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Posts Tagged ‘American Cancer Society’


Aspirin a Day Tied to Lower Cancer Mortality

Reporter: Aviva Lev-Ari, PhD, RN

Aspirin a Day Tied to Lower Cancer Mortality

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Daily aspirin use is associated with a modest decrease in mortality from cancer, particularly for malignancies of the gastrointestinal tract, a large retrospective study confirmed.

Individuals who were current daily users for 5 years or more at baseline had an 8% decrease in cancer mortality compared with non-users (RR 0.92, 95% CI 0.83 to 1.02), according to Eric J. Jacobs, PhD, and colleagues from the American Cancer Society in Atlanta.

The association was stronger, with a 16% decrease for those with daily use for 5 years or more, when the analysis included data collected periodically during 2 decades of follow-up (RR 0.84, 95% CI 0.75 to 0.95), the researchers reported in the Journal of the National Cancer Institute.

A recent pooled analysis of more than 50 trials involving aspirin use for cardioprotection found a 37% reduction in deaths from cancer among users, which was considerably greater than in observational studies and trials of alternate-day aspirin.

To clarify the magnitude of the association between aspirin use and overall cancer mortality, Jacobs and colleagues analyzed data from the Cancer Prevention Study II, which began in 1992 and included 100,139 participants who completed questionnaires with information on demographics, medical history, and behavioral influences.

Beginning in 1997, participants also provided information about aspirin use, and continued to provide updates every 2 years.

The 1997 questionnaire was considered the baseline for the analysis, at which time 23.8% of participants were using either low-dose or adult-strength aspirin.

More than half of participants were older than 60 and female, and almost all were white.

During the 20 years of follow-up, there were 5,138 deaths from cancer.

Among those who reported aspirin use in 1997, three-quarters said they were still taking it in 2003, while among those who were non-users at baseline, 25% had begun doing so.

Baseline aspirin users tended to be more educated, former smokers, and obese, as well as to have a history of cardiovascular disease and diabetes.

Male users also were more likely to have a history of prostate specific antigen (PSA) testing, and women users were more likely to have a history of mammography.

Overall mortality was slightly lower even for individuals who had been users for less than 5 years (RR 0.84, 95% CI 0.76 to 0.94).

Relative risks were similar for users of low-dose and full-strength aspirin, and for those with and without a history of cardiovascular disease, ranging from 0.82 (95% CI 0.72 to 0.91) to 0.95 (95% CI 0.86 to 1.04).

Current users who had never smoked had considerably lower mortality (RR 0.68, 95% CI 0.57 to 0.81), a reduction that was not seen for former smokers (RR 0.92, 95% CI 0.82 to 1.04) or those currently smoking (RR 0.91, 95% CI 0.70 to 1.19).

Even after discounting lung cancer deaths, the only lower mortality among aspirin users was for never-smokers (RR 0.67, 95% CI 0.56 to 0.81).

A possible explanation for the lack of effect on cancers other than those in the lung among ever-smokers is that smoking may attenuate the antiplatelet activity of aspirin, and activated platelets are thought to promote tumor metastases, the researchers explained.

Aspirin use at the 1997 baseline was not significantly associated with mortality from specific cancers, but differences were seen when data through 2008 were included in the analysis:

  • Cancers within the gastrointestinal tract, RR 0.61 (95% CI 0.44 to 0.84)
  • Cancers outside the gastrointestinal tract, RR 0.88 (95% CI 0.78 to 1)
  • Colorectal cancer, OR 0.64 (95% CI 0.42 to 0.98)
  • Esophageal and stomach cancer, RR 0.56 (95% CI 0.37 to 0.86)

“The reduction in overall cancer mortality was driven by both a substantial reduction in mortality from gastrointestinal tract cancers and a small, but statistically significant, reduction in mortality from cancers outside the gastrointestinal tract,” they stated.

They noted that their study was observational, which was an important limitation, in that confounding factors could have resulted in either an underestimate or an overestimate of the effects of aspirin on mortality.

Also, the absolute risk for cancer mortality between non-users and daily long-term aspirin users — approximately 100 per 100,000 person-years for men and about 40 per 100,000 person-years for women — would represent an important benefit of aspirin use if it were causal, the authors stated.

“However, even if causal, differences in absolute rates are likely to differ between our predominantly elderly population and younger populations at much lower risk of cancer mortality,” they warned.

They concluded that the “relatively modest benefit” seen in their analysis could “meaningfully influence the balances of risks and benefits of prophylactic aspirin use.”

In an accompanying editorial, John Baron, MD, of the University of North Carolina in Chapel Hill, offered a word of caution. Baron was the lead author of the meta-analysis on aspirin use and cancer risk.

“Just because aspirin is effective does not mean it necessarily should be used,” he argued.

“Aspirin is a real drug, with definite toxicity. As for any preventative intervention, the benefits must be balanced against the risks, particularly when the benefits are delayed whereas the risks are not,” Baron stated.

The American Cancer Society funds the Cancer Prevention Study II cohort.

The authors are employees of the American Cancer Society.

Editorialist Baron has been a consultant for Bayer, and holds a use patent for aspirin chemoprevention.

Primary source: Journal of the National Cancer Institute
Source reference:
Jacobs E, et al “Daily aspirin use and cancer mortality in a large US cohort” JNCI 2012; DOI: 10.1093/jnci/djs318.

Additional source: Journal of the National Cancer Institute
Source reference:
Baron JA, et al “Aspirin and cancer: trials and observational studies” JNCI 2012; DOI: 10.1093/jnci/djs318.

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UPDATED on 2/25/2019

https://www.medpagetoday.com/cardiology/prevention/78202?xid=nl_mpt_SRCardiology_2019-02-25&eun=g99985d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=CardioUpdate_022519&utm_term=NL_Spec_Cardiology_Update_Active

Painkiller celecoxib (Celebrex) unexpectedly was linked to aortic stenosis in an observational study and in vitro experiments showing a possible mechanism of dystrophic calcification of aortic valve interstitial cells. (JACC: Basic to Translational Science)

Commonly Used Painkillers May Protect Against Skin Cancer

Reporter: Prabodh Kandala, PhD

A new study suggests that aspirin and other similar painkillers may help protect against skin cancer. Published early online in CANCER, a peer-reviewed journal of the American Cancer Society, the findings indicate that skin cancer prevention may be added to the benefits of these commonly used medications.

Previous studies suggest that taking nonsteroidal anti-inflammatory drugs, or NSAIDs, which include aspirin, ibuprofen, and naproxen, as well as a variety of other nonprescription and prescription drugs, can decrease an individual’s risk of developing some types of cancer. Sigrún Alba Jóhannesdóttir, BSc, of Aarhus University Hospital in Denmark, and her colleagues looked to see if the medications might decrease the risk of the three major types of skin cancer: basal cell carcinoma, squamous cell carcinoma, and malignant melanoma.

The researchers analyzed medical records from northern Denmark from 1991 through 2009 and identified 1,974 diagnoses of squamous cell carcinoma, 13,316 diagnoses of basal cell carcinoma, and 3,242 diagnoses of malignant melanoma. They compared information, including prescription data, from these patients with information from 178,655 individuals without skin cancer.

Individuals who filled more than two prescriptions for NSAIDs had a 15 percent decreased risk for developing squamous cell carcinoma and a 13 percent decreased risk for developing malignant melanoma than those who filled two or fewer prescriptions for the medications, especially when the drugs were taken for seven or more years or taken at high intensity. Individuals who took NSAIDs did not seem to benefit from a reduced risk of developing basal cell carcinoma in general, although they did have a 15 percent and 21 percent reduced risk of developing this type of cancer on less-exposed sites (body areas other than the head and neck) when they took them long term or at high intensity, respectively.

“We hope that the potential cancer-protective effect of NSAIDs will inspire more research on skin cancer prevention,” said Ms. Jóhannesdóttir. “Also, this potential cancer-protective effect should be taken into account when discussing benefits and harms of NSAID use.”

Ref:

http://www.sciencedaily.com/releases/2012/05/120529073847.htm

http://onlinelibrary.wiley.com/doi/10.1002/cncr.27406/abstract;jsessionid=5D858902700DB3FF54D77A74AD38E905.d01t04

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Reporter: Prabodh Kandala, PhD

A study from Massachusetts General Hospital (MGH) researchers suggests that specific populations of tumor cells have different roles in the process by which tumors make new copies of themselves and grow. In their report in the May 15 issue of Cancer Cell, researchers identify a tumor-propagating cell required for the growth of a pediatric muscle tumor in a zebrafish model and also show that another, more-differentiated tumor cell must first travel to sites of new tumor growth to prepare an environment that supports metastatic growth.

“Most investigators have thought that tumor-propagating cells — what are sometimes called cancer stem cells — must be the first colonizing cells that travel from the primary tumor to start the process of local invasion and metastasis, but in this model, this is simply not the case,” says David Langenau, PhD, of the MGH Department of Pathology and Center for Cancer Research, who led the study. “Instead, the colonizing cells lack the ability to divide and instead prime newly infiltrated regions for the eventual recruitment of slow-moving cancer stem cells. It will be important to test how broadly this phenomenon is found in a diversity of animal and human cancers.”

Langenau’s team has long been using zebrafish to study rhabdomyosarcoma (RMS), an aggressive pediatric cancer. In embryonic zebrafish, RMS can develop within 10 days, and since the tiny fish are transparent at that stage, fluorescent markers attached to particular cellular proteins can easily be imaged. The current study used these properties to monitor how specific populations of tumor cells develop and their role in initiating new tumor growth.

Previous research from the MGH team had discovered that RMS cells expressing marker proteins also seen on muscle progenitor cells had significantly more tumor-propagating potential than did other tumor cells. Fluorescently labeling proteins associated with different stages of cellular differentiation revealed distinct populations of RMS cells in the zebrafish model. Cells expressing the progenitor cell marker myf5, were labeled green, and those expressing myogenin, a marker of mature muscle cells, were labeled red.

In a series of experiments, the research team confirmed that myf5-expressing RMS cells had powerful tumor-propagating potential, but the ability to visualize how tumor cells move in living fish produced a surprising observation. While myf5-expressing cells largely remained within the primary tumor itself, myogenin-expressing RMS cells easily moved out from the tumor, entering the vascular system and passing through usually impenetrable layers of collagen. Only after the more-differentiated but non-proliferative myogenin-expressing cells had colonized an area did the myf5-expressing tumor-propagating cells appear and start the growth a new tumor. Imaging the labeled tumor cells also revealed that different cellular populations tended to cluster in different areas of later-stage tumors.

“Our direct in-vivo imaging studies are the first to suggest such diverse cellular functions in solid tumors, based on differentiation and the propensity for self-renewal,” says Myron Ignatius, PhD, of MGH Pathology and Center for Cancer Research, the study’s first author. “I think we will find that this kind of division of labor is a common theme in cancer, especially given that the vast majority of cells within a tumor are not tumor-propagating cells. We suspect there will be molecularly defined populations that make niches for tumor-propagating cells, secrete factors to recruit vasculature and create boundaries to suppress immune cell invasion.”

Langenau adds, “Division of labor is a new and emerging concept in cancer research that we hope will lead to new targets for rationally designed therapies. In rhabdomyosarcoma it will be important to target both the tumor-propagating cells and the highly migratory colonizing cells for destruction — a major focus of ongoing studies in our group.” Langenau is an assistant professor of Genetics at Harvard Medical School and a principal faculty member at the Harvard Stem Cell Institute.

Additional co-authors author of the Cancer Cell article are Eleanor Chen, Adam Fuller, Ines Tenente Rayn Clagg, Sali Liu, Jessica Blackburn, MGH Pathology and Center for Cancer Research; Andrew Rosenberg, and Petur Neilsen, MGH Pathology; Natalie Elpek and Thorsten Mempel, MGH Center for Immunology and Inflammatory Diseases; and Corinne Linardic, Duke University Medical Center. The study was supported by grants from the National Institute of Health, the Alex’s Lemonade Stand Foundation, the Sarcoma Foundation of America, the American Cancer Society and the Harvard Stem Cell Institute.

http://www.sciencedaily.com/releases/2012/05/120515131756.htm

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Reporter: Prabodh Kandala, PhD

The human body does a great job of generating new cells to replace dead ones but it is not perfect. Cells need to communicate with or signal to each other to decide when to generate new cells. Communication or signaling errors in cells lead to uncontrolled cell growth and are the basis of many cancers.

At The University of Texas Health Science Center at Houston (UTHealth) Medical School, scientists have made a key discovery in cell signaling that is relevant to the fight against melanoma skin cancer and certain other fast-spreading tumors.

The scientists report that they have discovered why a class of drug called BRaf inhibitors that are widely used to treat melanomas do not always work and most importantly how these drugs may potentially accelerate cancer growth in certain patients. Melanoma, according to the American Cancer Society, accounts for almost 9,000 deaths each year. The scientists’ research was published online ahead of the June 5 print issue of Current Biology, which is published by Cell Press.

“This information may aid the development of more effective anti-cancer drugs and better inform the choice of new combinations of drugs,” said John Hancock, M.B, B.Chir, Ph.D., the study’s senior author, John S. Dunn Distinguished University Chair in Physiology and Medicine, chairman of the Department of Integrative Biology and Pharmacology and interim director of the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases at the UTHealth Medical School.

Growth signals are transmitted from a cell’s surface to the nucleus by a chain of proteins that form a signaling pathway. The command for cells to divide to generate new cells is relayed by a chain of four proteins (Ras → BRaf → MEK → ERK). All cells have this pathway and it does an effective job of generating new cells most of time.

Problems happen when a mutation occurs in one of the first two proteins in the chain — both of which lock the signaling pathway in the “on” position. The good news is that doctors have drugs that block signaling from the second protein known as BRaf. These are the BRaf inhibitors, which are successful at treating melanomas with mutant BRaf proteins.

The not-so-good news is that doctors cannot block the signal from the first protein called Ras. Researchers therefore studiedin vivo what happens when BRaf inhibitors are applied to human cancer tissues with Ras mutations.

“Surprisingly recent studies found that BRaf inhibitors do not block signaling in melanoma cells with Ras mutations. In fact, the drugs actually enhance the abnormal signaling activity. Our work now describes the mechanism for this seemingly paradoxical enhanced signaling activity,” said Kwang-jin Cho, Ph.D., the study’s lead author and research fellow at the UTHealth Medical School.

Most melanomas isolated from patients turn out to have either a BRaf or Ras mutation but rarely have both. Ras mutations cause an otherwise normal BRaf protein to stay switched on.

“Our study also emphasizes the importance of genetic testing of melanomas before using BRaf inhibitors. Our study may also help design a better drug,” Cho said.

The study was supported by the Cancer Prevention & Research Institute of Texas.

Hancock and Cho’s co-authors from the UTHealth Medical School are: Jin-Hee Park, senior research assistant; Sravanthi Chigurupati, senior research assistant; Dharini van der Hoeven, Ph.D., research fellow; and Sarah J. Plowman, Ph.D., assistant professor.

Other collaborators include: Rinshi S. Kasai, Ph.D., and Akihiro Kusumi, Ph.D., Kyoto University, Japan; and Sonja J. Heidorn, Ph.D., and Richard Marais, Ph.D., Institute for Cancer Research, London.

http://www.sciencedaily.com/releases/2012/05/120510122853.htm

 

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