Medically Speaking Team

According to a new study, women who used chemical hair straightening treatments had a greater risk of uterine cancer than women who did not use these products. The researchers discovered no links between other hair products used by the women and uterine cancer, such as hair colours, bleach, highlights, or perms.

The data set includes 33,497 U.S. women aged 35 to 74 who took part in the Sister Study, a study run by the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health (NIH), to investigate risk factors for breast cancer and other health issues.

The women were followed for almost 11 years and during that time 378 uterine cancer cases were diagnosed. The researchers found that women who reported frequent use of hair straightening products, defined as more than four times in the previous year, were more than twice as likely to go on to develop uterine cancer compared to those who did not use the products.

“We estimated that 1.64% of women who never used hair straighteners would go on to develop uterine cancer by the age of 70; but for frequent users, that risk goes up to 4.05%,” said Alexandra White, Ph.D., head of the NIEHS Environment and Cancer Epidemiology group and lead author on the new study. “This doubling rate is concerning. However, it is important to put this information into context — uterine cancer is a relatively rare type of cancer.”

Uterine cancer accounts for about 3% of all new cancer cases but is the most common cancer of the female reproductive system, with 65,950 estimated new cases in 2022. Studies show that incidence rates of uterine cancer have been rising in the United States, particularly among Black women.

Approximately 60% of the participants who reported using straighteners in the previous year were self-identified Black women, according to the study published in the Journal of the National Cancer Institute. Although, the study did not find that the relationship between straightener use and uterine cancer incidence was different by race, the adverse health effects may be greater for Black women due to higher prevalence of use.

“Because Black women use hair straightening or relaxer products more frequently and tend to initiate use at earlier ages than other races and ethnicities, these findings may be even more relevant for them,” said Che-Jung Chang, Ph.D., an author on the new study and a research fellow in the NIEHS Epidemiology Branch.

The findings are consistent with prior studies showing straighteners can increase the risk of hormone-related cancers in women.

The researchers did not collect information on brands or ingredients in the hair products the women used. However, in the paper they note that several chemicals that have been found in straighteners (such as parabens, bisphenol A, metals, and formaldehyde) could be contributing to the increased uterine cancer risk observed.

Chemical exposure from hair product use, especially straighteners, could be more concerning than other personal care products due to increased absorption through the scalp which may be exacerbated by burns and lesions caused by straighteners.

“To our knowledge this is the first epidemiologic study that examined the relationship between straightener use and uterine cancer,” said White. “More research is needed to confirm these findings in different populations, to determine if hair products contribute to health disparities in uterine cancer, and to identify the specific chemicals that may be increasing the risk of cancers in women.”

This team previously found that permanent hair dye and straighteners may increase breast and ovarian cancer risk.

Also read: Scientists find no heart damage in hypertension patients with shortened fingers

Following a series of related tests that were initially thought to have launched the global epidemic in China, Boston University researchers claim to have generated a new COVID strain with an 80% fatality rate.

The version, a combination of omicron and the original virus in Wuhan, killed 80% of the mice infected with it, according to Fox News. Mice only showed modest effects when exposed to omicron. A team of scientists from Florida and Boston conducted the study at the school’s National Emerging Infectious Diseases Laboratories.

As per the reports of Fox News, they extracted the spike protein from omicron and attached it with the strain first detected at the onset of the pandemic that began in Wuhan, China. They then documented how the mice reacted to the hybrid strain. “In…mice, while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80 percent,” they wrote in a research paper.

According to researchers, the new strain has five times more contagious virus particles than the omicron variety. In a statement, the university stressed that the replicated strain was less dangerous than the original strain.

“First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-COV-2 virus strain or make it more dangerous. In fact, this research made the virus replicate less dangerous,” the statement read.

“Secondly, the research was reviewed and approved by the Institutional Biosafety Committee (IBC), which consists of scientists as well as local community members. The Boston Public Health Commission also approved the research.

Furthermore, this research mirrors and reinforces the findings of other, similar research performed by other organizations, including the FDA. Ultimately, this research will provide a public benefit by leading to better, targeted therapeutic interventions to help fight against future pandemics.”

According to Fox News, COVID-19 was thought to have originated in a wet market in Wuhan, although many believe the virus was created at the Wuhan Institute of Virology. The World Health Organization is still being chastised for how it handled the crisis in its early, critical days. Even among fully vaccinated people, the omicron variation is extremely transmissible. According to experts, the spike protein is responsible for virus infectivity rates; other modifications to the virus’s structure control its timeliness. One disadvantage of the study was the type of mouse utilised, as other species are more human-like.

Also read: Scientists find no heart damage in hypertension patients with shortened fingers

Turning on the stress response in cells at a post-reproductive age may be the key to reducing ageing and enhancing longevity, according to researchers.

The NTU Singapore team discovered that turning on this stress response in aged worms by giving them a high-glucose diet enhanced their longevity compared to worms fed a regular diet in lab trials on a kind of roundworm that shares parallels with humans. The NTU team’s findings, published on October 19 in Nature Communications, are the first to establish a relationship between this stress response and ageing.

While further studies are needed to gain a deeper understanding of this link, the scientists said their findings open the door to the development of therapies that could delay the onset or even tackle age-related disorders such as cancer, dementia, and stroke.

Cell biologist and study lead Associate Professor Guillaume Thibault from the NTU School of Biological Sciences said: “Ageing is a critical risk factor for a variety of human pathologies, from metabolic diseases such as diabetes to cancer and neurodegenerative diseases. From a public health perspective, determining the cellular pathways that underpin the ageing process could take us one step closer to developing novel therapeutic strategies to treat age-related disorders.

“While our study found that a high-glucose diet could be useful to slow down ageing and promote longevity in aged worms, we are not recommending that the aged population should now turn to a high-sugar diet. This study shows that triggering certain stress responses in cells may translate to longevity, and that activating this stress response with a drug might be critical to decelerate cellular ageing.”

Aside from showing that the effect of manipulating this stress response in aged worms, the NTU scientists also showed that the same response, when ‘switched off’ in young worms fed a high-glucose diet, helped them to live longer than worms on a normal diet.

Commenting as an independent expert, Professor Rong Li, Director of the Mechanobiology Institute at the National University of Singapore said: “Metabolic diseases have serious consequences in the elderly if left untreated. This work is impactful because the scientists identified a cellular pathway, called the unfolded protein response, which affects lifespan in animals fed a high-glucose diet. They found that inhibiting this pathway dramatically extended the lifespan of these animals. They, therefore, propose that targeting this pathway may extend lifespan in humans with metabolic disorder.”

This research is in line with the University’s NTU2025 five-year strategy plan, which focuses on health and society as one area with substantial intellectual and societal influence.

Also Read: People who have diabetes more often affected by trigger finger: Study

A recent study suggests that getting less than five hours of sleep in your mid-to-late twenties may increase your chance of developing at least two chronic diseases.

The study, published in PLOS Medicine, looked at the effect of sleep duration on the health of almost 7,000 men and women aged 50, 60, and 70 from the Whitehall II cohort study. Over a 25-year period, researchers looked at the association between how long each person slept, mortality, and whether they had been diagnosed with two or more chronic conditions (multimorbidity), such as heart disease, cancer, or diabetes.

People who reported getting five hours of sleep or less at age 50 were 20% more likely to have been diagnosed with a chronic disease and 40% more likely to be diagnosed with two or more chronic diseases over 25 years, compared to people who slept for up to seven hours.

Additionally, sleeping for five hours or less at the age of 50, 60, and 70 was linked to a 30% to 40% increased risk of multimorbidity when compared with those who slept for up to seven hours.

Researchers also found that sleep duration of five hours or less at age 50 was associated with 25% increased risk of mortality over the 25 years of follow-up — which can mainly be explained by the fact that short sleep duration increases the risk of chronic disease(s) that in turn increase the risk of death.

Lead author, Dr Severine Sabia (UCL Institute of Epidemiology & Health, and Inserm, Universite Paris Cite) said: “Multimorbidity is on the rise in high income countries and more than half of older adults now have at least two chronic diseases. This is proving to be a major challenge for public health, as multimorbidity is associated with high healthcare service use, hospitalisations and disability.

“As people get older, their sleep habits and sleep structure change. However, it is recommended to sleep for 7 to 8 hours a night — as sleep durations above or below this have previously been associated with individual chronic diseases.
“Our findings show that short sleep duration is also associated with multimorbidity.

“To ensure a better night’s sleep, it is important to promote good sleep hygiene, such as making sure the bedroom is quiet, dark and a comfortable temperature before sleeping. It’s also advised to remove electronic devices and avoid large meals before bedtime. Physical activity and exposure to light during the day might also promote good sleep.”

As part of the study, researchers also assessed whether sleeping for a long duration, of nine hours or more, affected health outcomes. There was no clear association between long sleep durations at age 50 and multimorbidity in healthy people.

However, if a participant had already been diagnosed with a chronic condition, then long sleep duration was associated with around a 35% increased risk of developing another illness. Researchers believe this could be due to underlying health conditions impacting sleep.

Jo Whitmore, senior cardiac nurse at the British Heart Foundation said: “Getting enough sleep allows your body to rest. There are a host of other ways that poor sleep could increase the risk of heart disease or stroke, including by increasing inflammation and increasing blood pressure.

“This research adds to a growing body of research that highlights the importance of getting a good night’s sleep.”

Also Read: People who have diabetes more often affected by trigger finger: Study

For decades, scientists in Berlin have been researching a bizarre hereditary illness that causes half of certain families’ members to have abnormally short fingers, hypertension and dangerously high blood pressure. Patients who are not treated frequently die of a stroke when they reach the age of 50.

The study’s findings were published in the journal Circulation. Researchers at the Max Delbruck Center (MDC) in Berlin discovered the cause of the disease in 2015 and were able to prove it five years later using animal models: a mutation in the phosphodiesterase 3A gene (PDE3A) causes its encoded enzyme to become overactive, affecting bone growth and causing blood vessel hyperplasia, resulting in high blood pressure.

Immune to hypertension-related damage

“High blood pressure almost always leads to the heart becoming weaker,” said Dr. Enno Klussmann, head of the Anchored Signaling Lab at the Max Delbruck Center and a scientist at the German Centre for Cardiovascular Research (DZHK). As it has to pump against a higher pressure, Klussmann explains, the organ tries to strengthen its left ventricle. “But ultimately, this results in the thickening of the heart muscle – known as cardiac hypertrophy – which can lead to heart failure greatly decreasing its pumping capacity.”

But in hypertension patients with shortened fingers and mutated PDE3A gene, this doesn’t happen. “For reasons that are now partly – but not yet fully – understood, their hearts appear immune to the damage that usually results from high blood pressure,” said Klussmann.

The study is the result of a collaboration between researchers at the Max Delbruck Center, Charite – Universitatsmedizin Berlin, and the DZHK. In addition to Klussmann, professors Norbert Hubner and Michael Bader from the Max Delbruck Center were involved as final authors, along with Dr. Sylvia Bahring from the Experimental and Clinical Research Center (ECRC) – a joint institution of Charite and the Max Delbruck Center. Together with 43 other researchers from Berlin, Bochum, Heidelberg, Kassel, Limburg, Lubeck, Canada, and New Zealand, the team has now reported its findings on the protective effects of the gene mutation – and why these results could change the way heart failure is treated in the future.

The publication has four first authors, three of whom conduct research at the Max Delbruck Center and one at the ECRC.

Two mutations with the same effect

The scientists performed their tests on human patients with hypertension and brachydactyly (HTNB) syndrome – i.e., high blood pressure and abnormally short digits – as well as on rat models and heart muscle cells. The cells were grown from specially engineered stem cells known as induced pluripotent stem cells. Before testing began, researchers altered the PDE3A gene in the cells and the animals to mimic HTNB mutations.

“We came across a previously unknown PDE3A gene mutation in the patients we examined,” reports Bahring. “Previous studies had always shown the mutation in the enzyme to be located outside the catalytic domain – but we have now found a mutation right in the center of this domain.” Surprisingly, both mutations have the same effect in making the enzyme more active than usual. This hyperactivity ramps up the degradation of one of the cell’s important signalling molecules known as cAMP (cyclic adenosine monophosphate), which is involved in the contraction of the heart muscle cells. “It is possible that this gene modification – regardless of its location – causes two or more PDE3A molecules to cluster together and thus work more effectively,” Bahring suspects.

The proteins stay the same

The researchers used a rat model – created with CRISPR-Cas9 technology by Michael Bader’s lab at the Max Delbruck Center – to try to better understand the effects of the mutations. “We treated the animals with the agent isoproterenol, a so-called beta-receptor agonist,” says Klussmann. Such medications are sometimes used in patients with end-stage heart failure. Isoproterenol is known to induce cardiac hypertrophy. “Yet surprisingly, this occurred in the gene-modified rats in a manner similar to what we observed in the wild-type animals. Contrary to what we expected, existing hypertension did not aggravate the situation,” reports Klussmann. “Their hearts were quite obviously protected from this effect of the isoproterenol.”

In further experiments, the team investigated whether proteins in a specific signaling cascade of the heart muscle cells changed as a result of the mutation and if so which ones. Through this chain of chemical reactions, the heart responds to adrenaline and beats faster in response to situations such as excitement. Adrenaline activates the cells’ beta receptors, causing them to produce more cAMP. PDE3A and other PDEs stop the process by chemically altering cAMP. “However, we found little difference between mutant and wild-type rats at both the protein and the RNA levels,” Klussmann said.

More calcium in the cytosol

The conversion of cAMP by PDE3A does not occur just anywhere in the heart muscle cell, but near a tubular membrane system that stores calcium ions. A release of these ions into the cytosol of the cell triggers muscle contraction, thus making the heartbeat. After the contraction, the calcium is pumped back into storage by a protein complex. This process is also regulated locally by PDE.

Klussmann and his team hypothesized that because these enzymes are hyperactive in the local region around the calcium pump, there should be less cAMP, inhibiting the pump’s activity. “In the gene-modified heart muscle cells, we actually showed that the calcium ions remain in the cytosol longer than usual,” said Dr. Maria Ercu, a member of Klussmann’s lab and one of the study’s four first authors. “This could increase the contractile force of the cells.”

Activating instead of inhibiting

“PDE3 inhibitors are currently in use for acute heart failure treatment to increase cAMP levels,” Klussmann explains. Regular therapy with these drugs would rapidly sap the heart muscle’s strength. “Our findings now suggest that not the inhibition of PDE3, but – on the contrary – the selective activation of PDE3A may be a new and vastly improved approach for preventing and treating hypertension-induced cardiac damage like hypertrophic cardiomyopathy and heart failure,” Klussmann said.

But before that can happen, he says, more light needs to be shed on the protective effects of the mutation. “We have observed that PDE3A not only becomes more active, but also that its concentration in heart muscle cells decreases,” the researcher reports, adding that it is possible that the former can be explained by oligomerization – a mechanism that involves at least two enzyme molecules working together. “In this case,” said Klussmann, “we could probably develop strategies that artificially initiate local oligomerization – thus mimicking the protective effect for the heart.”

Also Read: People who have diabetes more often affected by trigger finger: Study

People with diabetes are more likely than the general population to suffer from trigger finger or locked fingers. A study done by Lund University in Sweden found that when blood sugar levels are high, the risk of getting affected increases.

The study’s findings were published in the journal Diabetes Care. Trigger finger occurs when one or more fingers, most commonly the ring finger or thumb, become bent and difficult to straighten. The thickening of the tendons that bend the finger and their connective tissue sheath causes the finger to become stuck in a bent posture towards the palm. It is a painful ailment that is generally managed with cortisone injections but occasionally necessitates surgery.

“At the hand surgery clinic, we have noted for a long time that people with diabetes, both type 1 and type 2, are more often affected by trigger finger. Over 20 percent of those who require surgery for this condition are patients who have, or will develop, diabetes,” says Mattias Rydberg, doctoral student at Lund University, resident physician at Skane University Hospital and first author of the study.

The researchers investigated two registers to see if high blood sugar (blood sugar dysregulation) increased the incidence of trigger finger. The first was Region Skane’s healthcare database, which included all diagnoses, and the second was the Swedish national diabetes register. Trigger finger affects between 1% and 1.5% of the population, although the diagnosis occurs in 10-15% of individuals with diabetes, and the occurrence is most common in type 1 diabetic patients.

The newly published study strengthens the pattern of blood sugar being a crucial factor for an increased risk of being affected by trigger finger. High blood sugar increased the risk of being affected by trigger finger among both men and women in the groups with type 1 diabetes and type 2 diabetes.

Blood sugar is measured in HbA1C, also referred to as long-term blood sugar, and when regulated, is under 48. The group of men with the worst regulated blood sugar (HbA1C > 64) had up to 5 times as high a risk of being affected than men with well-regulated (HbA1< 48) blood sugar.

“However, we can’t know for certain if any of the groups seek healthcare more often than others which could be a factor that affects the results,” says Mattias Rydberg.

The mechanism, or mechanisms, behind the increased risk are unknown, but there are theories that high blood sugar makes both the flexor tendons and their connective tissue sheaths thicker, thus causing them to lock more easily. It was previously known that those with unregulated blood sugar are more prone to nerve entrapments in the hand.

“It is important to draw attention to the complications from diabetes and how they can arise in order to discover them early, which enables faster treatment and thus a better outcome. In addition to nerve compressions and trigger finger, there may also be a link with thickening of the connective tissue in the palm (Dupuytren’s contracture), impairment of joint movement and the risk of arthritis at the base of the thumb,” says Lars B. Dahlin, professor at Lund University and consultant in hand surgery at Skane University Hospital.

“The mechanisms behind these complications probably differ in the case of diabetes. The results of this study are interesting, as we can show that blood sugar dysregulation has a connection with the development of trigger finger,” he added.

The next step in the research will be to chart how effective it is to operate on patients with diabetes who are affected by trigger finger.

“From our experience at the clinic, surgery goes well and there are few complications, but it takes a little longer for patients with type 1 and type 2 diabetes to regain full movement and function. We want to investigate this hypothesis further.

Another interesting idea is to see if trigger finger could be a warning signal for type 2 diabetes. It is far from all who are affected by trigger finger that have diabetes, but it would be interesting to see if by using modern registers we can discover those who are in the risk zone for developing diabetes,” concludes Mattias Rydberg.

Also Read: Must follow COVID-appropriate behaviour, high-risk patients can get serious infection: Dr Randeep Guleria

According to a new UN report titled Protect the Promise, women’s and children’s health has suffered globally as the effects of conflict, the COVID-19 pandemic, and climate change converge with disastrous consequences for children, young people, and women.

Data presented in the report, which was released at the World Health Summit in Berlin, show that the majority of maternal, child, and adolescent deaths and stillbirths occur in just two regions: Sub-Saharan Africa and South Asia.

It also shows a critical regression across virtually every major measure of childhood wellbeing, and many key indicators of Sustainable Development Goals (SDGs). Since the last Every Woman Every Child Progress Report published in 2020, food insecurity, hunger, child marriage, risks from intimate partner violence, and adolescent depression and anxiety have all increased.

An estimated 25 million children were un- or under-vaccinated in 2021 – 6 million more than in 2019 – increasing their risk of contracting deadly and debilitating diseases. Millions of children missed out on school during the pandemic, many for more than a year, while approximately 80% of children in 104 countries and territories experienced learning-loss because of school closures. Since the start of the global pandemic, 10.5 million children lost a parent or caregiver to COVID-19.

“At the core of our unkept promise is the failure to address the gaping inequities at the root of global crises, from the COVID-19 pandemic to conflicts and the climate emergency. The report describes the impacts of these crises on women, children and adolescents, from maternal mortality to education losses to severe malnutrition,” said Antonio Guterres, United Nations Secretary-General.

The report Protect the Promise provides wide-ranging evidence that children and adolescents face wildly divergent chances of leading a healthy life simply based on where they are born, their exposure to conflict, and the economic circumstances of their families. For example:

– A child born in a low-income country has an average life expectancy at birth of around 63 years, compared to 80 in a high-income country. This devastating 17-year survival gap has changed little over recent years. In 2020, 5 million children died even before the age of 5, mostly from preventable or treatable causes. Meanwhile, most maternal, child, and adolescent deaths and stillbirths are concentrated in just two regions – sub-Saharan Africa and South Asia.

– More than 45 million children had acute malnutrition in 2020, a life-threatening condition which leaves them vulnerable to death, developmental delays and disease. Nearly three-quarters of these children live in lower-middle-income countries. A staggering 149 million children were stunted in 2020. Africa is the only region where the numbers of children affected by stunting increased over the past 20 years, from 54.4 million in 2000 to 61.4 million in 2020.

– The six countries with the highest numbers of internally displaced persons – Afghanistan, the Democratic Republic of the Congo, Ethiopia, Sudan, the Syrian Arab Republic and Yemen – are also among the top 10 food-insecure countries.

– A woman in sub-Saharan Africa has around a 130 times higher risk of dying from causes relating to pregnancy or childbirth than a woman in Europe or North America. Coverage of antenatal care, skilled birth attendance, and postnatal care is far from reaching all women in low- and middle-income countries, leaving them at elevated risk of death and disability.

– Millions of children and their families are experiencing poor physical and mental health from recent humanitarian disasters in Afghanistan, Ethiopia, Pakistan, Somalia, Ukraine and Yemen. In 2021, a record 89.3 million people worldwide were driven from their homes by war, violence, persecution, and human rights abuse.

The report calls upon the global community to address this damaging trajectory and protect the promises made to women, children, and adolescents in the Sustainable Development Goals. In particular, it advocates for countries to continue investing in health services, to address all crises and food insecurity, and empower women and young people around the world.

“The report advocates for countries to continue investing in health services, in all crises, and to re-imagine health systems that can truly reach every woman, child, and adolescent, no matter who they are or where they live,” said the Rt. Hon Helen Clark, Board Chair of PMNCH (The Partnership for Maternal, Newborn & Child Health) and former Prime Minister of New Zealand. “Experts and world leaders are calling for more women in policy- and decision-making at every level, meaningful engagement with young people, and primary health care systems which deliver what people need when and where they need it most.”

Protect the Promise is a bi-annual summary of progress in response to the UN Secretary General’s Every Woman Every Child Global Strategy for Women, Children, and Adolescents’ Health, published by global partners including WHO, UNICEF, UNFPA, Partnership for Maternal, Newborn, and Child Health (PMNCH), and Countdown to 2030. It is the most complete evidence synthesis on the present situation of maternal, infant, child, and adolescent health, and it updates the previous Every Woman Every Child Global Strategy Progress Report, which was published in 2020.

Also Read: Exercise improves cardiorespiratory fitness both during and after treatment : Study

Physical activity intervention during chemotherapy is safe, increases long-term cardiorespiratory fitness, and alleviates some of the side effects of cancer treatment, according to research published in JACC: CardioOncology. If exercise is not possible during chemotherapy, the individual can participate in a post-treatment exercise programme to regain function.

One of the most important independent predictors of cardiovascular health is cardiorespiratory fitness, as measured by peak oxygen uptake (VO2peak). VO2peak drops by up to 25% during cancer treatment. Cancer treatment frequently has negative effects on the patient’s health-related quality of life (HRQoL), such as decreased cardiorespiratory fitness, increased fatigue, and cardiovascular morbidity. Physical activity has been shown to reduce these risks.

Exercise therapy has been linked to improved cardiorespiratory fitness, increased VO2peak, and a reduction in cardiovascular morbidity, cancer mortality, and overall mortality.

“Exercise is widely recognised as beneficial to cancer patients. However, there is insufficient evidence on the best time to start exercising for improving long-term cardiorespiratory fitness in cancer patients “Annemiek M.E. Walenkamp, MD, PhD, senior author of the study and a medical oncologist at University Medical Center Groningen in Groningen, the Netherlands, said

The ACT trial looked at the efficacy of exercise intervention during chemotherapy versus after treatment for improving long-term cardiorespiratory fitness.

The study included adult patients who had recently been diagnosed with breast cancer, colon cancer, testicular cancer, or B-cell non-Hodgkin lymphoma and were scheduled to receive curative chemotherapy. Between February 2013 and November 2018, trial participants were randomly assigned to a 24-week exercise intervention that began either during or after chemotherapy.

Rigorous exercise

Moderate to vigorous effort on a stationary bicycle, resistance training with weight machines and free weights, and badminton were all types of exercise. The difference in VO2peak one year after the intervention was the primary endpoint. At all time points, the secondary endpoints were VO2peak after chemotherapy and intervention, muscle strength, HRQoL, fatigue, physical activity, and self-efficacy.

The researchers discovered that the group that began exercise therapy during treatment reported less fatigue and increased physical activity, as well as a decrease in VO2peak, HRQoL, and muscle strength. Three months after chemotherapy, the group that started exercising after treatment had similar values to the group that started exercising during treatment. Regardless of timing, both groups returned to their baseline cardiorespiratory fitness one year after completing the exercise intervention.

“These findings suggest that the best time to exercise is during chemotherapy. When exercising during chemotherapy is not possible, starting a physical exercise programme after chemotherapy is a viable option “Walenkamp explained. “We hope that our findings will encourage health-care providers to advise patients on exercise interventions during anti-cancer treatment.”

The American College of Cardiology envisions a world in which knowledge and innovation improve cardiovascular care and outcomes. The mission of the College and its more than 56,000 members, as the professional home for the entire cardiovascular care team, is to transform cardiovascular care and improve heart health.

The ACC confers credentials on cardiovascular professionals who meet stringent qualifications and is a driving force behind the development of health policy, standards, and guidelines. In addition, the College offers professional medical education, disseminates cardiovascular research through its world-renowned JACC Journals, operates national registries to measure and improve care, and provides cardiovascular accreditation to hospitals and institutions.

The ACC’s JACC Journals are ranked among the top cardiovascular journals in the world in terms of scientific impact.

Also read: Researchers have figured out why breast cancer cells resist treatment

Because one-fourth of recurrent oestrogen receptor-positive (ER+) breast cancers lack ER expression, they are resistant to endocrine therapy and can spread uncontrollably.

A recent study published in the Proceedings of the National Academy of Sciences by a group of Baylor College of Medicine researchers reveals a mechanism that not only explains the process but also suggests ways to avoid it.

“For years, our goal has been to piece together the complex puzzle of breast cancer progression to understand how the players interact with one another to confer resistance to therapy and persistent growth,” said corresponding author Dr Weei-Chin Lin, a Baylor professor of medicine-haematology and oncology as well as molecular and cellular biology.

“Our goal is to overcome this barrier and restore ER receptor expression in these cancers so they can be treated again, giving patients a better chance of survival.”

The process by which breast cancer cells lose their ER

Resistance to endocrine therapy in breast cancer has previously been linked to two cellular proteins known as 14-3-3 and ER-36.

“We were surprised to find that over-expressing 14-3-3t in these tumours resulted in all of the cancer cells becoming ER-negative (ER-),” said Lin, a member of the Dan L Duncan Comprehensive Cancer Center. “I recall seeing the data for the first time. The transformation was dramatic: all of the tumours had lost their ER!”

Because studying the mechanism in animal models would be laborious, time-consuming, and costly, the researchers devised an alternative model. Lidija A., the first author,

Wilhelms Garan, a graduate student in Baylor’s Cancer and Cell Biology Graduate Program who works in the Lin lab, created a spheroid model of human breast cancer cells that mimics the progression from ER+ to ER- and serves as a useful experimental tool for future research.

“A breast tumour in a patient can take years to progress from ER+ to ER-; in our animal model, it takes several months; but in our spheroid model, it switches from ER+ to ER- in 1 to 2 weeks,” Garan explained.

The researchers discovered that when 14-3-3t is over-expressed in cancer cells under the right conditions, the cells increase their levels of ERa36, which is followed by ER loss.

“Other molecular players like AKT and GATA3 are also required,” Garan explained. “Most importantly, we discovered that factors produced by the tumour microenvironment, which includes fibroblasts and immune cells that are part of the tumour mass and interact with cancer cells, are also required for the progression from ER+ to ER-.”

“Other molecular players like AKT and GATA3 are also required,” Garan explained. “Most importantly, we discovered that factors produced by the tumour microenvironment, which includes fibroblasts and immune cells that are part of the tumour mass and interact with cancer cells, are also required for the progression from ER+ to ER-.”

“We knew 14-3-3t, ERa36, AKT, and GATA3 were key players in the transformation of ER+ breast cancer cells to ER- cells.” “Here, we’ve determined how they functionally interact with one another, laying out a road map that leads to ER loss,” Lin explained.

“I am very excited that we now have a valuable tool with our spheroid breast cancer model to study not only the cellular changes involved in breast cancer progression, but also to test drugs for their ability to inhibit the process that leads to ER loss.”

“In approximately 60% of breast cancers, the protein 14-3-3t is overexpressed. Not all patients with high 14-3-3t will develop the ER, but for those who do, our findings may one day aid in returning their tumours to a therapy-sensitive state “Garan stated. “Bringing discoveries to the clinic and improving people’s lives has always been a passion of mine in this research.”

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