CCCF Research

At the 2022 American Society of Clinical Oncology (ASCO) Annual Meeting, several research studies were presented that shared a targeted approach to colorectal cancer (CRC) treatment that can ensure efficacy and reduction of side effects. The infographic below highlights those studies and their key findings.

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In May 2021, the US Preventive Services Task Force (USPSTF) revised the colorectal cancer (CRC) screening age for average-risk adults to 45 years. However, stakeholders are concerned about the lack of awareness, access, and motivation among the younger age group to get screened. Now, a new research study has found that the prevalence of CRC screening remained lowest for individuals ages 50 to 54 years old and young adults (age<50) experienced smaller increases in screening prevalence over time, regardless of race, ethnicity, education, income, and insurance coverage. 

An investigation using population-based data from the National Health Interview Survey (NHIS), an annual, cross-sectional survey of the U.S. population conducted by the National Center for Health Statistics at the U.S. Centers for Disease Control and Prevention, studied CRC screening participation using surveys from multiple years. A sample of 80,220 participants ages 50 to 75 years old was analyzed for CRC screening participation. For each survey year, the prevalence of CRC screening was estimated for age, race, ethnicity, educational attainment, family income, and health insurance.

Racial, ethnic, and socioeconomic disparities influence screening rates. Despite the prevalence of CRC screening increasing from 36.7% in 2000 to 66.1% in 2018, screening prevalence was observed to be the lowest for:

  • Participants ages 50 to 54 years old
  • Hispanic populations (56.5%)
  • Asian populations (57.1%)
  • Participants with less than a high school degree (53.6%)
  • Participants from low-income families (56.6%)
  • Participants without insurance (39.7%) 

This may be the result of a lack of concern for cancer and cancer screening among younger adults and their healthcare providers, limited access to healthcare, absence of or limited insurance coverage, and other priorities for young adults, such as work and family. Disparities in screening rates can potentially extend to adults ages 45 to 49 as the new USPSTF recommendations are implemented. Multilevel barriers, such as patient-, provider-, and system-level factors, impact the completion of CRC screening for young adults (age<50), creating disparities and inequities in CRC screening. The administration of new CRC screening guidelines must acknowledge and account for multilevel disparities in screening programs to ensure all populations have equal access to CRC screening and benefit from CRC screening, especially newly eligible adults ages 45 to 49 years old. 

The benefits and outcomes of the updated USPSTF guidelines to extend CRC screening to ages 45 to 49 years old have been debated by clinicians and researchers. Concerns about the updated guidelines include redirecting endoscopic resources away from higher-risk and older patients, resulting in a more significant exacerbation of health disparities. Another criticism is that adults ages 45 to 49 years old who participate in screening may be less likely to belong to groups at higher CRC risk. 

One benefit of expanding CRC screening to the 45-49 age group is to increase the screening participation rate among older populations. Awareness of CRC screening may also increase, resulting in newly eligible adults having more time to schedule their first screening test. However, the impact of screening among those in the 45-49 age group on disparities, benefits, and participation of older adults may take several years to be fully recognized and understood, as the USPSTF’s effect on insurance coverage only occur in mid-2022.

Sahar Alam is a Colon Cancer Prevention Intern with the Colon Cancer Foundation.

Locally advanced rectal cancer may involve multistep neoadjuvant therapy to shrink the tumor before the main treatment, which is often surgery. Although this approach results in a complete pathological response in up to 25% of patients, it involves the risk of complications and toxic effects, including bowel, urinary, and sexual dysfunction; infertility; and altered quality of life in a significant number of patients. A new study, published in the New England Journal of Medicine, has found that patients with mismatch repair-deficient, locally advanced rectal cancer can be effectively treated with neoadjuvant programmed death-1 (PD-1) blockade.  

Approximately 5-10% of rectal adenocarcinomas are attributed to mismatch-repair deficiency, and this subset of tumors respond poorly to standard chemotherapy treatments. Immune checkpoint blockade could be an effective treatment option for this subset of patients. PD-1 elicits an immune checkpoint response of T-cells, allowing tumor cells to bypass the immune system defense, as well as resist the effects of chemotherapy. To test this hypothesis, researchers at Memorial Sloan Kettering Cancer Center and Yale University School of Medicine conducted a phase 2 investigation to analyze the overall response and frequency of sustained clinical complete response to neoadjuvant treatment with a PD-1 inhibitor, dostarlimab. 

PD-1 Blockade Eliminated Rectal Tumors

Of the sixteen patients enrolled in the study, twelve were enrolled for more than six months and completed nine cycles of dostarlimab. The resulting clinical complete response was measured by a combination of rectal MRI, visual endoscopic inspection, and digital rectal examination in twelve patients who had at least six months of follow-up. Endoscopic biopsies were performed at baseline and during visual inspection of tumor response at six weeks, three months, and 6 months, and then every four months thereafter. Serial FDG-PET scans to evaluate tumor eradication presented similar results to that seen with pathological examination and genomic analysis of the evolution of tumor eradication. 

The elimination of tumors after six months of therapy with PD-1 blockade allowed Dr. Cercek and her team to be able to omit both chemoradiotherapy and surgery and to move forward with observation alone. Single-agent dostarlimab was significantly influential in treating mismatch repair-deficient, locally advanced rectal cancer. It provided a clinical complete response in all 12 patients who completed treatment to date. 

Surgery and radiation can permanently impact fertility, sexual health, and bowel and bladder function. With the rise in incidence of rectal cancer among young patients of child-bearing age, anti-PD-1 antibodies can be a good alternative to chemoradiotherapy and surgery and may specifically benefit this cohort of patients. Dostarlimab promotes a refined approach toward treatment that can significantly improve the quality of life of patients, especially younger patients who may not yet have started a family. These findings also encourage the potential for using PD-1 inhibitors in the treatment of other mismatch repair-deficient tumors, such as localized pancreatic, gastric, and prostate cancers.

 

Sahar Alam is a Colorectal Cancer Prevention Intern with the Colon Cancer Foundation. 

With an observed increase of distant-stage colorectal cancer (CRC) among young patients in recent years, researchers have been searching for the reasons behind rising numbers and ways to counteract them. Carcinoids, a subtype of slow-growing cancer, have been found to contribute to the steadily rising incidence rate of early-onset colorectal cancer, which is diagnosed before the age of 50. This has created a need to assess the shifts toward distant-stage adenocarcinoma and its impact on public health.

Why Are We Seeing This Increase?

A study recently published in Cancer Epidemiology, Biomarkers & Prevention sought to understand how the proportions of distant-stage disease changed over time. Several studies have identified a significant increase (49%) in the average annual percent change for distant stage colorectal cancer in the 20-34 years age group. However, many of these studies do not report histological subtypes of CRC. 

With carcinoids increasing in younger patients, it is important to look at adenocarcinoma (most common cancer of the colon and rectum) staging independently from carcinoids (neuroendocrine tumors). Therefore, these researchers focused specifically on adenocarcinomas. Yearly adenocarcinoma incidence rates from the 2000-2016 Surveillance Epidemiology And End Results (SEER) data were stratified by stage, age, subsite, and race for 103,975 patients. Changes in the three-year annual incidence rate were calculated with the percent contribution of each cancer stage. Lastly, the subgroup with the highest proportion of distant-stage disease was determined.

The greatest percent increases were seen in distant-stage cancer when comparing data from 2000-2002 with 2014-2016. Here are a few significant findings of the study:

  • Colon-only distant adenocarcinoma increased most in 30-39-year-olds (49%)
  • Rectal-only distant-stage adenocarcinoma increased most in 20-29-year-olds (133%)
  • Based on race:
    • Distant stage proportions increased most for both colon- and rectal-only subsites in 20-29-year-old non-Hispanic Blacks (14% and 46%, respectively) 
    • The second most-impacted group was 20-29-year-old Hispanics with a 13% increase in the proportion of those affected by rectal-only, distant stage adenocarcinoma.

From these findings, we can conclude that the greatest burden of disease was on younger patients, highest in the non-Hispanic Black and Hispanic subgroups (despite relatively low absolute case counts). The researchers also uncovered that there is a decrease in early-stage disease in these early-onset groups. As we now know, younger patients are presented with higher risks, but the absolute incidence rates in the youngest subgroups remain relatively low.

These findings are important because they set a new precedent for patients under 50 who may not be aware that preventive screening for those at average risk of CRC starts at 45 years. Studies moving forward should also note that not all adenocarcinomas are categorized as early-onset CRC. Although this study is limited in its observational nature, it raises important questions in analyzing staging results, promoting screening opportunities, and keeping the general public aware of their risks. This study also presents potential solutions, including optimizing earlier screening and the risk-stratification of younger patients by family history and symptoms.

 

Juhi Patel is  Colon Cancer Prevention Intern.

The Colon Cancer Foundation recently had the opportunity to speak with Dr. Cynthia Sears, Professor of Medicine and Oncology, Johns Hopkins University School of Medicine; Professor of Molecular Microbiology and Immunology at the Bloomberg School of Public Health. She is also the leader of the Bloomberg-Kimmel Institute for Cancer Immunotherapy at Johns Hopkins. Her current research focus is on the microbiome and how specific bacteria can contribute to colon cancer.

Dr. Sears, received her medical degree at Thomas Jefferson Medical College and completed her training in internal medicine at the Cornell Medical School, and trained in infectious diseases at The Memorial Sloan Kettering Cancer Institute and the University of Virginia. Over the past 20 years, Dr. Sears has conducted research on colonic microbiota and colon cancer, making her an expert in this field.

Q. What enticed you to start studying bacteria and the microbiome in relation to colon cancer.  

Dr. Sears: I am an infectious disease doctor who got into internal medicine because of previous work I conducted. I conduct research on how the microbiome is impacted by organisms and bacteria. I am also looking at improving immunotherapy response among colon cancer patients, since, unfortunately, only 20% to 30% of colon cancer patients respond to immunotherapya majority of patients do not respond. I am currently working to help improve treatments for cancer patients.

Dr. Cynthia Sears

Q. Can you help us improve our understanding of the interaction between a person’s dietary habits and the gut microbiome and how it relates to colorectal cancer?

Dr. Sears: There’s been substantial research showing that diet is a major driver of the composition and function of the microbiome. Individuals who shifted from a meat based diet to a vegetarian diet can see a shift in their microbiome in the first 24 to 48 hours. This shows that we have the ability to impact our microbiome based on the foods we eat. It also shows that we all have the capacity to have a “good” microbiome. It is also important to note that each person is different in their response to a particular diet. For example, some individuals can eat ice cream and pizza and have no change in their physiology, while others may have a terrible response.

Q. Talking about the “ideal” diet, is there really an “ideal” diet? What impact does an individual’s genetics or environmental factors have on the gut microbiome?

Dr. Sears: We are not very good at targeting the individual level. As a society we can’t afford the type of testing it would require to figure out exactly what each individual should and should not be eating. We really must rely on public health and what’s best for most people. In relation to genetics, it’s published that less than 10% of the effect in our microbiome is related to our genetic makeup. There’s a lot of redundancy in the microbiome. We can have three perfectly healthy individuals and when we sequence their microbiomes, they would all look totally different. In one person a certain bug may be taking up a niche and promoting the production of short-chain fatty acids and in another individual, a totally different bug could be doing the exact same thing.

Q. There has been a lot of research comparing the Mediterranean diet with the Western Diet, with the Mediterranean diet being rich in grains, fiber, fruit, vegetables, and fish meanwhile the Western diet is high in fat and red meat. Do you have any advice for individuals on what diet they should follow?

Dr. Sears: People should try and follow a Mediterranean diet or the DASH [Dietary Approach to Stop Hypertension] diet. I’m a big fan of the idea that food is medicine.

Q. What would you like the public to know about the gut microbiome?

Dr. Sears: We are at least as many microbes as we are human cells but the microbes are just much smaller so the human cells are more evident. Microbes are critical to our overall health. Individual’s should strive to foster a good microbiome whether it’s on your skin, your mouth, or in your colon. There is also literature about the impact that exercise and physical activity can have on your gut microbiome as well as brain health and vascular health. The more an individual is focused on healthy living, the better they will be overall.

Q. What do you think is the future of this field?

Dr. Sears: The future direction in this field is immunotherapy, where we can use the microbiome as a biomarker. When you do a stool test or a plasma test the doctors will be able to tell you if you are more or less likely to respond to this therapy based on a microbial signal. This can relate to colorectal cancer because early-age onset colorectal cancer [EAO-CRC] is becoming frighteningly common but it is still rare enough that we are not doing colonoscopies on everyone under the age of 50. We can hopefully do something to see if a person is at a higher risk and then we can focus our care and try to prevent EAO-CRC. 

 

Here are some additional resources on diet and lifestyle and how they can influence your colon health and overall wellness:

  1. Healthy Inside and Out: How Diet and Lifestyle Impact Colorectal Cancer
  2. Dietary Mindfulness Can Reduce the Risk of Colorectal Cancer
  3. Could the Western Diet Be a Risk Factor for EAO-CRC?
  4. Have You Had Your Fiber Yet? Food Habits and the Risk of Colorectal Cancer

The Colon Cancer Foundation (CCF) spoke with Dr. Rami James Aoun, 11th winner of the Dr. Thomas K. Weber Colorectal Cancer Research Scholar Award, for his work looking at biomarkers of radiation response in rectal cancer patients. He is a surgical resident at The Ohio State Wexner Medical Center. Instituted in 2011 by CCF and the Society of Surgical Oncology to recognize translational research focused on the molecular biology of colorectal cancer, the award was renamed in 2020 to honor CCF’s founder, the late Dr. Thomas K. Weber.

Born in West Palm Beach, Florida, Dr. Aoun was raised in Beirut, Lebanon, where he was a student at the American University of Beirut. After completing his undergraduate years and medical school, Dr. Aoun joined Columbia University in New York where he received a Master of Public Health degree in Healthcare Management and Policy. As part of his ongoing residency at The Ohio State Wexner Medical Center, he is completing a research fellowship with Dr. Matthew Kalady, a colorectal surgeon at The James Cancer Center.

Dr. Rami James Aoun

Q: What motivated you to work in the oncology research space, and colorectal cancer in particular?

Dr. Aoun: I am motivated to work in oncology research because I have seen some of my own family members suffer from cancer. However, what specifically interests me in colon cancer research are the patients that I encounter here at The James Cancer Center and my mentors. Their guidance when I was a junior resident was extremely important to set the direction for me as a future colorectal surgeon. That’s how I met Dr. Kalady, and now I am a part of his lab conducting research on colorectal cancer, with the goal of improving patient care outcomes.

Q: Can you summarize the significance of your findings for which you have received this award? Can you also share the prior work or observations that laid the foundation for this project?

Dr. Aoun: We observed a difference in how patients with rectal cancer reacted to neoadjuvant radiation therapy. Some of the patients who were exposed to neoadjuvant therapy had a complete response—the cancer disappeared. However, there were patients who had almost no response to the therapy. The response can be determined and graded by examining the tumor under a microscope. Patients who had a better response end up living longer without cancer.

We sought to identify the reason certain cancers responded to neoadjuvant radiation and certain cancers did not. To do that, we tried to understand these cancers at the genetic level by studying how a rectal cancer expressed particular genes, as measured by mRNA. By comparing the gene expression in both, patients who responded to radiation therapy and those who did not, we were able to obtain a gene signature that helps us identify patterns of gene expression that are different between responders and non-responders.

While this is just a starting point, it can help us develop a more predictive model to use clinically. Once we validate this model, we could be able to distinguish between a responder and non-responder to radiation based on the gene expression that we obtained from their biopsies even before any treatment is administered. This would allow us to provide individualized patient-specific therapy and avoid any unnecessary treatments and procedures.

We also think that certain genes in this signature can be further studied to see if they might be able to be blocked or changed to improve the response to treatment.

Q: What was the size of your current cohort and what is the ‘n’ that you are looking for to be able to validate your study results?

Dr. Aoun: Our ‘n’, or sample size, was 33 patients for this study. In genetic studies like this, it is difficult to design a statistical power needed to validate, but we hope to test this in about 100 different patients.

Q: Did you see any commonality in the gene signatures between rectal cancer and colon cancer?

Dr. Aoun: The gene signature we investigated was related to radiation resistance in rectal cancer, whereas colon cancer is not usually treated with radiation therapy. So, we did not study this for colon cancer. However, some of the pathways we identified are known to be relevant to colon cancer. In terms of the common pathways, what we know is the WNT pathway specifically is involved in the development and progression of colon cancer and rectal cancer. In the gene signature that we identified, six of the genes are involved in the WNT pathway. So, the question is whether the WNT pathway is also involved in radiation resistance in rectal cancer.

Q: Rectal cancer has been steadily increasing in the younger population. Do we know why that may be happening?

Dr. Aoun: An increasing number of younger patients are being afflicted with colorectal cancer and we don’t fully know why. There are lots of different theories about diet, lifestyle, and the microbiome (i.e. the bacterial content in the colon and rectum). This is a hot area of research and many groups are trying to figure out this question.

 

A study published in the Journal of Medical Economics simulating a cohort of one million Medicare patientsUS adults aged 65 years and olderwith average risk of colorectal cancer, investigated the cost-effectiveness of non-invasive fecal tests (fecal immunochemical test (FIT), fecal occult blood test (FOBT), and multi target stool DNA test (mt-sDNA)). The researchers used the Colorectal Cancer and Adenoma Incidence and Mortality Microsimulation Model (CRC-AIM) with test-specific adherence data to estimate the cost-effectiveness of the various options.

Assuming 100% adherence follow-up colonoscopies and using real-world screening adherence data, the researchers found that mt-sDNA was cost-effective when compared to FOBT but not FIT. Cost-effectiveness was defined at the $100,000/quality adjusted life-year (QALY) threshold. 

  •     $62, 814/QALY when compared to FIT
  •   $39,171/QALY when compared to FOBT

The assumption of100% adherence to follow-up colonoscopies is not a significant limitation to this study because this is just one scenario and also because follow-up colonoscopies are covered under Medicare. Since follow-up colonoscopies are covered under Medicare there is not a financial disincentive to get a colonoscopy and therefore most people under Medicare do get the colonoscopy.  Moreover, when the authors ran the model using real-world follow up-colonoscopy and screening adherence rates, they found that mt-sDNA was even more cost-effective:

  •   $31,725/QALY when compared to FIT
  •   $28,465/QALY when compared to FOBT

Generally an incremental cost-effectiveness ratio (ICER) of less than $100,000 is considered good value, and those under $61,000/QALY is considered cost-effective. Therefore, when real-world adherence rates were considered, mt-sDNA was the more cost-effective option compared to both FIT and FOBT and resulted in greater reductions in CRC incidence and mortality.

Cost-effectiveness analyses are important for determining which screening test performs better than the others, and where to relocate resources to achieve the best health outcomes for the lowest possible cost. These types of studies on Medicare populations are important because they help policy makers make informed decisions on resource allocation.

 

Gargi Patel is a Colon Cancer Prevention Intern with the Colon Cancer Foundation.

We learn time and again that prevention is the best medicine, and this holds true for colorectal cancer (CRC). It is estimated that 50% of CRC cases can be prevented with diet and lifestyle modifications. Previous studies that looked at the relationship between CRC development and nutrition concluded that there is a strong correlation between diet and the development of certain types of cancer, specifically CRC. 

A recent study published in Preventive Medicine Reports investigated the impact that an insufficient diet plays in the development and prevalence of certain cancers as well as the effect that race and ethnicity has on diet.  Wholegrains, dietary fiber, non-starchy fruits, and vegetables, dairy products, milk, cheese, dietary calcium, coffee, and calcium supplements were found to be associated with preventing cancer development. The study examined population attributable factors and the number of excessive cases diagnosed in Texas in 2015 that were attributed to an inadequate diet, defined as a diet that does not meet or conform to the national or global dietary recommendations. 

With a diverse study population, the researchers had the opportunity to explore how race and ethnicity play into diet and thus contribute to the prevalence of cancers, specifically colorectal cancer (CRC).  

The study found:

  • While men were more likely than women to not follow guidelines on red and processed meat consumption.
  • Women were more likely to miss dietary recommendations on fiber and calcium intake.
  • A significant correlation between processed meats consumption and the prevalence of CRC and a connection between red meat consumption and the prevalence of CRC. 

There has been additional research conducted to show that there is a link between dietary fiber intake, and dietary calcium intake and the prevention of CRC. Looking at the racial and ethnic difference the study found that Non-Hispanic Whites consumed higher than the recommended dietary intake of red and processed meats. While it was found that Non-Hispanic Blacks were the most likely to have insufficient fiber and calcium intake.

In the Texas population, the authors found:

  • 3.3% of all new cancers (>3,428) could be attributed to an inadequate diet 
  • 34% of new CRC cases can be attributed to dietary insufficiencies 

The authors describe a similar correlation identified in an Australian population, where:

  • 17.6% of CRCs were related to an insufficient fiber level in diet 
  • 17.7% of CRCs were attributed to red and processed meats 
  • Men had a higher proportion of cancers attributable to an insufficient diet than women 
  • Excess consumption of processed meat contributed to 1,002 new cancer cases and red meat consumption contributed to 379 additional cancer cases 

This study along with multiple other studies conducted in relation to dietary factors and their contribution to cancer highlight the importance of dietespecially insufficient fiber intake and excess red or processed meat intakeon overall cancer burden.

 

Abigail Parker is a Colon Cancer Prevention Intern with the Colon Cancer Foundation.

Immunotherapy aids your immune system to fight off cancer. There are five types of immunotherapy: treatment vaccines, immune checkpoint inhibitors, T-cell transfer therapy, monoclonal antibodies, and immune system modulators. While there have been no treatment vaccines approved for colorectal cancer (CRC) yet, BioNTech’s mRNA-based treatment vaccine has recently reached phase 2 clinical trials for CRC. The vaccine, individualized to each patient, is being developed as a treatment for CRC as well as to prevent relapse in those who have undergone CRC surgery. 

How Does Immunotherapy Work?

The immune system is built to detect and destroy abnormal/mutated cells. Tumor-infiltrating lymphocytes are often found around tumors and they are an indication that the immune system is working to eliminate the tumor. Cancer cells typically undergo genetic changes that allow them to escape the immune system—they often have proteins on their surface that inactivate immune cells, and they can even change cells surrounding them to interfere with the immune system. Therefore, a therapy that can train the immune system to identify and destroy cancer cells capable of defying the immune system is important.

Cancer Treatment Vaccines

Cancer treatment vaccines are designed for people who already have cancer, and trains their body’s immune system to find well-hidden cancer cells. These vaccines can be made in three different ways. 

  1. From the patient’s own cancer cells to cause an immune response against features that are unique to their cancer.
  2. From tumor-associated antigens that are found on cancer cells. These are made for cancer subtypes.
  3. From dendritic cells, which are a type of immune cell that respond to an antigen on tumor cells. This type of a vaccine is already being used for treating prostate cancer.

Matias Riihimäki et al. in their 2016 epidemiologic study published in Scientific Reports found that up to 18% of all CRC patients have recurrence and up to 25% have metastasis. A treatment vaccine would be able to help prevent recurrence and help patients with metastasis suppress small tumors that are often difficult to remove surgically.

BioNTech Chief Medical Officer and Co-founder Özlem Türeci, M.D., noted in a press release, “This trial is an important milestone in our efforts to bringing individualized immunotherapies to patients. Many cancers progress in such a way that the patient initially appears tumor-free after surgery, but after some time tumor foci that were initially invisible grow and form metastases. In this clinical trial in patients with colorectal cancer, we aim to identify high-risk patients with a blood test and investigate whether an individualized mRNA vaccine can prevent such relapses.”

Gargi Patel is a Colon Cancer Prevention Intern at the Colon Cancer Foundation.

Slow-transit constipation (STC) is reported to occur in 15-30% of people in the U.S. The most widely accepted definition of STC is two or fewer bowel movements per week or straining at stool more than 25% of the time. Research continues to point to STC as a risk factor for colorectal cancer (CRC).

A study published in 2020 that looked at 2,165 patients (median age 54 years), found that the cumulative probability of CRC was 0.2% 5 years after STC diagnosis and 0.4% 10 years after STC diagnosis. This was not significantly different (p=0.575) than among those without STC diagnosis. However, this may be due to the small number of patients (5) who were diagnosed with CRC.

Although the authors of the 2020 study did not find a significant difference among those with and without STC diagnosis, it is well established that STC increases CRC risk. Gurérin et al. in their 2014 study of over 100,000 patients identified a statistically significant risk of CRC among those with STC:

  • 56% higher for CRC
  • 260% higher for benign neoplasm
  • 256% higher for benign neoplasm in colon
  • 262% higher for anal and rectal polyps

Current management options for STC range from dietary counseling, pharmacological therapy, and surgery. 

While the etiology of STC remains unclear, there is increasing evidence that it is caused by an imbalance in the gut microbiome. Zhang et al. in their 2021 review published in Gastroenterology Report found that gut microbiota may play a major role in modulating colonic motility, secretion, and absorption. However, there is still much research needed to understand how the gut microbiome modulates movement of fecal matter through the small intestine and colon.

Conversations about the role of the gut microbiome in CRC development were a part of the Early-Age Onset Colorectal Cancer Summit held by the Colon Cancer Foundation in May 2022.

 

Gargi Patel is a Colon Cancer Prevention Intern with the Colon Cancer Foundation.