. Research on the physical-feedback mechanisms between cancer cells and their environment is part of Penn Engineering's larger efforts to understand such dynamics, housed at the Physical Sciences Oncology Center and the new Center for Engineering Mechanobiology, which is co-directed by Shenoy. Shenoy and colleagues published findings that detailed the feedback mechanism exhibited by cancer cells and the ECM surrounding them. There, they showed how this mechanism stiffens and aligns the collagen fibers found in ECM. The new work looks at the cell side of the equation and how cells must switch from rounded to elongated in order to leave the tumor squeeze through the ECM. "What we're showing is that the mechanical factors alone can lead to the change in phenotype in cancer cells," Shenoy said. "This is the first quantitative analysis of the shapes of cancer cells as they invade from the tumor." The Penn researchers postulated that the key factor of this interplay is finding a "sweet spot" in the stiffness of the ECM. "The cells in a tumor are sticky," Shenoy said. "Without the collagen fibers of the ECM pulling on those cells, you can't break that cell-cell adhesion. But, if the ECM is too stiff, the pores in the matrix become too narrow and the cells can't escape." After the Penn team modeled these interactions in computer simulations, the Weeraratna lab at Wistar conducted matching experiments to see if the results held up. "We used melanoma spheroids embedded in a collagen matrix as a 3-D model to mimic in vitro what happens in the body when tumor cells leave the primary tumor to invade other tissues," said Weeraratna. "Our observations perfectly matched and complemented the computer model. This study reaffirms, from a mechanobiology standpoint, the crucial role of the tumor microenvironment in orchestrating the fate of cancer cells and dictating prognosis and response to therapy." Insights from cancer mechanobiology could inform future diagnostics and potentially even treatments. "The takeaway is that, if you look at what's going on outside the tumor, you could make a prognosis of whether it will spread," Shenoy said. Co-authors of this study include Marie R. Webster and Reeti Behera of Wistar and Angela M. Jimenez Valencia and Denis Wirtz of Johns Hopkins University. This work was supported by National Cancer Institute grants U01CA202177, U54CA193417 and U54CA210173; National Institutes of Health grants R01EB017753, R01CA174746 and K99 CA208012-01; and National Science Foundation grant CMMI-1548571. Core support for The Wistar Institute was provided by the Cancer Center Support Grant P30CA010815.

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