Category Archives: Men’s Health

Positive Trial Data with 100% Safe Delivery

Moleculin Announces Positive Trial Data with 100% Safe Delivery of p-STAT3 Inhibitor and Efficacy in Majority of Patients

Preliminary results from phase 1 clinical trial of WP1220 for treatment of cutaneous T-cell lymphoma (“CTCL”); supports phase 2 study.

“For years, p-STAT3 (the activated form of STAT3) has been considered an ‘undruggable’ target because of the difficulty of reaching and affecting this cell-signaling protein,” commented Walter Klemp, Moleculin’s Chairman and CEO. “Some consider it to be a master regulator of cancer-related gene transcription, so we believe the ability to show a therapeutic effect from a p-STAT3 inhibitor could be considered a significant breakthrough in cancer research.”

Results: There were 6 patients screened, and 5 patients enrolled between March and July 2019. Three are evaluable for both safety and efficacy after completing 3 months of treatment, with 2 ongoing and evaluable for safety. The only AE reported potentially related to study drug in one of the five patients was a mild contact dermatitis not requiring treatment. CAILS scores on index lesions were significantly decreased in the first 3 patients, who were stages IA, IB, and IIB, respectively, at entry. A composite score was obtained for all treated lesions for each patient, and percent changes were calculated from baseline to Day 84. There was a median reduction of 70.8% (range 62.1%-76.2%) for the 3 patients. Improvement was noted as early as 7 days after initiation of treatment, and maintenance of improvement was also shown at follow up (1 month after discontinuation, as per protocol). The fourth patient has also shown an initial reduction in the composite CAILS score after 56 days (26.7%), and is continuing on treatment. Evaluations of the biopsy samples for histopathology and status of p-STAT3 in treated lesions are in progress.

Conclusions: WP1220, an inhibitor of p-STAT3, has shown demonstrable safety and significant efficacy after at least 3 months of topical treatment in 3 patients with progressive MF, with a continuing trend towards improvement in additional patients currently in treatment. This is the first demonstration that inhibition of the STAT3 activation pathway with topical therapy has impacted the course of this disease. The trial is continuing, and updated and more comprehensive data from this study as well as assessment of STAT3 phosphorylation in treated lesions will be reported.

“This is the first topical delivery of a p-STAT3 inhibitor that we know of for CTCL, where there is a significant unmet need for improved treatment of the lesions associated with this potentially deadly skin cancer. But, we believe the significance of this data goes well beyond CTCL, as it speaks to the targeting of p-STAT3 as a general strategy. We are excited to share these preliminary results in association with ASH, especially because we believe showing activity here could have exciting implications for the future of STAT3 inhibitors in general. Although this is a relatively small pilot study, we believe the results justify an expansion to a larger patient population in a Phase 2 clinical trial,” added Dr. Sandra Silberman, CMO at Moleculin.

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Consumer Warning for Erectile Dysfunction Pills

The U.S. Food and Drug Administration is warning consumers not to purchase or use drugs advertised nationwide as a “healthy man alternative to the little blue pill” or “healthy man,” or “the power pill” for erectile dysfunction on broadcast and internet radio platforms such as iHeart Radio, as these drugs have not been approved by the FDA.

The FDA confirmed that consumers have received these drugs, without a prescription, which contain 100 mg of sildenafil, the active ingredient in Viagra. This is a dangerous dosage strength for certain patients including the elderly and those with impaired liver and kidney function. When sildenafil interacts with nitrates in some prescription drugs, such as nitroglycerin, a person’s blood pressure can reach dangerously low levels. People with diabetes, high blood pressure, high cholesterol, or heart disease often take nitrates.

Do not use these products. If you have used these products and became ill or otherwise experienced an adverse event, contact your health care provider. FDA continues to warn consumers that medications purchased from unapproved and/or unlicensed sources may be dangerous as they can be counterfeit, contaminated, improperly stored and transported, ineffective, and/or unsafe.

The label on the blister packs for these unapproved drugs states that the products are manufactured in India by Acme Generics. The label also bears the name Sun Pharma. FDA is concerned the seller may also be distributing to U.S. consumers unapproved tadalafil as a generic for the prescription drug Cialis.

Adverse Events
To date, FDA is not aware of any adverse events associated with these particular unapproved versions of sildenafil or tadalifil. Health care professionals and consumers should report any adverse events related to this product to FDA’s MedWatch. Adverse Event Reporting program by:
•  Completing and submitting the report online at MedWatch Online Voluntary Reporting Form
•  Downloading and completing the form, then submitting it via fax at 1-800-FDA-0178.

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New Public Health Crisis? Study Urged on Marijuana Smoking & Lung Cancer

As marijuana becomes mainstream and usage rates skyrocket, some of the nation’s top cancer doctors are urging the Surgeon General to investigate the link between smoking marijuana and lung cancer.

Among the renowned doctors calling for more study is Dr. Joseph Friedberg, head of the Division of Thoracic Surgery at the University of Maryland School of Medicine. Publishing his concerns on SurvivorNet, the cancer site providing the latest information and treatment options from foremost cancer experts, Dr. Friedberg is calling for a federal study citing increased rates of lung cancer in their practices from patients whose only discernible risk factor is marijuana smoking. SurvivorNet released a documentary outlining the concerns surrounding the lack of research on the link between smoking marijuana and lung cancer in hopes of bringing widespread attention to the need for this study.

Dr. Friedberg states “Given the expanding legalization of marijuana, and the anticipated wave of increased use, there is clearly a need to study the cancer risks of marijuana with the same rigor that has been devoted to tobacco smoke. Both types of smoke contain some of the same carcinogens, so the widely held belief that tobacco smoke causes cancer and marijuana smoke does not is inherently flawed. “We have an opportunity to avoid a potential marijuana-related public health crisis similar to what we are still dealing with from cigarettes being introduced to the public without any health risk warnings.”

Previously, the only study on long term use of cannabis and lung cancer was a 2008 NIH study conducted in New Zealand which found that long term cannabis use increases the risk of lung cancer in young adults. The study cites other reputable scientific findings that state cannabis smoke is similar to tobacco smoke but with twice as many carcinogens and because people smoke joints without filters and hold the smoke in their lungs longer it can increase the risk of lung cancer. The major finding from this study was that for each joint-year of cannabis exposure, the risk of lung cancer increased by 8%, after adjustment for confounding variables including tobacco smoking.

A major differential risk between cannabis and cigarette smoking was observed, with 1 joint of cannabis similar to about 20 cigarettes for risk of lung cancer. This study was not extensive or long enough to be definitive but it raises concerns about the drug. This study would be the first of its kind to bring groundbreaking research and information to millions of Americans who smoke marijuana without understanding the potentially lethal side effects. Much like tobacco’s earliest days, if something is not done about this now, we risk another major health emergency.

SurvivorNet was founded to fill an urgent need for better information about cancer prevention and treatment. “By bringing attention to crucial findings from some of the country’s leading cancer doctors, we are hoping to save lives. We know marijuana is alleviating suffering for a great many cancer patients. We also think people who smoke and vape marijuana recreationally should have accurate information about whether there is an increased risk for cancer and then make their own choices. It’s clear a major national study is needed so we can really understand this issue.”

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Hong Kong Dept of Health Approves Biktarvy® for HIV, following FDA and EC

In Phase 3 Clinical Trials, Biktarvy® Demonstrated High Efficacy and Zero Resistance Through 48 Weeks

The triple-combination, single-tablet therapy combines the potency of the novel integrase strand transfer inhibitor (INSTI) bictegravir, with the demonstrated safety and efficacy profile of a guideline recommended dual nucleoside reverse transcriptase inhibitor (NRTI) backbone – Descovy® (emtricitabine 200 mg/tenofovir alafenamide 25 mg; FTC/TAF). BIC/FTC/TAF provides a convenient once-daily dosing STR without regards to food. Furthermore, BIC/FTC/TAF’s use is not restricted by the patient’s baseline viral load, CD4 cell count or HLA-B 5701 status.

“Safety and resistance profiles are important considerations for HIV patients, as the disease requires long-term care. In addition, potent treatments with convenient dosing can potentially improve adherence and outcomes for patients,” said Dr Chan Kai Ming, Specialist in Infectious Disease, Consultant in Internal Medicine, Union Hospital, Hong Kong.

The Hong Kong Dept of Health has approved Biktarvy® (bictegravir 50mg/emtricitabine 200 mg/tenofovir alafenamide 25 mg; BIC/FTC/TAF), a once-daily single tablet regimen (STR) for the treatment of HIV-1 infection in adults*. Hong Kong is the first market in Asia to approve Biktarvy. BIC/FTC/TAF was approved by the U.S. Food and Drug Administration (FDA) on February 7, 2018 and the European Commission on June 21, 2018.

The approval was based upon data from four ongoing Phase 3 studies: Studies 1489 and 1490 in treatment-naive HIV-1 infected adults, and Studies 1844 and 1878 in virologically suppressed adults. The trials are comprised of a population of 2,414 participants, and BIC/FTC/TAF met its primary efficacy objective at 48 weeks in all four studies, with no participants in any of the four BIC/FTC/TAF studies developing treatment-emergent virologic resistance. There were no cases of renal discontinuation, proximal renal tubulopathy or Fanconi syndrome in the BIC/FTC/TAF arms at 48 weeks. Additional ongoing studies not included in the marketing authorization application involve dedicated studies in women, adolescents and children.

“We welcome the timely approval of BIC/FTC/TAF in Hong Kong, a novel treatment option for people living with HIV,” said Andrew Hexter, Vice President and GM for Gilead Sciences Asia. “We are committed to serving the needs of HIV patients and medical communities in Asia, and are working with public health authorities to make the treatment available in this region.”

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A Phase 2/3 Clinical Trial of Trigriluzole for Alzheimer’s Disease

The first patient has been enrolled in a Phase 2/3 clinical trial of trigriluzole (BHV-4157), a novel glutamate modulator for the treatment of mild-to-moderate Alzheimer’s disease (AD). The trial is a randomized, double-blind, placebo-controlled trial evaluating the efficacy and safety of trigriluzole in patients diagnosed with AD of mild-to-moderate severity (Mini-Mental State Examination scores of 14-24 at screening), and is being conducted in collaboration with the Alzheimer’s Disease Cooperative Study (ADCS) at sites throughout the USA.Howard Feldman, MD, FRCP, Director of the ADCS and Professor of Neurosciences at University of California San Diego School of Medicine added, “The preclinical evidence for the active metabolite of trigriluzole to modulate glutamate and confer neuroprotective effects in patients with AD is compelling, and the new formulation of trigriluzole should improve its pharmaceutical properties with potential for efficacy in AD.”

Alzheimer’s disease is a progressive, fatal neurodegenerative dementia that accounts for 60 ? 80 percent of dementia cases. Alzheimer’s disease currently has no cure. Although there are FDA-approved medications for symptomatic treatment of AD, their clinical benefits are generally limited. Novel therapeutic approaches aimed at normalizing synaptic and extra-synaptic glutamate levels, such as trigriluzole, may offer the potential for symptomatic benefit in AD by improving cognitive function, as well as the potential for disease modification by preventing the loss of synapses.

The Phase 2/3 clinical trial (clinicaltrials.gov identifier NCT03605667) is a randomized, double-blind, placebo-controlled trial evaluating the efficacy and safety of trigriluzole in patients diagnosed with AD of mild-to-moderate severity (Mini-Mental State Examination scores of 14-24 at screening). Patients who have been taking stable doses of FDA-approved AD medications (AchEI also known as acetylcholinesterase inhibitors and/or memantine) for a minimum of three months prior to screening and who are willing to remain on the same regimen for the duration of the trial may be eligible to participate. Approximately 292 patients will be randomized on a 1:1 basis to receive 280 mg of trigriluzole or placebo, taken orally at bedtime. Duration of treatment will be 48 weeks.

About Trigriluzole
Trigriluzole is a third-generation prodrug and new chemical entity that modulates glutamate, the most abundant excitatory neurotransmitter in the human body. Trigriluzole has a wide range of pharmacological actions, including interactions with several types of ion channels, cellular signaling mechanisms and facilitation of glutamate reuptake. Some potential targets related to trigriluzole’s mechanism of action include (1) reducing presynaptic glutamate release through actions at the voltage-gated ion channels, (2) facilitating glutamate uptake via EAATs located on glial cells, (3) enhancing transmission through synaptic AMPA receptors, (4) altering GABAergic neurotransmission, and (5) effecting neurotrophic agents such as BDNF. Several of these targets of trigriluzole balance abnormalities observed in human AD post-mortem tissue as well as in AD animal models. As such, trigriluzole potentially offers neuroprotective effects at the level of the synapse as well as improved synaptic functioning, mechanisms that could exert both symptomatic and disease-modifying effects in AD.

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CRISPR Tech for Eye Disease Moves Closer to Reality

A study published in the journal of the American Academy of Ophthalmology shows that a CRISPR-based treatment can restore retinal function in mice.

Researchers from Columbia University have developed a new technique for the powerful gene editing tool CRISPR to restore retinal function in mice afflicted by a degenerative retinal disease, retinitis pigmentosa. This is the first time researchers have successfully applied CRISPR technology to a type of inherited disease known as a dominant disorder. This same tool might work in hundreds of diseases, including Huntington’s disease, Marfan syndrome, and corneal dystrophies. Their study was published online today in Ophthalmology, the journal of the American Academy of Ophthalmology.

Stephen H. Tsang, M.D., Ph.D., and his colleagues sought to create a more agile CRISPR tool so it can treat more patients, regardless of their individual genetic profile. Dr. Tsang calls the technique genome surgery because it cuts out the bad gene and replaces it with a normal, functioning gene. Dr. Tsang said he expects human trials to begin in three years. “Genome surgery is coming,” Dr. Tsang said. “Ophthalmology will be the first to see genome surgery before the rest of medicine.”

Retinitis pigmentosa is a group of rare inherited genetic disorders caused by one of more than 70 genes. It involves the breakdown and loss of cells in the retina, the light sensitive tissue that lines the back of the eye. It typically strikes in childhood and progresses slowly, affecting peripheral vision and the ability to see at night. Most will lose much of their sight by early adulthood and become legally blind by age 40. There is no cure. It is estimated to affect roughly 1 in 4,000 people worldwide.

Since it was introduced in 2012, the gene editing technology known as CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) has revolutionized the speed and scope with which scientists can modify the DNA of living cells. Scientists have used it on a wide range of applications, from engineering plants (seedless tomatoes) to producing animals (extra lean piglets). But as incredible as genome surgery is, CRISPR has some flaws to overcome before it can live up to its hype of curing disease in humans by simply cutting out bad genes and sewing in good ones.

Typically, CRISPR researchers design a short sequence of code called guide RNA that matches the bit they want to replace. They attach the guide RNA to a protein called Cas9, and together they roam the cell’s nucleus until they find a matching piece of DNA. Cas9 unzips the DNA and pushes in the guide RNA. It then snips out the bad code and coaxes the cell to accept the good code, using the cell’s natural gene repair machinery.

Diseases like autosomal dominant retinitis pigmentosa present a special challenge to researchers. In autosomal dominant disorders, the person inherits only one copy of a mutated gene from their parents and one normal gene on a pair of autosomal chromosomes. So, the challenge for CRISPR-wielding scientists is to edit only the mutant copy without altering the healthy one. In contrast, people with autosomal recessive disorders inherit two copies of the mutant gene. When two copies of the gene are mutated, treatment involves a more straightforward, one-step approach of simply replacing the defective gene. Dr. Tsang and colleagues have come up with a better strategy to treat autosomal dominant disease. It allowed them to cut out the old gene and replace it with a good gene, without affecting its normal function.

Instead of using one guide RNA, Dr. Tsang designed two guide RNAs to treat autosomal dominant retinitis pigmentosa caused by variations in the rhodopsin gene. Rhodopsin is an important therapeutic target because mutations in it cause about 30 percent of autosomal dominant retinitis pigmentosa and 15 percent of all inherited retinal dystrophies.

This technique allowed for a larger deletion of genetic code that permanently destroyed the targeted gene. Dr. Tsang found that using two guide RNAs instead of one increased the chance of disrupting the bad gene from 30 percent to 90 percent. They combined this genome surgery tool with a gene replacement technique using an adeno-associated virus to carry a healthy version of the gene into the retina. Another advantage is that this technique can be used in non-dividing cells, which means that it could enable gene therapies that focus on nondividing adult cells, such as cells of the eye, brain, or heart. Up until now, CRISPR has been applied more efficiently in dividing cells than non-dividing cells.

Dr. Tsang used an objective vision test to evaluate the mice after treatment to show a significant improvement in retinal function. An electroretinogram is typically used to evaluate retinal health in humans. It tests the health of the retina much like an electrocardiogram (EKG) tests the health of the heart. Previous CRISPR studies for retinal diseases have relied on a less objective measure that involves evaluating how often the mouse turns its head in the direction of a light source. Dr. Tsang used electroretinography to show that retinal degeneration slowed in treated eyes compared with untreated eyes.

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Orphan Drug Designation for Treatment of ALS – Amyotrophic Lateral Sclerosis

On March 29, 2018 the U.S. Food and Drug Administration (FDA) Office of Orphan Products Development granted Orphan Drug Designation (ODD) to experimental therapeutic EH301 for the treatment of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s Disease.

The Orphan Drug Designation submission included data from a 2017 double-blind placebo-controlled European pilot study in humans. To expand on the results of the pilot study, Elysium Health expects to initiate a placebo-controlled study in collaboration with Mayo Clinic to evaluate EH301 in up to 150 adults with ALS by the fourth quarter of 2018. The granting of ODD to EH301 does not alter the standard regulatory requirement through adequate and well-controlled studies to support FDA approval, and there is no guarantee EH301 will be approved for the treatment of ALS by FDA.

Elysium Health Chief Scientist Dr. Leonard Guarente remarked that “There is a great deal of work to be done to address the need for continued research to better understand and to treat all neurodegenerative diseases. We believe that the FDA’s granting of Orphan Drug Designation for EH301 for ALS underscores the need for novel treatments for this rare condition.”

ALS is a rare neurodegenerative disease that affects nerve cells that control voluntary muscles throughout the body to produce movements including talking, eating, walking, and breathing. ALS is progressive, meaning it gets worse over time. As the nerves lose the ability to control muscles, the muscles become weak and eventually lead to paralysis. Most people with ALS succumb to respiratory failure, usually within three to five years from when symptoms first appear. Please visit the ALS website for more information.

The FDA’s ODD program provides orphan status to drugs intended for the safe and effective treatment, diagnosis, or prevention of rare diseases or disorders that affect fewer than 200,000 people in the United States. It is estimated that there are approximately 15,000-20,000 Americans with ALS. Please see the NIH ALS Fact Sheet for details.

Additional information can be found on the Christopher & Dana Reeve Foundation website regarding current therapies and disease trends.

Disclosure: Mayo Clinic has a financial interest in Elysium Health. All revenue Mayo Clinic receives will be used to fund its not-for-profit mission in medical research and education.

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Beneficial Skin Bacteria Protect Against Skin Cancer

Science continues to peel away layers of the skin microbiome to reveal its protective properties.? Researchers now report on a potential new role for some bacteria on the skin: protecting against cancer.

“We have identified a strain of Staphylococcus epidermidis, common on healthy human skin, that exerts a selective ability to inhibit the growth of some cancers,” said Richard Gallo, MD, PhD, Distinguished Professor and chair of the Department of Dermatology at UC San Diego School of Medicine. “This unique strain of skin bacteria produces a chemical that kills several types of cancer cells but does not appear to be toxic to normal cells.”

The team discovered the S. epidermidis strain produces the chemical compound 6-N-hydroxyaminopurine (6-HAP). Mice with S. epidermidis on their skin that did not make 6-HAP had many skin tumors after being exposed to cancer-causing ultraviolet rays (UV), but mice with the S. epidermidis strain producing 6-HAP did not.? 6-HAP is a molecule that impairs the creation of DNA, known as DNA synthesis, and prevents the spread of transformed tumor cells as well as the potential to suppress development of UV-induced skin tumors.

Mice that received intravenous injections of 6-HAP every 48 hours over a two-week period experienced no apparent toxic effects, but when transplanted with melanoma cells, their tumor size was suppressed by more than 50 percent compared to controls.

“There is increasing evidence that the skin microbiome is an important element of human health. In fact, we previously reported that some bacteria on our skin produce antimicrobial peptides that defend against pathogenic bacteria such as, Staph aureus,” said Gallo.

In the case of S. epidermidis, it appears to also be adding a layer of protection against some forms of cancer, said Gallo. Further studies are needed to understand how 6-HAP is produced, if it can be used for prevention of cancer or if loss of 6-HAP increases cancer risk, said Gallo.

More than 1 million cases of skin cancer are diagnosed in the United States each year. More than 95 percent of these are non-melanoma skin cancer, which is typically caused by overexposure to the sun’s UV rays. Melanoma is the most serious form of skin cancer that starts in the pigment-producing skin cells, called melanocytes.

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Huntington’s Disease Molecule Can Kill Cancer Cells

Scientists have destroyed numerous types of human cancer cells with a toxic molecule characteristic of fatal genetic illness Huntington?s disease.

The researchers hailed the molecule?which has killed both human and mouse ovarian, breast, prostate, liver, brain, lung, skin and colon cancer cell lines in mice?as a ?super assassin.? Their results were published in the journal EMBO Reports.

Huntington?s disease is a progressive illness caused by an excess of a specific repeating RNA sequence in the Huntington gene, which is present in every cell. The defect causes the death of brain cells, and gradually worsens a person?s physical and mental abilities. The disease has no cure.

Researchers believe that the defect may be even more powerful against cancer cells than nerve cells in the brain, and the team hopes it can be harnessed to kill cancer cells without causing Huntington?s symptoms.? ?This molecule is a super assassin against all tumor cells,? said senior author Marcus Peter, a professor of cancer metabolism at Northwestern University Feinberg School of Medicine, Chicago, in a press statement. ?We?ve never seen anything this powerful.?

Peter collaborated with Feinberg colleague Shad Thaxton, associate professor of urology, to deliver the molecule in the form of nanoparticles to mice with human ovarian cancer. The targeted molecule decreased tumor growth with no toxicity to the mice.

First author Andrea Murmann, a research assistant professor who discovered the cancer-killing mechanism, used the molecule to kill numerous other human and mouse cancer cell lines. Building on previous research into a cancer ?kill switch?, Murmann looked to diseases associated with low rates of cancer and a suspected RNA link.? ?I thought maybe there is a situation where this kill switch is overactive in certain people, and where it could cause loss of tissues,? Murmann said in the statement. ?These patients would not only have a disease with an RNA component, but they also had to have less cancer.?

There is up to 80 percent less cancer in people with Huntington?s disease than the general population.? Murmann recognised similarities between the kill switch and the toxic Huntington?s disease RNA sequences.? Based on their results, the team believe the ?super assassin? molecule could be used to fight cancer in humans. ?We believe a short-term treatment cancer therapy for a few weeks might be possible, where we could treat a patient to kill the cancer cells without causing the neurological issues that Huntington?s patients suffer from,? Peter said.? The scientists next aim to refine the molecule?s delivery method to improve tumor targeting, and to stabilize the nanoparticles for storage.

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Cancer Deaths Decline Again in US

Death rates from cancer in the United States dropped again between 2014 and 2015, continuing a downward trend that began in 1991 and has meant 2.4 million fewer deaths.

Advances in early detection and treatment, along with a drop in smoking, are believed to be responsible for much of the 26 percent drop since 1991, said the findings in the American Cancer Society’s comprehensive annual report. “This new report reiterates where cancer control efforts have worked, particularly the impact of tobacco control,” said Otis W. Brawley, chief medical officer of the American Cancer Society.

“A decline in consumption of cigarettes is credited with being the most important factor in the drop in cancer death rates.”? However, he noted that “tobacco remains by far the leading cause of cancer deaths today, responsible for nearly three in 10 cancer deaths.”

Overall, the US cancer death rate reached a peak of 215.1 per 100,000 population in 1991, and has declined to 158.6 per 100,000 in 2015.

Deaths from lung cancer made a 45 percent decline among men and 19 percent among women.? Cancers of the breast, prostate and colon and rectum are also down steeply. The report forecasts about 1.7 million new cancer cases and 609,640 cancer deaths in the United States in 2018. “Over the past decade, the overall cancer incidence rate was stable in women and declined by about two percent per year in men,” it said.

While progress is evident, stark racial disparities remain. The cancer death rate in 2015 was 14 percent higher in blacks than in whites, down from a peak of 33 percent in 1993.

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