New antibiotic may make bacterial resistance nearly impossible

A newly discovered antibiotic that disrupts two distinct biological targets will make it 100 million times harder for bacteria to evolve resistance, according to a study.

The study from the University of Illinois at Chicago (UIC), in the US, reveals that this antibiotic disrupts two different cellular targets, significantly complicating bacteria's ability to evolve resistance, a dangerous, unwanted side effect.

The study, published in the journal Nature Chemical Biology, focuses on a class of synthetic drugs known as macrolones. These drugs combat bacterial infections by either interfering with protein production or corrupting DNA structure, making it challenging for bacteria to develop resistance to both mechanisms simultaneously.

"The beauty of this antibiotic is that it kills through two different targets in bacteria," said Alexander Mankin, a professor of pharmaceutical sciences at the University of Illinois, Chicago.

"If the antibiotic hits both targets at the same concentration, then the bacteria lose their ability to become resistant via the acquisition of random mutations in any of the two targets," he added.

Macrolones combine features of macrolides, like erythromycin, which block protein synthesis, and fluoroquinolones, such as ciprofloxacin, which target the bacterial enzyme DNA gyrase.

Researchers Yury Polikanov and Nora Vazquez-Laslop at UIC demonstrated that these drugs bind more tightly to ribosomes than traditional antibiotics and are effective even against macrolide-resistant bacterial strains. "By basically hitting two targets at the same concentration, the advantage is that you make it almost impossible for the bacteria to easily come up with a simple genetic defence," Polikanov said.

This discovery underscores the importance of the integration across various scientific fields that fosters significant advancements like this one.

https://www.newkerala.com/news/2024/43847.htm

Researchers reveals ways of preventing cancer cells from colonizing liver

Nine times out of ten, metastasis is the cause of cancer deaths. This is the point when the primary tumour has sent out cells, like seeds, and invaded other organs of the body. Despite significant advancements in the treatment of primary tumours, medicine remains mainly powerless against metastases. As of right now, there are no drugs that stop this process.

Researchers from the Department of Biosystems Science and Engineering at ETH Zurich in Basel, under the direction of Andreas Moor, have now published findings in the journal Nature that demonstrate how colorectal cancer cells colonise the liver. Their research will aid in the creation of therapies that might impede the spread of disease.

Cancer is said to metastasise when cells from the primary tumour break off and travel via the circulatory system to other parts of the body. "Colorectal cancer metastasises to the liver because of how our blood flows," Moor says. Blood is first enriched with nutrients in the intestines before it goes to the liver, which metabolises the nutrients. For colorectal cancer cells, the liver is the last stop. "They get caught in the liver's capillary network," Moor says.

Costanza Borrelli, a doctoral student, and other members of Moor's team have now shown that the liver cells also play a large role in whether or not the cancer cells lodged there can colonise their new location. Science has known for over a century that, much like plant seeds in soil, cancer cells are dependent on their environment, yet it was previously unknown which molecular mechanisms play a role here.

Using sophisticated tests on genetically modified mice, Moor and his team have discovered that the secret lies in certain proteins on the cell surface. When liver cells have a protein called Plexin-B2 and the colorectal cancer cells possess certain proteins from the semaphorin family, the colorectal cancer cells can attach themselves to the liver cells.

Cancer cells that have semaphorins on their surface are especially dangerous, as attested by clinical studies cited by Moor's researchers in their paper. The study data shows that colorectal cancer metastasises earlier and more frequently to the liver if the tumour has large amounts of semaphorin.

Plexin and its counterpart semaphorin were previously known to the research community for their function in the nervous system, where the two proteins steer growing nerve cells and ensure they form the right pathways. "Why liver cells also create plexin and what this protein does in healthy livers is anything but clear - and interests us immensely," Moor says. In other words, the question of its function remains open.

What Moor and his team have discovered, however, is that direct contact between plexin and semaphorin triggers fundamental changes in colorectal cancer cells. To break off from the primary tumour, the cancer cells have to change their identity: they free themselves from the surface layer of the intestine, or epithelium, severing their close connections to neighbouring cells.

Once in the bloodstream, the cancer cells resemble those from connective tissue called mesenchyme. Yet once they find their new niche - thanks to the plexin on some liver cells - the cancer cells turn back into their sedentary form. "An epithelisation process takes place," the researchers wrote in their paper. Moor expands: "You can spot this immediately if you look at the cancer cells, as they form invaginations similar to the folds or crypts in the intestines."

The researchers' discovery will have an impact on more than colorectal cancer patients: further tests have shown that plexin also encourages the formation of metastases in melanoma and pancreatic cancer. For Moor and his team, this throws up many new research questions. One in particular is drawing their focus: when cancer cells cluster together to form a tumour, they also influence cells in their environment. "Cancer cells set up their own ecosystem," Moor explains.

If efforts to inhibit the crucial interaction between plexin and semaphorin succeed, it may be possible to prevent the cancer from establishing new tumours in the first place. That's because early on, when the relationships among the cells in this ecosystem have not yet been firmly established, tumour metastases are especially vulnerable, Moor explains. He appears confident that an answer lies within this "critical period of time in the development of metastases", even though the path to any potential treatment is still long.

https://www.newkerala.com/news/2024/44003.htm

Daily statin use may lower heart risk in HIV patients by 35 pc: Study

Daily use of statins, or cholesterol-lowering drugs, may help reduce the risk of cardiovascular events such as heart attacks, and strokes in people with HIV by 35 per  cent, according to a study.

People living with HIV can have a 50-100 per cent increased risk for cardiovascular disease.

The research, published in the New England Journal of Medicine, showed that daily statin use could prevent one in five major cardiovascular events or premature deaths in this population.

"This research suggests that statins may provide an accessible, cost-effective measure to improve cardiovascular health and quality of life for people living with HIV," said Gary H. Gibbons, director of the National Heart, Lung, and Blood Institute, part of the US National Institute of Health.

The study involved 7,769 adults aged 40-75, who were randomised to receive either pitavastatin or a placebo. Participants who took pitavastatin experienced 35 per cent fewer major cardiovascular events and a 21 per cent reduction in deaths compared to the placebo group.

Additionally, those taking the statin saw a 30 per cent decrease in Low-density lipoprotein (LDL) cholesterol or bad cholesterol levels.

Steven K. Grinspoon, a professor of medicine at Harvard University, noted that while lowering LDL cholesterol reduces risks for heart attacks and strokes, the findings suggest additional benefits of statin therapy for people living with HIV.

The study highlights the need to address comorbidities like cardiovascular disease in successful HIV management, a disease that plagues more than 38 million people worldwide, with a new 1.5 million diagnosed in 2021, as per the World Health Organisation (WHO).

https://www.newkerala.com/news/2024/43882.htm

Study links specific pesticides to increased risk of over 6 types of cancers

A new study has linked pesticides to heightened cancer risk. 

Agricultural pesticide use in the U.S. is linked to various cancers as strongly as smoking cigarettes, a new population-based study shows.

The study analyzed local records throughout the country to make the first national map of cancer risks associated with pesticide use.

The authors note that as potentially toxic as individual pesticides may be, most often they are deployed in combination, and the study’s findings document the resulting enhanced risks of cancer.

Given the importance of food security, the study recognizes the tradeoff between having enough food and an increased risk of cancers.

In areas near agricultural production, pesticides increase the risk of developing cancer as much as smoking, according to a new nationwide study.

Its authors found strong links between environmental pesticides and leukemia, non-Hodgkin’s lymphoma, bladder, colon, lung, and pancreatic cancers, as well as cancer combinations.

The researchers compared the risks of pesticides to the known cancer risk associated with smoking cigarettes to provide an easily understood measure of risk.

While the authors assert that “pesticides are an essential feature of modern-day agriculture” — resulting in robust crop yields on which the planet’s food security depends — it spotlights the inherent danger in relying on them.

“There are few innovations as significant in agriculture as the development and use of pesticides,” they write.

To assess associations between pesticides tracked by the United States Geological Survey and cancers, the researchers analyzed county-level data from across the U.S. They identified pesticides reported in each area, and cancer cases, as well as the incidence of cigarette smoking and other possible factors.

Though individual pesticides have been linked to cancers, the study emphasizes that mixtures of pesticides — the manner in which they’re typically delivered to crops — significantly multiply their carcinogenic risk.

This risk is not confined to areas where agriculture actually occurs. Many communities under the greatest threat are visited by hazardous air- and water-borne pesticides that emanate from neighboring farms.

States such as Iowa, Illinois, Nebraska, and Missouri exemplified the strongest pesticide/cancer links, suggesting a connection between the corn grown in the area and the carcinogenic risk in its production. The study also spotlights fruit production in California and Florida.

The study is published in Frontiers in Cancer Control and Society.

Pesticides vs. cancer risk

Senior author of the study Isain Zapata, PhD, assistant professor of research and statistics in the Department of Biomedical Sciences of Rocky Vista University, Englewood, CO, described the importance of maintaining agricultural productivity, which currently means living with pesticide use.

Unfortunately, Zapata said, “Organic farming does not have the output necessary to feed in an economically sustainable way our population. It is not a simple solution.”

“There is no magic bullet,” said Zapata.

“We need agricultural products, and we need to produce them in an affordable way, so everyone has access to them. There is no way around it,” he said.

The value of the study

Wael Harb, MD, board certified hematologist and medical oncologist at MemorialCare Cancer Institute at Orange Coast and Saddleback Medical Centers in Orange County, CA, who was not involved in the study, considered the findings valuable.

“It identifies significant associations between the pesticides and several cancers like leukemia, Hodgkin’s lymphoma, bladder, colon, lung, and pancreatic cancers,” he said. “In

that sense, it’s a comprehensive holistic analysis to understand how the widespread exposure of pesticides contribute to cancer risk.”

“Establishing pesticide usage patterns fine-tunes the environment of usage in those communities,” said Zapata.

How specific pesticides are linked to cancer

Until this study, investigations of the pesticide/cancer connection have primarily focused on subsets of community populations, such as farmers and their spouses. This is the first comprehensive look at pesticides’ effect on the health of entire communities.

Perhaps the best-known pesticide considered in the study is Glyphosate, which is marketed as Roundup, and has been linked in some studies to lymphomaTrusted Source.

The International Agency for Research on Cancer (IARC) has classified Glyphosate as a probable carcinogen and $11 billion was awarded to plaintiffs suing over its use.

However, the U.S. National Institutes of Health’s Agricultural Health Study of 88,000 farmers and their spouses found no link between Glyphosphate and cancersTrusted Source.

The new study concluded that the frequent use of Glyphosate was associated with a higher risk of all cancers, colon cancer, and pancreatic cancer.

Similarly, all cancers, colon cancer, and lung cancer were linked to the use of Imazethapyr. Metolachlor, Metolachlor-S, and the combination of both were consistently associated with all cancers, colon cancer, and pancreatic cancer.

Other associations between the heavy use of specific pesticides and cancers were:

Atrazine was frequently deployed in areas with an elevated risk for all cancers and colon cancers.

Boscalid was heavily used in regions that had higher incidences of leukemia, non-Hodgkin’s lymphoma, and pancreatic cancer, as well as low added-risk regions for lung cancer.

Dimethomorph was associated with a high added risk of leukemia and non-Hodgkin’s lymphoma, as well as a lower additional risk of colon cancer.

Dicamba was consistently used in areas with a high added risk of colon cancer and pancreatic cancer.

Dinotefuran was commonly used in counties with high rates of leukemia and non-Hodgkin’s lymphoma.

While Dimethenamid was associated in the study only with a low added risk of bladder cancer, when it was used in combination with Dimethenamid-P, it was linked to a high added risk of pancreatic cancer.

Does combining pesticides increase cancer risk?

The study underscores the multiplying effects of pesticide combinations in potential carcinogenesis.

Said Harb, “[When] there’s more exposure to chemicals, there’s a higher risk of cancer because all of these pesticides are potential carcinogens.”

“The more exposure, the length of exposure, and the different chemicals combined can increase the risk of damage to the DNA or similar signal pathways,” he said.

“Cancer is a multi-step process. Sometimes it takes multiple hits,” said Harb. “Not everybody gets cancer, but some people might be more vulnerable than others.”

How pesticides trigger cancers

Harb explained, “It’s oxidative stress [from pesticides] that causes DNA damage and disruption in cellular signaling pathways.”

“As an example,” he said, “certain pesticides can lead to the formation of reactive oxygen species (ROS), and this reactive oxygen causes damage to the DNA, protein, and lipids.”

“This basically leads to mutations, alteration, gene expression, and ultimately carcinogenesis. We know the problem with cancer is developing mutations in the genome which lead to abnormal protein and carcinogenesis,” said Harb.

The future of pesticides

Zapata hoped that the study might move forward a considered conversation regarding pesticides.

For now, he suggested: “Bring awareness, special healthcare initiatives, and education on the risk and management of exposures.”

“This is very important, although easier said than done,” he noted, especially since “Rural areas where most agricultural production happens tend to be most deprived of these resources.”

In the longer term, he called for “continuing research and the development of less harmful chemicals or usage strategies.”

https://www.medicalnewstoday.com/articles/specific-pesticides-glyphosate-increased-risk-lung-colon-cancer#The-future-of-pesticides

Twice-a-year anti-HIV injection shows 100 per cent efficacy, reveals study

Lenacapavir, injectable twice a year, is developed by US-based biopharmaceutical company Gilead Sciences, Inc.

An HIV-preventive drug showed 100 per cent efficacy and “no safety concerns” in women, according to a study published in The New England Journal of Medicine.

Lenacapavir, injectable twice a year, is developed by the US-based biopharmaceutical company Gilead Sciences, Inc. as a pre-exposure prophylaxis (PrEP) drug. These drugs prevent the spread of infection in people not yet exposed to the disease-causing agent.

The study, a phase-3 trial involving teenage girls and young women in South Africa and Uganda, showed that lenacapavir “demonstrated zero (HIV) infections” and “100 per cent efficacy,” Gilead Sciences, Inc. said in a statement.

HIV, or human immunodeficiency virus, spreads from the body fluids of an infected person. Untreated, the infection can progress to AIDS or acquired immunodeficiency syndrome over years.

In the PURPOSE 1 trial, 5,338 participants, who were HIV-negative, to begin with, were divided into three groups - 2,134 receiving lenacapavir injections 26 weeks apart; 2,136 receiving the daily oral tablet Descovy (F/TAF); and 1,068 receiving the daily oral tablet Truvada (F/TDF).

Researchers, including those from the Desmond Tutu HIV Centre, University of Cape Town, South Africa, observed a total of 55 infections - zero in the Lenacapavir group, 39 in the Desovy group and 16 in the Truvada group.

“No participants receiving twice-yearly lenacapavir acquired HIV infection,” the study authors wrote.

The most common adverse effects were injection-site reactions experienced by close to 70 per cent of the participants in the Lenacapavir group. However, there were “no serious injection-site reactions,” according to the statement.

“These stellar results show that twice-yearly lenacapavir for PrEP, if approved, could offer a highly effective, tolerable and discreet choice that could potentially improve PrEP uptake and persistence, helping us to reduce HIV in cisgender women globally,” first author Linda-Gail Bekker, Director of the Desmond Tutu HIV Center at the University of Cape Town, South Africa, said in the statement.

Results of PURPOSE 2 trial, involving cisgender men, transgender men, transgender women and gender non-binary individuals in countries, including Latin American ones, South Africa and Thailand, are expected in late 2024 or early 2025, the statement said.

https://www.tribuneindia.com/news/health/twice-a-year-anti-hiv-injection-shows-100-per-cent-efficacy-reveals-study-642922

Parkinson's disease could have 3 subtypes, researchers find

Does Parkinson’s disease have different subtypes?

• A machine-learning study at Weill Cornell Medicine was able to classify Parkinson’s disease into three subgroups, a development with the potential to effectively target patients with treatments specific to their disease’s progression.
• By analyzing data from an existing study, researchers split the cohort into Rapid Pace, Inching Pace, and Moderate Pace — an approach that acknowledges the heterogeneous nature of the disease.
• Experts say the findings are logical and hold great promise, but caution that larger populations need to be explored to create more accurate models.

On the heels of new research from Boston University showing that an artificial intelligence model was able to predict a person’s chances of developing Alzheimer’s disease, Weill Cornell Medicine researchers have been able to classify Parkinson’s disease into three subtypes using machine learning.

The findings — which appear in npj Digital Medicine — hold promise in aiding researchers and clinicians to target treatments specific to those subtypes.

 

What are the 3 subtypes of Parkinson’s?

Researchers at Cornell analyzed data from 406 people who participated in the Parkinson’s Progression Markers Initiative (PPMI), which is an international observational study that “systematically collected clinical, biospecimen, multi-omics, and brain imaging data of participants.”

 

They developed a deep-learning model called deep phenotypic progression embedding (DPPE), which was able to “holistically” model “multidimensional, longitudinal progression data of the participants,” as the authors explain in the study paper.

 

The authors further note that in recent years there has been a move toward observing Parkinson’s as a condition with heterogeneous symptoms and progression.

 

Not all individuals with Parkinson’s will have the same experience, in other words, and therefore treatment could be much more tailored to suit different patients’ needs.

 

The three subgroups of Parkinson’s identified by the machine learning are based on the pace of the disease’s progression:

 

• Rapid Pace (PD-R), which is marked by rapid progression of symptoms. Of the cohort observed, 54 people (13.3%) had this subtype.
• Inching Pace (PD-I), which has mild baseline symptoms and relatively mild progression. Of the cohort observed, 145 people (35.7%) had this variety.
• Moderate Pace (PD-M), which is characterized by mild baseline symptoms and moderate progression. This was the largest portion of the cohort observed, with 207 people (50.9%) living with this form of Parkinson’s.

The study authors note that their classifications “highlighted the necessity of treating [Parkinson’s disease] subtypes as unique sub-disorders within clinical practice, where our pace subtypes could inform patient stratification and management.”

 

By identifying specific varieties of the disease, clinical approaches could be much more targeted and effective.

 

Findings on Parkinson’s subtypes need confirming

Clemens Scherzer, MD, a physician-scientist and the Stephen & Denise Adams Professor of Neurology at Yale School of Medicine, who was not involved in the study, told Medical News Today that the study’s computational findings were very interesting, but cautioned that they are extremely preliminary and need larger populations to develop and validate such classifiers.

 

“The goal of precision medicine is to predict the disease course in a patient and to therapeutically intervene ahead of time to prevent complications from developing. To achieve this we need to identify the disease driver in each patient and develop targeted therapeutics,” Scherzer pointed out.

 

“For example, we have found that 10% of Parkinson’s patients in the [United States] have a mutation in the GBA gene and that different types of GBA mutations accelerate the course of the disease,“ he explained. “Patients with GBA mutations can now be enrolled in clinical trials for targeted therapies and ultimately will benefit from disease-modifying GBA-directed therapeutics.”

 

Nevertheless, Daniel Truong, MD, a neurologist and medical director of the Truong Neuroscience Institute at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, and editor in chief of the Journal of Clinical Parkinsonism and Related Disorders, who also was not involved in the study, told MNT that the subgroupings are a logical, systematic approach to treating Parkinson’s.

 

“For instance, patients with the Rapid Pace subtype (PD-R) might benefit from more aggressive therapeutic strategies and closer monitoring compared to those with the Inching Pace subtype (PD-I), who may need less intensive management. Knowledge of a patient’s subtype can guide the selection of medications, including the potential repurposing of existing drugs like metformin, which the study suggests might be particularly beneficial for the PD-R subtype.”– Daniel Truong, MD

 

“It allows predictive and preventive healthcare to be designed for each subtype,” Truong explained.

 

“Early intervention may be required for rapid progressive patients. This is crucial for managing symptoms before they become severe and debilitating. Subtyping helps in stratifying patients based on their risk, enabling more focused and effective clinical trials for new treatments, as well as better allocation of healthcare resources,” he added.

 

Steven Allder, BMedSci, BMBS, FRCP, DM, a consultant neurologist at Re:Cognition Health, not involved in the study, agreed that advance identification of different subgroups would allow medical professionals to work on specific treatment plans for each one.

 

He listed the possible treatments for each, noting:

• Inching Pace (PD-I): “Treatments could focus on maintaining quality of life and preventing symptom progression through lifestyle modifications, physical therapy, and possibly neuroprotective drugs.”
• Moderate Pace (PD-M): “These patients exhibit moderate disease advancement. They might benefit from a combination of pharmacological treatments to manage symptoms and slow progression, such as dopamine agonists, MAO-B inhibitors or other disease-modifying therapies.”
• Rapid Pace (PD-R): “This subtype progresses quickly and often involves cognitive deficits. Metformin has shown promise in improving symptoms in this group, especially related to cognition and falls. Early intervention with Metformin and other neuroprotective agents could be crucial for managing this subtype.”

Is it problematic to use AI to predict Parkinson’s?

Allder’s main concern about using machine-learning technology to predict diseases such as Parkinson’s revolved around the accessibility of such a tool for people who need it.

 

“I don’t foresee problems with the AI model, but I do foresee problems with patients accessing it,“ he told us.

 

“While AI models are powerful tools for identifying disease subtypes and predicting progression, there are potential issues related to patient access. Not all patients may have access to advanced diagnostic tools or treatments derived from AI research, especially in under-resourced settings,“ Allder pointed out.

 

However, according to him, another issue might be “[t]he use of extensive patient data for AI model training,“ which “raises concerns about data privacy and security.“

 

“AI models need to be validated across diverse populations to ensure they are not biased towards specific cohorts,” said Allder.

 

Scherzer, echoing his earlier statement, said that the significant power of artificial intelligence toward precise medical treatments will ultimately depend on more research and trials.

 

“The success of AI to predict outcomes depends on the size and quality of the input data,” he noted. “A key gap in the field is that we need much larger, high quality, longitudinal data sets of Parkinson’s patients — data on large populations spanning prodromal stages and the entire disease course. These will be essential for training and validating AI models useful for augmented medicine.”

https://www.medicalnewstoday.com/articles/parkinsons-disease-could-have-3-subtypes-researchers-find

Nipah virus: A recurring, deadly threat in India

The recent death of a boy in Kerala renews concerns about outbreaks, as health officials work to contain the virus's spread among humans and animals.

Health authorities in India face outbreaks of Nipah virus almost every other year. Transmitted by fruit bats, it's often fatal among humans. After a 14-year-old boy died of Nipah virus Sunday, July 21, 2024, in the southern Indian state of Kerala, authorities tried to stop a new outbreak — just a year after the last outbreak in 2023. Kerala State Health Minister, Veena George, said the boy died after suffering a cardiac arrest, which was apparently brought on by the virus. A further 60 people had been identified as being at high-risk, she said.

Nipah is most common in fruit bats, which live in wooded areas close to the highly populated state of Kerala. It's also found in pigs. Humans can pick up an infection from animals either directly, through droplets, or indirectly via contaminated surfaces. Human-to-human transmission is also possible. An infection can trigger encephalitis and lead to mild to severe illness, but also death. The World Health Organization classifies Nipah as a priority pathogen, which means it has the potential to trigger an epidemic.

How is the virus transmitted?

Nipah virus is commonly found in fruit bats (Pteropodidae), which feed on nectar and pollen, as opposed to vampire bats which eat insects and drink the blood of animals. Fruit bats are much bigger and use their eyes, and not ultrasound, to orient themselves.

Kerala was probably due to the contamination of a drinking water source. Dead fruit bats were later found in a well belonging to the house of an infected family in Changaroth. First, many of the family members fell ill. Later, their acquaintances also got sick.

Why is the virus so dangerous?

The Nipah virus aggressively inflames the brain. The US Centers for Disease Control cites an incubation period of five days to two weeks. Initial symptoms resemble those of the flu: fever, nausea and severe headache. Some patients experience respiratory problems. Later, disorientation, dizziness and confusion follow. Within one to two days, patients can slip into a coma and die. The mortality rate for Nipah disease is 70%.

How can the disease be treated?

There is no vaccination or medication against the Nipah virus — neither for animals, nor for humans. Medications have so far only been able to alleviate the symptoms. In  principle, patients have to be immediately isolated and taken to an intensive care unit, where vital body functions can be supported. Contact persons or suspected cases have to be quarantined to stop the spread of the infectious disease.

Where does the Nipah virus come from?

Nipah virus was first discovered in 1998 in the Malaysian village of Sungai Nipah. Febrile encephalitis — an illness caused by the virus entering the brain — and, in some cases, severe respiratory infections were observed in 229 individuals. Men who worked in slaughterhouses were the first to catch the infection. It became apparent that one could contract the disease from animals.

Around the same time, a comparatively mild outbreak of a respiratory infection caused by an unknown pathogen was observed in pigs in Malaysia. Only later did scientists find that the workers and the pigs had been infected by the same virus. As a precaution, more than 1 million pigs — half the country's total pig population — were culled in Malaysia.Since then, cases of the virus have been reported in Bangladesh in 2001 and 2003, and in Kerala in 2018, 2021 and 2023.

https://www.hindustantimes.com/lifestyle/health/nipah-virus-a-recurring-deadly-threat-in-india-101721725481334.html

Endometriosis likely poses a heightened ovarian cancer risk, study finds

More research warns about the link between endometriosis and ovarian cancer risk.

• Endometriosis is a complex condition that involves uterine-like tissue growing in other areas outside the uterus.
• Researchers are interested in understanding how endometriosis relates to risk for other conditions, including cancer.
• Results of a recent study found that individuals with endometriosis may be at an increased risk for ovarian cancer. Those with ovarian endometriomas, deep infiltrating endometriosis, or both were at the highest level of risk for ovarian cancer.
• Individuals experiencing endometriosis and those potentially at risk for ovarian cancer can seek proper guidance and follow up with specialists.

Endometriosis is a chronic condition that can be difficult to manage and may also increase risks for additional health problems. It occurs when tissue similar to the uterine lining grows outside the uterus, such as in the ovaries or fallopian tubes.

Endometriosis can lead to symptoms like pelvic pain, pain during intercourse, and problems with fertility.

 

Experts are still working to understand the complexities of endometriosis and how it relates to risks for other conditions, including how it may increase risk for certain cancers.

 

A study recently published in JAMA examined the relationship between endometriosis and the risk for ovarian cancer.

 

The study found that individuals with endometriosis had a risk for ovarian cancer that was four times higher than that of women who did not have endometriosis.

Those with specific endometriosis types, like deep infiltrating endometriosis, had an almost 10 times higher risk for ovarian cancer than women without endometriosis.

The results highlight another potential risk factor for ovarian cancer, making prompt follow-up with specialists essential.

 

Endometriosis and ovarian cancer risk

This study was a population-based cohort study. The research matched 78,476 women with endometriosis with 372,430 women without known endometriosis. Researchers included participants between the ages of 18 and 55 who had at least one endometriosis diagnosis.

 

Researchers used data from the Utah Population Database, allowing data collection from multiple health records. They collected data on several covariates, including information on reproductive and surgical histories, body mass index (BMI), smoking history, and ethnicity.

 

The average age of women at first endometriosis diagnosis was 36 years old, and the average follow-up time with participants was 12 years.

 

Overall, those with endometriosis were at a much higher risk for ovarian cancer than women who did not have endometriosis.

 

Compared to women without endometriosis, those with endometriosis were over seven times more at risk of developing type 1 ovarian cancer, which included cancer types like endometrioid, clear cell, and mucinous.

 

These women were also 2.7 times more at risk of developing high-grade serous ovarian cancer.

 

Women with deep infiltrating endometriosis saw the most significant risk for ovarian cancer. Those who had both deep infiltrating endometriosis and ovarian endometriomas had the second highest risk.

 

Overall, women with deep infiltrating endometriosis, ovarian endometriomas, or both were almost 10 times more at risk for developing ovarian cancer.

 

Steve Vasilev, MD, a board-certified integrative gynecologic oncologist and medical director of Integrative Gynecologic Oncology at Providence Saint John’s Health Center and Professor at Saint John’s Cancer Institute in Santa Monica, CA, who was not involved in this research, commented with his thoughts on the study’s findings to Medical News Today.

 

According to him:

“This population-based cohort study adds substantial evidence to a growing body of research, including epidemiologic and histopathologic data, which indicates a strong association between endometriosis and specific subtypes of ovarian cancer […] This helps solidify the concern that, in any given individual, endometriosis may progress to certain types of ovarian cancer or stimulate malignant degeneration. Even though the absolute risk is felt to be very low among the millions of women with endometriosis, it is very important to consider because the type of surgery that may be required is different. When cancer is known to be present, or strongly suspected, a cancer specialist (gynecologic oncologist) should be involved.”

 

How accurate is this study?

Nevertheless, this research has several limitations that could have affected the study’s results. First, it only included participants in a specific age range from one state in the United States, making it difficult to generalize the results.

 

Second, there was a risk of misclassification of endometriosis due to factors, such as the difficulty of correctly diagnosing endometriosis. While the data compared women with endometriosis to those with no known endometriosis, it is still possible that some women in the control group had endometriosis and had just not been diagnosed.

 

There is also the possibility researchers misclassified ovarian cancer histotypes, body mass index (BMI), and smoking. Researchers also lacked data on hysterectomies and oophorectomies that happened outside of Utah facilities or other care that occurred outside of the state. Researchers also lacked data on the use of oral contraceptives and gonadotropin-releasing hormone agonists.

Because a diagnosis of endometriosis is often delayed, researchers did assume that those who received an ovarian cancer diagnosis on their index date had actually had an endometriosis diagnosis before cancer onset.

 

Regardless, the results highlight new questions and areas for research and another potential factor to consider in clinical practice.

 

Diana Pearre, MD, a board-certified gynecologic oncologist at The Roy and Patricia Disney Family Cancer Center at Providence Saint Joseph Medical Center in Burbank, CA, who was not involved in the research, noted that “[t]he problem with this study is that we do not know the denominator.”

 

She cautioned that:

“There are plenty of people living with endometriosis who are asymptomatic and may not be seeking treatment/having surgery. Studies like this make us consider, as clinicians and surgeons, whether we should be offering prophylactic surgery for women living with endometriosis. I think without knowing the clear absolute risk of cancer with endometriosis — evidenced by not knowing exactly how many people live with it — we cannot make such a blanketed recommendation.”

 

“Our counseling for surgical treatment for symptomatic endometriosis, however, should include a very thoughtful discussion with the patient about this association that we are seeing in these large population based studies that there is a definite association between endometriosis and ovarian cancer,” Pearre advised.

 

How to reduce ovarian cancer risk

Overall, the study highlights endometriosis as a potential risk factor for ovarian cancer. It highlights exploring ways to reduce risk and seeking proper follow-up with specialists.

 

Unfortunately, there are no screening tests in place that make it easy to detect ovarian cancer, making follow-up even more critical. Vasilev noted that:

“Currently, there is no reliable method recommended to screen for any type of ovarian cancer. With the advent and growth of understanding about molecular mechanisms underlying the disease, this will hopefully change soon. However, the more there is a family history of cancer it is prudent to consider genetic counseling and appropriate testing.”

 

Some possible ways to reduce the risk of ovarian cancer include using birth control pills for 5 years or longer, giving birth, and breastfeeding.

 

There is also the option of undergoing surgical removal of the ovaries or other organs in certain situations. All options for reducing the risk of ovarian cancer should be thoroughly discussed with appropriate specialists.

 

Rikki Baldwin, DO, an obstetrician-gynecologist with Memorial Hermann, who was likewise not involved in the recent study, also noted that self-care measures are “paramount” to reducing any type of cancer risk.

 

She advised that “[w]omen should eat a well-balanced diet, exercise regularly, avoid smoking and excessive alcohol use, and have regular visits with their primary physician.”

 

“Symptoms of ovarian cancer are vague, so it is very important to pay attention and notify your physician if there are new and abnormal symptoms like abdominal pain, bloating, nausea, decreased appetite, etc,” noted Baldwin.

https://www.medicalnewstoday.com/articles/endometriosis-likely-poses-a-heightened-ovarian-cancer-risk-study-finds#How-to-reduce-ovarian-cancer-risk