cancer

Unlike other medical disorders such as stone diseases, cancer treatment is time-sensitive. The later a patient sees a doctor, the more advanced their cancer is, necessitating more complicated therapy. At the end of the day, cancer is a’referred disease.’ A general physician or specialist is usually the one who suspects the development of cancer, which is subsequently explored by a cancer super-specialist after a referral to a better medical facility.

During the coronavirus disease (Covid-19) pandemic, cancer detection went up for a toss in many areas where new patients could not be taken in for treatment because most of these physicians were either not available or tied up with Covid-19 treatment.

At the height of the Covid-19 second wave in April-May 2021 and later during the third wave in January this year, registration of new cancer patients has plummeted across the country. However, following the second wave of the pandemic, new registrations of cancer patients jumped once again in June last year as both primary care physicians and patients were willing to step up for non-Covid treatments.

Ahead of World Cancer Day on February 4 (Friday), Dr. Shubham Garg, senior consultant of surgical oncology at the Fortis Hospital in Noida, shared a few insights on the significant trends reported in cancer treatments:

Treatment Interruptions: Cancer treatment is long-drawn. Surgery requires admission for seven to ten days, while radiotherapy requires daily visits to the hospital. Chemotherapy, too, requires periodic visits to the hospital.

Due to Covid-19, especially in April- May 2021, hospital services were badly hit and patients were not able to go visit the hospitals. This led to an interruption in treatment that influenced its effectiveness. According to Dr. Garg, there were also times when even the patients could not go to the hospitals due to other pressing family issues.

This led to a drop in chemotherapy cycles during the second wave of the Covid-19 pandemic.

However, what was observed during Phase-3 of the Covid-19 pandemic, says Dr. Garg, was “incidental positivity” – asymptomatic patients were subjected to a Covid-19 test before every admission, which not only added to a procedural hurdle in seeking treatment, but also led to many patients being detected with Covid-19 and unwanted treatment stoppage.

Higher risk in cancer patients: It is a well-documented fact that Covid-19 deaths were reported more among elderly patients with comorbidities and the immunocompromised.

“Cancer patients actually fit in the perfect template for a ‘high-risk patient’ in terms of Covid”, said the senior doctor.

UP trends for cancer: Tobacco has been the bane for cancer patients in Uttar Pradesh, particularly those from the western and eastern parts.

“Initially, we used to get patients with advanced diseases from the interiors of Uttar Pradesh, but now what we get are partially-treated patients or poorly-treated patients from these Tier-2 cities,” said Dr. Garg. “This is due to the fact that in the last couple of years a lot of cancer treatment facilities have mushroomed in UP’s tier-2 cities, such as Meerut, Bareilly, Kanpur, Gorakhpur, and the likes. These centers are bound by the limitations of technology or skillset and sometimes end up providing sub-optimal treatment, leading to incomplete treatment or early recurrence. Treating such patients is a different challenge altogether.”

Technological advances: As most cancer patients are diagnosed with the disease in the head and neck region, Dr. Garg said that top hospitals like Fortis offer specialised oncoplastic services allowing for “better reconstruction”, following cancer surgery in the head and neck. It also allows for better functional and cosmetic recovery, he said, specifying that advanced medical techniques like microvascular surgery also allows for free flap transfer.

HIPEC surgery: Despite proper chemotherapy, many patients may have residual diseases. However, these can now be tackled surgically, wherein during surgery only chemotherapy can be instilled at high temperatures so that the resistant disease can be removed. This is a specialised surgery technique and requires advanced machinery where chemotherapy is heated and administered at a constant temperature.

SBRT: Stereotactic body radiation therapy (SBRT) allows precise targeting of radiation so that side effects to surrounding structures can be minimised.

Immunotherapy: This type of therapy activates one’s immune system to fight against cancer cells allowing minimal side effects and better effectiveness.

In cancer research, it has long been known that lactic acid, or lactate, is produced in large quantities by cancer cells and that this lactic acid disrupts our defence against tumours. Until now, however, we did not know exactly how this happens. Prof Jo Van Ginderachter, immunologist and cancer researcher at the Vrije Universiteit Brussel and the Flemish Institute for Biotechnology (VIB), found the answer, in collaboration with PhD student Xenia Geeraerts (VUB), Prof Sarah-Maria Fendt (VIB-KU Leuven) and Prof Jan Van den Bossche of the University of Amsterdam. The findings were published in the renowned journal Cell Reports.

Cancer is a feared disease that has a significant influence on one’s personal, familial, and social life. Not only the patient, but everyone involved is physically, emotionally, and financially impacted. The likelihood of cure varies depending on the stage at which the patient presents. One of the most dangerous malignancies is pancreatic cancer. They are only treatable if caught early enough.

The chief problem is that they usually are detected very late and also they are less responsive to chemotherapy and radiotherapy. So it becomes paramount to catch them at a very early stage or to ensure strategies to prevent them from happening.

Unfortunately, there are no screening tests or diagnostic tests which can catch them in pre-cancerous or early stages. Lifestyle changes and dietary modifications have been known to affect the chances of gastrointestinal cancer. So, it becomes a lucrative option for pancreatic cancer, too. Many epidemiological shades have suggested that pancreatic cancer is associated with obesity (high BMI) and increased fat consumption.

It has been seen that high dietary intake of fat has been linked to causing pancreatic cancer not only directly but also by increased chances of obesity.

Obesity is a pro-inflammatory condition of the body with high levels of cytokines (a kind of chemical involved in inflammatory conditions). There are cytokines that have a role in the genesis of pancreatic cancer. Many observatory studies past two decades have shown that high saturated fat consumption leads to an increase in changes in pancreatic cancer.

A study published in the journal of the National Cancer Institute in 2009 (comparing more than five hundred thousand adults) has demonstrated a positive association between dietary intake of total fat (particularly animal fat) consumption and pancreatic cancers. When a comparison was done between people taking the highest to lowest fat content, it was seen that there was a 23 per cent increase in the chances of pancreatic cancer.

This effect was more profound when saturated fat was consumed more. It is very difficult to comment on the mechanism of how fat consumption leads to pancreatic cancer. The most likely explanation is that fat is an important stimulant for the hormone CCK (cholecystokinin) which leads to the secretion of pancreatic juice and bile. This hormone is also an important instrument in the growth of pancreatic cancer cells. In an experimental study CCK antagonist (counter the effect of CCK) Proglumide has been shown to decrease the growth of cancer cells and the metastatic potential of pancreatic cancer cells.

All the explanations lead to important questions on whether is it possible to decrease the chances of pancreatic cancer by decreasing fat consumption.

Recently, an important study published in AICR’s research update in November 2017 has found that obese and overweight elderly women had lowered the risk of pancreatic cancer by following a low-fat diet plan. There were two groups, one following their normal fat consumption (the comparison group) and another was made to eat low-fat and more vegetables, fruits, and grains (intervention group).

After 15 years of follow-up, the intervention group had 92 cases of pancreatic cancer as compared to 165 cases in the comparison group. This translated to a rate of pancreatic cancer of 41 per 1,00,000 in the comparison group while a rate of 35 per 1,00,000 in the intervention group was seen.

A low-fat diet was effective in reducing the chances of pancreatic cancer in overweight and obese postmenopausal women. Interestingly, a low-fat diet did not lower the disease risk for women with normal weight.

Almost all of this evidence comes from the observational studies which support that increased fat consumption leads to an increase in the incidents of pancreatic cancer and a decrease in the incidence by decreasing fat consumption, but they cannot be considered very strong evidence to be concluded as “cause and effect”.

But this evidence at least can be considered as a caution to decrease the total fat consumption, particularly animal fat. So it may be helpful to motivate the general public to avoid food high in saturated or trans fats like butter, margarine coconut oil, palm oil, vegetable oil, and hydrogenated oils. A diet with high fiber content, low fat, and a good lifestyle with daily exercise is likely to help in decreasing incidents of cancer.

According to a new study, the amino acid valine, a chemical building element of many animal proteins, is involved in malignant growth in T cell acute lymphoblastic leukaemia.

The research has been published in the ‘Nature Journal’.

Led by researchers at NYU Langone Health, its Department of Pathology, and the Laura and Isaac Perlmutter Cancer Center, the study showed that genes involved in using up valine in cells were more active in cancerous T cells than in normal T cells.

Blocking these valine-linked genes not only led to decreased valine in leukaemia blood T cells but also stalled these tumour cells from growing in the lab. Only 2 per cent of cancerous T cells remained alive.

Further, experiments suggested that changes (mutations) in the DNA code of the gene NOTCH1, the most commonly seen in patients who develop leukaemia, encouraged cancer growth in part by increasing valine levels.

In light of current studies, it’s worth mentioning that the vast majority of people will not be diagnosed with cancer during their lifetime. According to the National Cancer Institute, roughly 40% of people will get cancer, whereas the other 60% will not.

These percentages are important to remember because a study led by University of Colorado Cancer Center Deputy Director James DeGregori, PhD, a professor of biochemistry and molecular genetics, and Edward J. Evans, PhD, a postdoctoral fellow in the Department of Biochemistry and Molecular Genetics, discovered that most cancer-free people over 60 have at least 100 billion cells with at least one oncogenic, or tumor-causing, mutation.

The research, published in Aging and Cancer, involved a meta-analysis of previously published sequencing data on normal tissues, which DeGregori and Evans used to categorize somatic mutations, or mutations that occur after egg fertilization, based on their presence in cancer and showcase the quantity of cells with cancer-associated mutations in cancer-free individuals.

“When you have trillions of cells and they’re being maintained for up to a century, they’re going to accumulate mutations,” DeGregori explains. “The fact that we get mutations is not surprising, just based on known mutation rates. One thing this research points to is that we need to start looking at these mutations, and how or whether they cause cancer, from a different light.”

“To understand the genesis of cancer, we need to look at normal tissue,” Evans says. “By the time it’s developed into cancer, all the mutations are there and we don’t always know which ones are contributing to the actual genesis of cancer.

“We had the idea that a lot of the mutations in people would be oncogenic or associated with cancer, but we just didn’t know how many. We figured that it would increase as people get older, but we didn’t necessarily know which genes would be prevalent and we didn’t know the magnitude of how many cells could actually have these oncogenic mutations.”

After reviewing existing literature, Evans collected datasets from researchers who previously had conducted research on mutations in normal tissue. He taught himself to code in the programming language Python so that he could pull appropriate data and create data frames to categorize mutations by the genes, tissue, and age of individuals in which they were occurring, among other factors.

“We have about three trillion nucleated cells in our bodies, so to put it in perspective, 100 billion cells with oncogenic mutations isn’t a majority of our total number of cells,” Evans says. “But that’s a surprisingly high number considering that it only takes one cell to cause cancer. If there are billions of cells with these mutations but no indication of cancer, what does that mean? What does it mean to have these oncogenic mutations in the body?”

One of the interesting facets of the research findings, DeGregori says, has been learning that oncogenic mutations can be extremely prevalent in certain types of tissue, including skin, colon, and esophagus.

“Some tissues can be absolutely dominated by these mutations,” DeGregori says. “But if you look at the esophagus, for example, half of it is loaded with NOTCH1 mutations, which rarely contribute to cancer in non-smokers. So, to test for this mutation isn’t really useful if most of us have it and it rarely leads to cancer.

“If we’re simply looking for oncogenic mutations, we’re always going to find them and they may not tell us much about cancer risk. How those oncogenic mutations are interfacing with the tissue environment will tell us so much more about risk.”

A further avenue of research, DeGregori says, will be studying why some tissues have such a high occurrence of oncogenic mutations but a comparatively low occurrence of cancer, while other types of tissue have a relatively low level of oncogenic mutations.

“Before we began this research, I had no idea that almost 90 per cent of colon cells become occupied with cancer-causing mutations,” DeGregori said. “That the number was so high was quite surprising, but a relatively low percentage of us will get colon cancer. So, it’s going to be important to study this difference between tissue types. Why is it that epithelial tissue in the skin, for example, becomes dominated by oncogenic variants, but lung tissue actually keeps a fairly low level?”

Evans says future research could continue studying which oncogenic mutations are most likely to contribute to cancer and help to hone genetic screening tools to test for the most cancer-causing mutations.

“The vast majority of mutations don’t do anything, they don’t cause any problems, and many aren’t even in coding sequences,” DeGregori explained.

“Every cell in our bodies has dozens and dozens of mutations, if not hundreds or thousands, so we have an opportunity to begin asking whether these patterns of mutations that we see can dictate whether someone is at high risk of cancer,” DeGregori added.