Tag: colorectal cancer

Statins Might Reduce the Risk of Colorectal Cancer in Those with Ulcerative Colitis

Photo by Towfiqu Barbhuiya on Unsplash

New research published in eClinicalMedicine suggests that statins might protect patients with ulcerative colitis from developing and dying from colorectal cancer. The study, by Karolinska Insitut researchers, also found that statin treatment was associated with a lower risk of death regardless of cause in patients with ulcerative colitis or Crohn’s disease.

First author Jiangwei Sun notes that previous studies have shown that the risk of colorectal cancer in patients with IBD, such as ulcerative colitis and Crohn’s disease, is 50% higher than in the general population. This is likely to be because of the chronic gut inflammation that these patients have. Researchers have long sought drugs that can reduce the inflammation-related cancer risk.

“Even though more studies are needed to confirm our results, our study suggests that statins can prevent colorectal cancer in patients with inflammatory bowel disease (IBD), which is a high-risk group for this kind of cancer,” says Dr Sun.

The observational study conducted by Dr Sun and his colleagues compared over 10 500 IBD patients from around the country, of whom half were statin users; the other half of the group, who were matched with the first, were not. After a follow-up period of, on average, 5.6 years, 70 of the statin group and 90 of the non-statin group had been diagnosed with colorectal cancer.

The effect increased over time

The protective effect was directly proportional to the length of time the patient had been on statins and could be demonstrated after two years’ treatment.

There were also fewer deaths from colorectal cancer in the statin group (20) than in the non-statin group (37) during the study period, and deaths regardless of cause (529 versus 719).

The study shows that some 200 IBD patients need to be treated with statins to avoid one case of colorectal cancer or death from the cancer within ten years of treatment onset. The protective effect was only statistically valid for patients with ulcerative colitis.

“We think this is because the study contained fewer patients with Crohn’s disease,” explains Dr Sun. “More and larger studies compiling data from patient populations in many countries will probably be needed to achieve statistical significance for Crohn’s disease.”

Significantly fewer deaths

To avoid death regardless of cause during the same ten-year period, the number of treated patients dropped to 20, on account of how statins also protect against more common conditions, such as cardiovascular disease. Statins were linked to fewer deaths in both ulcerative colitis and Crohn’s disease patients.

The study was based on the ESPRESSO-cohort, which is run by its initiative-taker Jonas F Ludvigsson, paediatrician at Örebro University Hospital and professor at Karolinska Institutet, and the study’s last author.

“In that we can combine tissue data from patients with colorectal cancer with data from Swedish health registries, we’re uniquely placed to study the long-term effects of drugs for IBD,” he says. “Our hope is that these studies will improve the care of IBD patients.”

The most solid evidence so far

According to the researchers, the new results provide the most solid evidence so far that statins could be an effective prophylactic for colorectal cancer among people with IBD. However, more knowledge must be gathered before the treatment can be recommended in general guidelines.

“More studies are needed to ascertain if there is a causal relationship, at what point of the pathological process statins should be administered, what a reasonable dose would be and how long treatment needs to last if it’s to be of benefit,” says Dr Sun.

Source: Karolinska Institut


How High-fat Diets Affect Gut Bacteria and Increase Colorectal Cancer Risk

Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health

The increasing rate of obesity and high-fat diets are suspected to be behind the growing rates of colorectal cancers in people aged under 50. Now, in a study published in Cell Reports, researchers at have discovered how high-fat diets can change gut bacteria and alter digestive molecules called bile acids that are modified by those bacteria, predisposing mice to colorectal cancer.

In the study, researchers from the Salk Institute and UC San Diego found increased levels of specific gut bacteria in mice fed high-fat diets. They showed that those gut bacteria alter the composition of the bile acid pool in ways that cause inflammation and affect the replenishment rate of intestinal stem cells replenish.

“The balance of microbes in the gut is shaped by diet, and we are discovering how alterations in the gut microbial population (the gut microbiome) can create problems that lead to cancer,” says co-senior author and Professor Ronald Evans, director of Salk’s Gene Expression Laboratory. “This paves the way toward interventions that decrease cancer risk.”

In 2019, Evans and his colleagues showed in mice how high-fat diets boosted the overall bile acid levels. The shift in bile acids, they found, shut down a key protein in the gut, the Farnesoid X receptor (FXR). and increased the prevalence of cancer.

However, there were still missing links in the story, including how the gut microbiome and bile acids are changed by high-fat diets.

In the new work, Evans’ group teamed up with the labs of Rob Knight and Pieter Dorrestein at UC San Diego to examine the microbiomes and metabolomes (collections of dietary and microbially derived small molecules) in the digestive tracks of animals on high-fat diets. They studied mice genetically more susceptible to colorectal tumours.

The scientists discovered that although mice fed high-fat diets had more bile acids in their guts, it was a less diverse collection with a higher prevalence of certain bile acids that had been changed by gut bacteria. They also showed that these modified bile acids affected the proliferation of stem cells in the intestines. Without frequent replenishment, they accumulate mutations – a key step toward encouraging the growth of cancers, which often arise from these stem cells.

“We are only just beginning to understand these bacterially-conjugated bile acids and their roles in health and disease,” says co-author Michael Downes, a staff scientist at Salk.

There were also striking differences in the microbiomes of the mice on high-fat diets: the collections of gut bacteria in these mice’s digestive tracts were less diverse and contained different bacteria than the microbiomes of mice not on high-fat diets. Two of these bacteria – Ileibacterium valens and Ruminococcus gnavus – were able to produce these modified bile acids.

The scientists were surprised to discover that a high-fat diet actually had a greater impact on the microbiome and modified bile acids than a genetic mutation that increases cancer susceptibility in the animals.

“We’ve pinpointed how high-fat diet influences the gut microbiome and reshapes the bile acids pool, pushing the gut into an inflamed, disease-associated state,” says co-first author Ting Fu, a former postdoctoral fellow in the Evans lab.

The researchers believe high-fat diets change the composition of the microbiome, encouraging the growth of bacteria like I. valens and R. gnavus. In turn, that boosts levels of modified bile acids. In a vicious cycle, those bile acids create a more inflammatory environment that can further change the makeup of gut bacteria.

“We’ve deconstructed why high-fat diets aren’t good for you, and identified specific strains of microbes that flare with high-fat diets,” says Evans, March of Dimes Chair in Molecular and Developmental Biology. “By knowing what the problem is, we have a much better idea of how to prevent and reverse it.”

In the future, the team will study how quickly the microbiome and bile acids change after an animal begins eating a high-fat diet. They also plan to study ways to reverse the cancer-associated effects of a high-fat diet by targeting FXR – the protein that they previously discovered to be associated with bile acid changes.

Source: Salk Institute

Are Nitrates a Cancer Menace… or Cardiac Protector?

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Despite our understanding of nutrition expanding remarkably in recent times, few aspects of our diet continue to confuse and divide the experts like nitrate. For a long time nitrate has been viewed warily, with previous research showing it could potentially be linked to causing cancer.

However, subsequent research has revealed dietary nitrate also has various cardiovascular health benefits, which could help reduce the risk of related conditions such as heart disease, dementia and diabetes.

So, how can one dietary compound have such contrasting potential risks and benefits? Researchers set out to find out how and why nitrate such contrasting potential risks and benefits, publishing their findings in Trends in Food Science & Technology.

All about the source

Dr Catherine Bondonno led a review of nitrate research and says the key may lie in where it comes from.

“We get nitrate from three major dietary sources: meat, water and vegetables,” she said.

“Nitrate’s reputation as a health threat stems from 1970, when two studies showed it can form N-nitrosamines, which are highly carcinogenic in laboratory animals.

“However, no human studies have confirmed its potential dangers, and our clinical and observational studies support nitrate preventing cardiovascular disease if it’s sourced from vegetables.

“So the review looked to unpack all of that, identify new ways forward and ways that we can solve this puzzle, because it’s really time to address it: it’s been 50 years.”

Urgency required

Despite recent research indicating the source of nitrate may affect its health benefits and risks, current dietary guidelines relating to nitrate have been in place since the 1970s and don’t differentiate between nitrate from meat, vegetables and water.

Dr Bondonno said while the 1970s animal studies reported a small incidence of malignant tumours, there was evidence not all nitrates deserve to be “tarred with the same brush.”

“For instance, unlike meat and water-derived nitrate, nitrate-rich vegetables contain high levels of vitamin C and/or polyphenols that may inhibit formation of those harmful N-nitrosamines associated with cancer,” she said.

Dr Bondonno said it was vital more research was conducted so guidelines could be updated.

“The public are unlikely to listen to messages to increase intake of nitrate-rich vegetables, if they are concerned about a link between nitrate intake and cancer.”

However, she stressed while official guidelines hadn’t changed, the apparent benefits of nitrate had seen many people potentially put themselves at risk.

“We need to be sure nitrate-rich vegetables don’t actually have an increased risk of cancer if we consume a higher amount,” she said.

“High dosage nitrate supplements are already used to improve physical performance in sport, while vegetable nitrate extracts are being added to cured meat products with a “clean label” claim, purporting to be better for you.

“So we really need to get this right.”

What do we eat, then?

Given its divided experts in the field, Dr Bondonno said it’s understandable people may be confused as to whether nitrate is good or bad for them.

“They’re probably thinking, ‘If I can’t have a salad, what CAN I have?’,” she said.

Despite the debate, she said current evidence suggests people should aim to get their nitrate from vegetables — but there was no need to go overboard.

“Dark green, leafy vegetables and beetroot are good sources, our research shows one cup of raw, or half a cup cooked per day is enough to have the benefits on cardiovascular health,” she said.

“We know processed meat isn’t good for us and we should limit our intake, but whether it’s the nitrate in them that is causing the problem or something else, we don’t know.

“It just further emphasises the need to investigate dietary nitrate to clarify the message for people.

“The potential cancer link was raised 50 years ago; now it’s time to conduct an in-depth analysis to distinguish fact from fiction.”

Source: Edith Cowan University

Defensiveness Keeping People from Taking at-home Colorectal Cancer Stool Tests

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Despite colorectal cancer being highly treatable, especially when detected early, many people do not undergo recommended screening, even with the availability of at-home stool faecal immunochemical test (FIT) kits. New research published in CANCER reveals that people who react defensively to the invitation to get screened are less likely to take part.

For the study, Nicholas Clarke, PhD, of Dublin City University in Ireland, surveyed individuals in Dublin who had been invited to participate in a FIT screening program in 2008–2012. Questionnaires were mailed in September 2015 to all individuals who were invited to participate (over two screening rounds) but had declined and a random sample of individuals who had participated. Following two reminders, questionnaires were completed by 1988 people who participated in screening and 311 who did not.

Those who did not do FIT-based screening were more likely to provide responses indicating greater defensiveness. This was apparent for all questions related to the different domains of what is called defensive information processing (DIP). The four domains of DIP include:

  • attention avoidance (reducing risk awareness by avoidance),
  • blunting (active mental disengagement through avoidance and accepted denial),
  • suppression (acknowledging others’ risk but avoiding personal inferences through self-exemption beliefs), and
  • counter-argumentation (arguing against the evidence).

“People who react defensively to the invitation to colorectal cancer screening are less likely to take part, and this seems to be due to such misconceptions that having a healthy lifestyle or having regular bowel movements means that they do not need to be screened. Similarly, some people believe testing can be delayed while they wait for a ‘better’ test (even though the current test works very well) or wait until their other health concerns are under control,” explained Dr Clarke. “Some people also react defensively because they believe cancer is always fatal, which is not true. All of these factors can result in people making a decision not to take the home-based screening test.”

Dr Clarke noted that the study’s findings indicate that even well-designed health communication campaigns and proactive screening programs may be hindered by individuals’ defensive beliefs. “The measures used in this study could be used to help identify people who may need extra support to take part in colorectal cancer screening programs worldwide,” he said. “The results suggest that screening programs need strategies to decrease procrastination and address misconceptions about colorectal cancer and screening.”

He also stressed the importance of trying to make colorectal cancer screening something that everyone routinely does when they reach middle age.

An accompanying editorial by Beverly Beth Green MD, MPH advocates for additional research to test different strategies, such as financial incentives, for decreasing DIP in participants.

Source: Wiley

Temporary Low-protein Diet could Enhance Colon Cancer Treatment

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A brief switch to a low-protein diet could be a key to enhancing colon cancer treatment, say researchers investigating cancer metabolism. They reported their findings in the journal Gastroenterology.

Like all cells, cancer cells need nutrients to survive and grow. One of the most important nutrient sensing molecules in a cell is called mTORC1. Often called a master regulator of cell growth, it lets cells sense different nutrients, thereby growing and proliferating. When nutrients are limited, cells dial down nutrient sensing cascade and turn off mTORC1.

While mTORC1 is known to be hyperactive in colon cancer, the key question is whether colon tumours hijack nutrient sensing pathways to fire up the master regulator.

“In colon cancer, when you decrease the nutrients available in the tumours, the cells don’t know what to do. Without the nutrients to grow, they undergo a kind of crisis, which leads to massive cell death,” said senior author Yatrik M. Shah, PhD, professor at Michigan Medicine.

Researchers found in cells and in mice that a low-protein diet blocked the nutrient signalling pathway that fires up a master regulator of cancer growth.

The regulator, mTORC1, controls how cells use nutritional signals to grow and multiply. It’s highly active in cancers with certain mutations and is known to cause cancer to become resistant to standard treatments. A low-protein diet, and specifically a reduction in two key amino acids, changed the nutritional signals through a complex called GATOR.

GATOR1 and GATOR2 work together to keep mTORC1 in business. When a cell has plenty of nutrients, GATOR2 activates mTORC1. When nutrients are low, GATOR1 deactivates mTORC1. Limiting certain amino acids blocks this nutrient signalling.

Previous efforts to block mTORC have focused on inhibiting its cancer-causing signals. But these inhibitors cause significant side effects — and when patients stop taking it, the cancer comes back. The study suggests that blocking the nutrient pathway by limiting amino acids through a low-protein diet offers an alternative way to shut down mTORC.

“We knew that nutrients were important in mTORC regulation but we didn’t know how they directly signal to mTORC. We discovered the nutrient signalling pathway is just as important to regulate mTORC as the oncogenic signalling pathway,” said study first author Sumeet Solanki, Ph.D., a research investigator at the Rogel Cancer Center.

Researchers confirmed their findings in cells and mice, where they saw that limiting amino acids stopped the cancer from growing and led to increased cell death. They also looked at tissue biopsies from patients with colon cancer, which confirmed high markers of mTORC correlated with more resistance to chemotherapy and worse outcomes. Solanki said this could provide an opportunity to direct treatment for patients with this marker.

“A low-protein diet won’t be standalone treatment. It has to be combined with something else, such as chemotherapy,” Solanki said.

The risk with a low-protein diet is that people with cancer often experience muscle weakness and weight loss, which limiting protein could exacerbate.

“Putting cancer patients on a protein-deficient diet long-term is not ideal. But if you can find key windows – like at the start of chemotherapy or radiation – when patients could go on a low protein diet for a week or two, we could potentially increase the efficacy of those treatments,” Shah said.

Further research will refine this concept of a therapeutic window to limit amino acids. Researchers will also seek to understand how these pathways are creating resistance to treatment and whether an inhibitor could block the GATOR complexes.

Source: Michigan Medicine – University of Michigan

Disappointing Colorectal Cancer Screening Results with Colonoscopy

Colon cancer cells
Colon cancer cells. Source: National Cancer Institute on Unsplash

A randomised study of northern European data shows that colonoscopy screening reduces the risk of colorectal cancer by 18%, much smaller than experts previously assumed. The results of the study appear in the New England Journal of Medicine.

Colonoscopy may not even perform better than screening with faecal tests, said Louise Emilsson, docent at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, and national Swedish principal investigator of the study.

Prior to the publication of this study, experts assumed that screening with colonoscopy had significantly better effect than screening with faecal tests. Faecal tests are used in colorectal cancer screening programs in many countries, and other countries have introduced screening with colonoscopy based on the fact that researchers via observational and modelling studies estimated that up to nine out of ten cases of colorectal cancer could be prevented with a colonoscopy screening. With faecal tests, similar models has estimated the effect to be two to three out of ten.

In the NordICC study, the researchers investigated the extent to which colonoscopy screening actually prevents colorectal cancer. Overall, 1.2% of those randomised to no screening were diagnosed with colon cancer during ten years, compared to 0.98% in those offered screening.

This translates to an 18% reduced risk of colorectal cancer among the participants who were offered colonoscopy screening. Furthermore, 455 colonoscopies were required to prevent one single case of colorectal cancer. Colonoscopy is fairly invasive and costly procedure, involving preparation, bowel prep with laxatives, and a 30-45 minute examination of the bowel with a camera inserted via the rectum. The figure of 455 procedures to prevent one case of cancer is certainly disappointing, Louise Emilsson concluded.

Colorectal cancer mortality was also found to be lower than expected in the NordICC study. Only three in a thousand died of the disease within ten years, regardless of whether they were offered screening or not, and thus, there was no significant difference between the groups in terms of mortality. The low mortality rate is however encouraging and likely caused by significantly improved treatment options over the past ten years.

Source: Karolinska Institutet

Can a Banana per Day Keep the Oncologist Away?

Banana
Photo by Mike Dorner on Unsplash

A trial in people with hereditary colon cancer has shown that daily supplements of resistant starch, equivalent to a slightly green banana per day, had a major preventative effect against many cancers. Published in Cancer Prevention Research, the findings showed that, while bowel cancers were unaffected, the supplement reduced cancers in other parts of the body by more than half.

This effect was particularly pronounced for upper gastrointestinal cancers including oesophageal, gastric, biliary tract, pancreatic and duodenum cancers. What is even more remarkable is that the effects lasted for 10 years after the participants stopped taking the supplements.

The CAPP2 trial involved almost 1000 patients with Lynch syndrome from around the world and revealed that a regular dose of resistant starch, also known as fermentable fibre, taken for an average of two years, cut their risk for many cancers.

The present study is a planned double blind 10 year follow-up, supplemented with comprehensive national cancer registry data for up to 20 years in 369 of the participants.

A previous study as part of the same trial and published in The Lancet revealed that aspirin reduced cancer of the large bowel by 50%.

“We found that resistant starch reduces a range of cancers by over 60%. The effect was most obvious in the upper part of the gut,” explained Professor John Mathers at Newcastle University. “This is important as cancers of the upper GI tract are difficult to diagnose and often are not caught early on.

“Resistant starch can be taken as a powder supplement and is found naturally in peas, beans, oats and other starchy foods. The dose used in the trial is equivalent to eating a daily banana; before they become too ripe and soft, the starch in bananas resists breakdown and reaches the bowel where it can change the type of bacteria that live there.

“Resistant starch is a type of carbohydrate that isn’t digested in your small intestine, instead it ferments in your large intestine, feeding beneficial gut bacteria – it acts in effect, like dietary fibre in your digestive system. This type of starch has several health benefits and fewer calories than regular starch. We think that resistant starch may reduce cancer development by changing the bacterial metabolism of bile acids and to reduce those types of bile acids that can damage our DNA and eventually cause cancer. However, this needs further research.”

Professor Sir John Burn, from Newcastle University and Newcastle Hospitals NHS Foundation Trust who ran the trial with Prof Mathers, said: “When we started the studies over 20 years ago, we thought that people with a genetic predisposition to colon cancer could help us to test whether we could reduce the risk of cancer with either aspirin or resistant starch.

“Patients with Lynch syndrome are high risk as they are more likely to develop cancers so finding that aspirin can reduce the risk of large bowel cancers and resistant starch other cancers by half is vitally important.

“Based on our trial, NICE now recommend Aspirin for people at high genetic risk of cancer, the benefits are clear – aspirin and resistant starch work.”

Between 1999 and 2005, nearly 1000 participants began either taking resistant starch in a powder form every day for two years or aspirin or a placebo.

At the end of the treatment stage, there was no overall difference between those who had taken resistant starch or aspirin and those who had not. However, the research team anticipated a longer-term effect and designed the study for further follow-up.

During follow-up, only five new cases of upper GI cancers were diagnosed among the 463 participants who had taken the resistant starch compared with 21 among the 455 who were on the placebo.

The team are now leading the international trial, CaPP3, involving more than 1800 participants with Lynch syndrome to look at whether smaller, safer doses of aspirin can be used to help reduce the cancer risk.

Source: Newcastle University

Living Donors Liver Transplant a Viable Option in Colorectal Cancer

Doctors and nurses performing a surgery
Photo by Piron Guillaume on Unsplash

A recent study published in JAMA Surgery has demonstrated the viability of living-donor liver transplant for patients who have systemically controlled colorectal cancer and liver tumours that cannot be surgically removed.

“This study proves that transplant is an effective treatment to improve quality of life and survival for patients with colorectal cancer that metastasised to the liver,” said senior study author Dr Gonzalo Sapisochin.

The study focused on colorectal cancer partly for its tendency to spread to the liver. Nearly half of all patients with colorectal cancer develop liver metastases within a few years of diagnosis and 70% of liver tumours in these patients cannot be removed without removing the entire liver.

Unfortunately, most of these patients cannot get deceased-donor liver transplants because their liver function is fairly normal in spite of their tumours. This puts them near the bottom of the national organ transplant waiting list.

Thanks to recent advances in cancer treatments, many of these patients are able to get their cancer under systemic control, which means only their liver tumours prevent them getting a ‘cancer free’ label. It also increases the odds that these patients – and their new livers – will remain cancer free, which is crucial when balancing the benefit to the patient with the risk to a living donor.

“I’ve seen so many cancer patients, whose cancers were not spreading, but we couldn’t remove the tumours from their livers and we knew they would die,” said first study author Dr Roberto Hernandez-Alejandro. “We hoped living-donor liver transplant could give them another chance.”

Because it offered a last resort, the study attracted patients from near and far. All patients and donors went through a rigorous screening process to ensure they were good candidates for the procedure, and they were educated about the risks of the surgery and the possibility of cancer recurrence.

Patients and donors underwent staggered surgeries to fully remove patients’ diseased livers and replace them with half of their donors’ livers. Over time, both patients’ and donors’ livers regenerated and regain normal function.

Patient imaging and blood analysis was closely monitored for any signs of cancer recurrence and will continue to be followed for up to five years after their surgery. At the time of study publication, two patients had follow-up of two or more years and both remained alive and well, cancer-free.

“We have seen very good outcomes with this protocol, with 100 percent survival and 62 percent of patients remaining cancer free one year and a half after surgery,” said study author Dr Mark Cattral. “It is very strong data to support that we can offer this treatment safely and make appropriate use of scarce life-saving organs.”

Source: University Health Network

Taller Adults Have a Greater Colorectal Cancer Risk

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Taller adults may be more likely than shorter ones to develop colorectal cancer or precancerous colon polyps, according to a new meta-analysis published in Cancer Epidemiology, Biomarkers & Prevention. While the association between taller height and colorectal cancer has been previously investigated, the researchers say those studies offered conflicting results, used inconsistent measures of height and did not include the risk of adenomas.

“This is the largest study of its kind to date. It builds on evidence that taller height is an overlooked risk factor, and should be considered when evaluating and recommending patients for colorectal cancer screenings,” said Associate Professor Gerard Mullin, MD. Greater height is still not proven to be causative, nor is it a great a risk factor as genetics, he and his team cautioned. However, it does add to long-standing evidence linking height to colorectal cancer risk.

“One possible reason for this link is that adult height correlates with body organ size. More active proliferation in organs of taller people could increase the possibility of mutations leading to malignant transformation,” said co-first author Elinor Zhou, MD.

The researchers first identified 47 international, observational studies involving 280 660 cases of colorectal cancer and 14 139 cases of colorectal adenoma. They also included original data from the Johns Hopkins Colon Biofilm study, which recruited 1459 adult patients undergoing outpatient colonoscopies to investigate the relationship between cancer and biofilm on the colon.

Because the definition of tallness differs around the world, the researchers compared the highest versus the lowest height percentile of various study groups. “The findings suggest that, overall, the tallest individuals within the highest percentile of height had a 24% higher risk of developing colorectal cancer than the shortest within the lowest percentile. Every 10-centimeter increase (about 4 inches) in height was found to be associated with a 14% increased risk of developing colorectal cancer and 6% increased odds of having adenomas,” said A/Prof Mullin.

In the US, the average height for men is 175.3cm, and for women it is 162.6 inches. This means men who are 185.4cm and women who are 172.7cm (10cm above the average US height) or taller are at a 14% increased risk of colorectal cancer and a 6% increased risk of adenomas.

The percentage results were adjusted for known risk factors of colorectal cancer, including non-modifiable factors such as age, familial colorectal cancer history and a personal history of chronic inflammatory bowel disease. Though not directly comparable due to differences in measurement scale, tallness may impart an order of magnitude of colorectal cancer risk similar to better-known modifiable factors such as cigarette smoking, moderate alcohol consumption and high processed red meat intake. At present, gastroenterologists focus on genetic and age-related risks for colorectal cancer screenings recommendations.

While colorectal cancer is the third most common cancer in both men and women in the US, fewer people are diagnosed with colorectal cancer each year has dropped overall since the mid-1980s, mainly due to prevention and screening. However, the downward trend is mostly in older adults. Among adults under 50, colorectal cancer deaths have increased 2% per year from 2007 to 2016, an as yet unexplained phenomenon.

“Greater awareness by the public and government will help promote more interest and funding for more research, which ultimately could change guidelines for physicians to consider height as a risk for cancer,” said A/Prof Mullin. “There are well-known modifiable dietary associations for colorectal cancer, such as processed red meats and smoking, but guidelines currently are fixated on family history, and height is clinically neglected when it comes to risk screening.”

Dr Zhou says more research is needed to define particular taller populations at risk for colon cancer. “For instance, tall athletes and individuals with inherited tallness, such as those with Marfan syndrome, could be screened earlier and the impact of height further explored,” she said. “We need more studies before we can definitively say at what height you would need earlier colorectal cancer screening.”

Source: John Hopkins Medicine

In Metastatic Colon Cancer, Youth is no Advantage

Colon cancer cells. Source: National Cancer Institute on Unsplash

Even though young patients with metastatic colorectal cancer tend to be more fit and receive more intensive treatment than older patients, both groups survive for roughly the same amount of time, according to a new study by Dana-Farber Cancer Institute investigators.

The findings, published in the Journal of the National Cancer Institute, come as colorectal cancer rates in young people are rising. The researchers said the results are somewhat surprising, as younger patients, who usually have fewer complicating health factors, might be expected to survive longer than older patients.

“As a group, younger patients are more physically active and have higher performance status and are better able to perform the activities of daily living than older patients. They also tend to be treated with higher doses of therapy and have less severe side effects,” said study senior author Kimmie Ng, MD, MPH, director of the Young-Onset Colorectal Cancer Center at Dana-Farber. “This is the first study to compare survival in younger versus older patients participating in a clinical trial of treatment for metastatic colorectal cancer.”

The study drew on clinical trial data which tested a combination of chemotherapy and biologic therapy in patients with metastatic colorectal cancer, comparing patients under 50 with those over 50.

“We found no significant difference in overall survival between the two groups,” said Dana-Farber’s Marla Lipsyc-Sharf, MD, the first author of the study. The median survival for patients with young-onset colorectal cancer was 27.07 months vs. 26.12 months for the older-onset group. Progression-free survival – how long patients lived before the cancer worsened – was also similar for the two groups: 10.87 months for the younger patients vs. 10.55 for the older ones.

Confounding expectations even further, patients under age 35 had the shortest median overall survival of any age group: 21.95 months vs 26.12 months in older-onset patients. Because the study included relatively few patients younger than 35, the difference is not considered statistically significant, researchers noted, but it aligns with previous research suggesting that very young patients have worse outcomes.

Cases are markedly on the rise: between 2000 and 2013, incidence of the disease in people under age 50 increased approximately 22%, even as overall incidence of colorectal cancer has declined. Yet despite a wellspring of new research, no definitive cause for the increase has been found.

“If current trends hold, colorectal cancer is projected to be the second leading cancer and leading cause of cancer death in patients ages 20–49 by the year 2040,” Lipsyc-Sharf stated. “It is important to understand survival in this population in order to develop tailored treatments.”

That younger patients fare no better than older ones despite more favourable factors could suggest that colorectal cancer is more aggressive at an earlier age. But there is no conclusive evidence that that is the case.

“Research has yet to identify consistent molecular differences in the colorectal cancer cells of younger patients and older patients,” Dr Lipsyc-Sharf noted. Current studies also are exploring whether differences in the intestinal microbiome of younger and older patients might explain the increased incidence of early-onset colorectal cancer.

Source: Dana Farber Cancer Institute