Daily Times

A new research has provided further evidence that what people eat alters gut bacteria to affect colorectal cancer risk, after linking a high-fiber diet to a reduced risk of colorectal cancer containing Fusobacterium nucleatum.

Study leader Dr Shuji Ogino – from the Dana-Farber Cancer Institute of the Harvard TH Chan School of Public Health in Boston, MA – and colleagues report their findings in JAMA Oncology.

The study from Dr Ogino and team supports this association, after finding that individuals who followed a high-fibre diet were at a lower risk of developing colorectal cancer tumours containing the bacterium F nucleatum.

According to Dr Ogino, recent research has shown that F nucleatum may play a role in the development of colorectal cancer.

“One study showed that F nucleatum in the stool increased markedly after participants switched from a prudent to a Western-style, low-fibre diet,” he added. “We theorised that the link between a prudent diet and reduced colorectal cancer risk would be more evident for tumours enriched with F nucleatum than for those without it.”

The team found that participants who followed a prudent diet – defined as a high intake of vegetables, fruits, whole grains, and legumes – were at a significantly lower risk of colorectal cancer containing F nucleatum, compared with subjects who followed a Western-style diet.

However, participants who had a prudent dietary pattern did not show a reduced risk of colorectal cancer that was free of F nucleatum.

Dr Ogino says that these findings provide “compelling evidence” that diet influences the likelihood of developing specific forms of colorectal cancer by altering the gut microbiome.

“Though our research dealt with only one type of bacteria, it points to a much broader phenomenon – that intestinal bacteria can act in concert with diet to reduce or increase the risk of certain types of colorectal cancer.”

The researchers conclude that further studies are needed to confirm their findings, and larger-scale studies should delve into the complex relationship between diet, gut bacteria, and cancer.

In another study, scientists have discovered the conditions that programme migrating cancer cells to become dormant and hide from chemotherapy after spreading.

Researchers suggested that the work could lead to new drugs and therapies that transform the treatment of metastatic cancers, most of which cannot be cured with current approaches.

Hypoxia, a condition in which cells are starved of oxygen, is a known hallmark of solid tumors that triggers stress responses and induces resistance to chemotherapy and radiotherapy.

Until now, however, it has not been clear how hypoxia in primary tumors influences what happens to cancer cells that migrate to new sites, and how this affects the prognosis of the disease.

The study suggests that hypoxic microenvironments in primary tumors give rise to dormant disseminated tumor cells (DTCs) that “hide” from therapy and may be a cause of disease relapse and poor outcomes.

Senior author Julio A Aguirre-Ghiso, PhD, a professor of medicine, haematology, and medical oncology at Mount Sinai, says: “This research highlights the signals in the primary tumour that instruct disseminated cancer cells to become dormant.”

“Dormant cells must be targeted to address the whole spectrum of the disease and attacking the cancer,” he added.

With the help of biosensors, nanotechnology, and advanced imaging, the team implanted drugs that create hypoxic and non-hypoxic niches in breast tumors in mice and observed the effect on cells.

The researchers were able to isolate the cancer cells one by one and find out how they behaved when they travelled from the primary tumour to the lungs.

Genetically encoded biosensors allowed them to determine which cells were dormant, which ones were exposed to low oxygen, and their reactions to therapy.

They discovered that hypoxic tumour microenvironments not only produce DTCs that rapidly grow and spread, but also send a large proportion of them into a dormant state that makes them better able to evade chemotherapy.

The study suggests, therefore, that the poor prognoses associated with hypoxic tumours may arise not only because they produce more aggressive cancer cells, but also because they program many of them to enter a dormant state where they can hide from chemotherapy.

Researchers also found genes in the primary tumour that correlated with the behaviour of dormant, treatment-resistant cells in the secondary tumours.

They suggested that these genes could form the basis of a biomarker to predict which patients are likely to have more of the dormant, resistant cells.

Prof Aguirre-Ghiso describes the study as “an important step to further explore the biology of these dormant cells and design therapies that specifically address this biology”.

He added, “We hope this research may lead to the use of dormancy markers in primary tumours to assess the prevalence of disseminated cancer cells in secondary organs and thus tailor treatments to eliminate these dormant and therapy evading cancer cells.”