Category: 8. Health

Head and neck cancer remains a major global health challenge, ranking among the six most common cancers worldwide and claiming hundreds of thousands of lives each year. A growing body of evidence now points to an intricate connection between energy metabolism and immune regulation as a driving force behind the onset, progression, and treatment resistance of these cancers. The latest comprehensive review on this topic underscores the potential of targeting these intertwined processes to unlock more effective therapies.

Tumor cells in head and neck cancer exhibit profound metabolic reprogramming, altering the way they process glucose, lipids, and amino acids. This reprogramming fuels rapid growth, supports invasion into surrounding tissues, and fortifies tumors against hostile conditions. Changes in glucose transporters and key enzymes accelerate glycolysis, creating a microenvironment rich in lactate that fosters tumor progression and suppresses immune activity. Altered lipid metabolism not only sustains cell membrane production and energy storage but also promotes immune evasion by influencing macrophage polarization and dampening anti-tumor responses. Similarly, restructured amino acid metabolism, particularly in glutamine and arginine pathways, plays a critical role in both tumor growth and the regulation of immune cell activity.

The immune system, a natural line of defense, is often undermined in head and neck cancer. Tumor-driven metabolic shifts deprive CD8⁺ T cells and other immune cells of essential nutrients, weakening their ability to attack malignant cells. At the same time, immune checkpoints such as PD-L1 are upregulated, blocking immune activation. Dysregulation of antigen presentation pathways, altered cytokine signaling, and the recruitment of suppressive immune cells further deepen the immunosuppressive environment.

Importantly, the review highlights that this metabolism–immunity interplay is not just a byproduct of disease-it is a potential therapeutic target. Modulating glucose metabolism through transporter and enzyme inhibitors, interfering with lipid synthesis and cholesterol regulation, or restricting tumor access to key amino acids may tip the balance back in favor of the immune system. Moreover, combining metabolic interventions with immunotherapy could counteract immune suppression and improve patient outcomes, especially in cases resistant to standard treatments.

Pancreatic cancer, which mostly creeps in silently, remains a significant global health challenge with increasing incidence and mortality rates worldwide. It is often considered deadly due to its tendency to be diagnosed at a late stage, its aggressive nature, and the lack of effective treatments for advanced cases.In the middle of this growing concern of pancreatic cancer and a surge in new cases, a new study has uncovered a hidden danger behind a common habit that may put millions at increased risk of this particular type of cancer.What is it, and how is it affecting millions?More often than not, common habits that we’re accustomed to – on a daily basis – put us at great risk, without us even realizing it. Smoking is one such habit.Smoking has long been recognized as a risk factor for pancreatic cancer. Now, new evidence explains how it contributes to tumor growth at a cellular level. Researchers have found that chemicals in cigarette smoke not only spark tumor growth but also suppress the body’s immune defenses, creating fertile ground for cancer to flourish.

Smoking: More than just a risk factor

A recent study from the University of Michigan found that toxins from cigarettes activate specific cells that release a protein called interleukin-22 (IL-22). This protein promotes aggressive tumor growth while simultaneously unleashing a type of immune cell that suppresses the body’s anti-tumor response. The result: a double hit for patients, where tumors grow faster, and the immune system is blindsided.

What is pancreatic cancer?

Pancreatic cancer is a disease in which malignant (cancerous) cells form in the tissues of the pancreas. The pancreas is a gland located behind the stomach that plays a crucial role in digestion and blood sugar regulation by producing enzymes and hormones.While the exact causes are not always clear, risk factors include smoking, family history of pancreatic cancer, long-standing type 2 diabetes, and chronic pancreatitis.Pancreatic cancer is often difficult to diagnose early because symptoms may be subtle or absent in the early stages.

Rising pancreatic cancer cases: A growing concern

Pancreatic cancer is notoriously lethal. It’s often diagnosed late, and five-year survival rates remain under 20% globally. Experts estimate that by 2030, pancreatic cancer may surpass colorectal cancer as the second leading cause of cancer-related deaths in the US, a stark indicator of its growing impact.Unlike many cancers, where early detection has improved outcomes, pancreatic cancer lacks reliable screening methods for the general public. Most patients are diagnosed only after symptoms appear, usually at an advanced stage when treatment options are limited.

When should you consider screening?

Current guidelines make it clear: screening is not recommended for asymptomatic people at average risk. The U.S. Preventive Services Task Force gives it a “D” rating, meaning the potential harms outweigh the benefits.However, there are exceptions. Experts now advise proactive screening for high-risk individuals, including those with:Genetic conditions (e.g., Peutz-Jeghers, familial pancreatic cancer syndromes, BRCA1/2 mutations)A strong family history of pancreatic cancerNew-onset diabetes (especially when accompanied by unexplained weight loss), which may signal early-stage diseaseMajor health centers now recommend annual screening, using MRI or endoscopic ultrasound (EUS), for such high-risk groups, starting at an age tailored to the individual’s genetics and family history.

Why screening high-risk groups matters

For people at elevated risk, surveillance can detect tumors at an earlier, more treatable stage. Though testing comes with potential downsides, like increased anxiety, false positives, and invasive follow-ups, the emotional and clinical benefit of early detection often outweighs the risks for these individuals.Detecting pancreatic cancer in its early stages can significantly improve survival opportunities via surgery and therapy, lifesaving outcomes that are almost impossible when diagnosis comes too late.While the knowledge has been an age-old piece of information, the connection now is clearer than ever: smoking doesn’t just elevate the risk, it actively boosts pancreatic cancer growth by shutting down the immune system’s defenses. With rising incidence and still-poor survival rates, it’s crucial to act now.While mass screening isn’t yet feasible, those at higher risk, either by genetics, family history, or new-onset diabetes, should talk to their doctors about surveillance options like MRI or endoscopic ultrasound. And quitting smoking remains a vital, controllable step everyone can take.

Some of the populations with the highest risk for Alzheimer’s disease remain greatly underrepresented in clinical trials-and a new study helps explain why. Researchers from the Keck School of Medicine of USC found that participants from these high-risk groups are less likely to have elevated amyloid in the brain based on blood levels of p-tau217. Elevated amyloid is a requirement for clinical trials of Alzheimer’s disease treatments, and amyloid is known to accumulate in the brain years before any signs of cognitive decline.

The study, funded in part by the National Institutes of Health (NIH), builds on earlier research with similar findings, but leverages a new and improved blood test, p-tau217, that more accurately detects early signs of Alzheimer’s disease. Rising levels of p-tau217 are strongly linked to the buildup of amyloid, which disrupts brain activity in Alzheimer’s disease, and the p-tau217 test is increasingly used to determine who qualifies for treatment studies. Earlier this year, the U.S. Food and Drug Administration approved a similar test to help diagnose Alzheimer’s disease in the clinic.

Researchers found that cognitively unimpaired individuals from African American, Hispanic and Asian participants were less likely to have levels of p-tau217 in the blood that indicate elevated amyloid in the brain, showing they lacked the early signs of Alzheimer’s disease that would allow them to participate in a trial of lecanemab. The trial is testing whether the treatment can prevent symptoms of dementia related to Alzheimer’s disease in individuals with biological evidence of the disease. These findings suggest that these groups may have a lower prevalence of amyloid and are not at sufficient level of risk to appropriately qualify for amyloid lowering trials. The results were just published in the journal Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM).

Using this new and more accurate marker, we confirmed our earlier finding and affirmed that we may be seeing differences in the prevalence of amyloid across some populations.”

Doris P. Molina-Henry, PhD, assistant professor of research neurology, Alzheimer’s Therapeutic Research Institute (ATRI) , Keck School of Medicine and lead author of the study

In addition to helping explain the lack of diversity in Alzheimer’s disease research, the findings raise questions about whether the disease progresses differently across racial and ethnic groups. To address these and other important questions, some individuals who did not qualify for the AHEAD Study were invited to participate in the Amyloid Plasma Extension Study (APEX). The study will follow the trajectories of these and other blood markers in these individuals over time.

“It is somewhat paradoxical, because the populations showing low levels of amyloid on biomarker assessments are also the groups that face the highest risk of dementia,” Molina-Henry said. “If amyloid is not what drives disease risk in these groups, then we need to do our due diligence to find out what does.”

Eligibility for clinical trials

The study included 6,437 adults, ages 55 to 80, recruited from 75 sites across the country for AHEAD 3-45, a clinical trial designed to test the safety and efficacy of lecanemab, which removes amyloid from the brain. Of those, 4,832 identified as non-Hispanic white, 877 as Hispanic white, 511 as non-Hispanic Black, 155 as non-Hispanic Asian and 62 as Hispanic Black. All participants were cognitively unimpaired.

Using blood tests for p-tau217, the researchers found that non-Hispanic white participants were more likely than other groups to meet the threshold for inclusion in Alzheimer’s disease clinical trials. Those who identified as Hispanic Black, Hispanic white, non-Hispanic Asian and non-Hispanic Black were significantly less likely to qualify to participate.

In addition to blood tests, the researchers collected positron emission tomography (PET) scans from each participant to directly measure amyloid buildup in the brain. Among participants who qualified for the trials based on the p-tau217 test, all racial and ethnic groups were equally likely to meet the PET scan criteria. That suggests that the same blood test cutoff accurately identifies early signs of Alzheimer’s disease pathology across racial and ethnic groups.

What drives dementia risk

As one of the first and largest Alzheimer’s disease trials of cognitively unimpaired individuals to use blood-based biomarkers, the AHEAD study provides a valuable opportunity to better understand risk for future Alzheimer’s disease related dementia across populations. Those insights have important implications for the development of prevention therapies that will be necessary to address the needs of all individuals at risk of dementia.

Blood-based testing also enables much broader data collection than PET scans, which are more costly and burdensome.

“The additional data is helping us paint a clearer picture of why these populations may be underrepresented in research,” Molina-Henry said. “It may not be because of issues in recruitment, access or interest, but simply that the lower frequency of elevated amyloid in some groups makes them less likely to qualify for anti-amyloid trials.”

Further research can help clarify whether the observed differences relate to Alzheimer’s disease development and progression, and whether factors beyond amyloid-such as sociodemographic or genetic characteristics-contribute to dementia risk in these populations.

Next, Molina-Henry and her team will broaden their analysis of Alzheimer’s disease trial eligibility to include more than 20,000 participants screened for the AHEAD 3-45 trials from around the world.

About the study

In addition to Molina-Henry, the study’s other authors are Rema Raman, Andy Liu, Oliver Langford, Robert A. Rissman and Paul Aisen from the Alzheimer’s Therapeutic Research Institute, Keck School of Medicine of USC, University of Southern California; Joel B. Braunstein, Philip B. Verghese and Venky Venkatesh from C2N Diagnostics, LLC, St. Louis, Missouri; Shobha Dhadda and Michael Irrizary from Eisai, Inc., Nutley, New Jersey; Joshua D. Grill from the Institute for Memory Impairments and Neurological Disorders, University of California Irvine; Keith Johnson and Reisa A. Sperling from Mass General Brigham, Harvard Medical School, Boston, Massachusetts; and the AHEAD 3-45 Study Team.

The AHEAD 3-45 Study is conducted as a public–private partnership of the Alzheimer’s Clinical Trial Consortium, funded by the National Institute on Aging, National Institutes of Health, Eisai Inc., the GHR Foundation and other philanthropists.

The silent sabotage of alcohol

Dr Chopra said, “Alcohol. The most socially accepted drug that silently sabotages your health. Sure, it gives you pleasure in the present, but it steals clarity from your future. It dulls long-term decision-making and impairs judgment almost instantly. It damages your nerve cells, hits your mitochondria, which is your energy engines, leading to poor memory, risk of dementia, and even brain shrinkage over time.”

Alcohol hinders fat loss, damages organs like liver

Furthermore, he shared how alcohol disrupts brain chemistry, contributing to mental health problems like depression and anxiety, and said, “It disrupts brain chemistry, often triggering depression, anxiety, and unpredictable mood swings.”

From a physiological standpoint, Dr Chopra noted that alcohol hinders fat loss, provides empty calories, and damages vital organs such as the liver, potentially causing fatty liver disease and metabolic issues.

He said, “And if you’re working on fat loss, alcohol delays fat oxidation, directly opposing your fitness goals. It’s just empty calories with zero nutritional value. Worse still, alcohol fuels mindless eating, ruins your sleep, and burdens your liver. It can lead to fatty liver disease and long-term metabolic damage.”

‘Alcohol gives you nothing but short-lived pleasure’

Dr Chopra concluded that despite its social acceptance, alcohol offers only fleeting pleasure and does not contribute positively to overall health, even recommending against its consumption for health benefits.

He said, “Despite what the world shows you, alcohol gives you nothing but short-lived hedonic pleasure. That drink that you enjoy with your friends may feel great, but it doesn’t serve your health. So, yes, an occasional glass of red wine, beer or tequila might be okay, but truly speaking, I’d never recommend it for health.”

Note to readers: This report is based on user-generated content from social media. HT.com has not independently verified the claims and does not endorse them.

This article is for informational purposes only and not a substitute for professional medical advice.

Vitamin B12 is abundantly present in animal food products including meat, fish and poultry. A research published by the Cambridge University highlights how Indians who follow strict vegetarian diets have limited sources of B12, and thus, are more likely to suffer from this vitamin deficiency. This does not mean vegetarians can’t fulfil their B12 requirement. Here are 5 vegetarian-friendly B12 rich diet sources.

Newswise — Astrocytes in the lateral hypothalamus region of the brain, an area involved in the regulation of sleep and wakefulness, play a key role in neuron activity in mice and affect their behaviour, Canadian researchers have found.

Led by Ciaran Murphy-Royal of Université de Montréal’s affiliated hospital research centre, the CRCHUM, the scientists detail their finding in a study published in Nature Communications.

In so broadening medical science’s understanding of cerebral mechanisms, the discovery could someday help in the treatment and prevention of depression in humans, the researchers say.

According to the scientific literature, early-life stress leads to a five-fold increase in the risk of developing a mental-health disorder as an adult, notably causing treatment-resistant disorders.

Less active, day or night

As brain cells, astrocytes are sensitive to variations in the blood concentration of metabolites and, in response to changes in the blood, astrocytes can modulate the extent of their interaction with neurons, their neighbouring cells.

In mice, those changes are particularly responsive to the level of corticosterone, the stress hormone in the rodents’ blood.

“In adult mice who experienced early-life stress, we saw abnormally high levels of corticosterone,” said Murphy-Royal, a professor in UdeM’s Faculty of Medicine. “The impact of stress on behaviour also differed according to sex.”

Notably, he said, “females were less active at night, while males were hyperactive during the day.”

In people with depression who have experienced a similar type of stress, this sex differences have also been observed.

Lack of maternal care

Lewis R. Depaauw-Holt, the study’s first author and a PhD student on Murphy-Royal’s team, was able to recreate early-life stress conditions in young rodents by separating them from their mothers.

Over 10 days, for four hours a day, he kept the young mice apart from their mothers. This lack of maternal care occurred during a critical period of brain development for the rodents, the equivalent of ages three to seven in human children.

“The differences in activity levels between female and male mice were also seen within a group of neurons that produces neuropeptides called orexins,” said Murphy-Royal.

“Located in the lateral hypothalamus, these orexin neurons contribute to regulating sleep-wake cycles,” he said. “In males, these neurons showed hyperactivity, while in females we saw hypoactivity.”

In mice that experienced early-life stress, astrocytes were smaller and had fewer branches, especially in females. These branches are essential for transmitting information to neighbouring neurons and interacting with nearby cells.

“In our field of expertise, we believe that the changes in astrocyte morphology are a marker of dysfunction,” said Murphy-Royal. “In humans, we see these variations in diseases like Parkinson’s or Alzheimer’s.”

A single pathway?

What if these changes in behaviour, neuron activity and morphology in both sexes were tied to a single stress-signalling pathway?

To test their hypothesis, the CRCHUM research team deleted glucocorticoid receptors in astrocytes to which corticosterone, the stress hormone, would normally bind.

“Without these receptors, neuronal activity and mouse behaviours returned to baseline similar to that of mice who did not experience early-life stress,” said Murphy-Royal.

“And, even if their astrocytes didn’t return to their normal size, they did regain their complexity, visible in the number of branches they use to interact with neighbouring cells.” 

Contrary to what scientists believed until now, astrocytes are disturbed by stress before neurons are, the study reveals.

In humans, the challenge of countering the effects of early-life stress will surely be more complex than in rodents, Murphy-Royal cautioned, but one thing is for sure: astrocytes could turn out to be an excellent therapeutic target for preventing depression.

Overview

Candida is a yeast that can cause infections ranging in severity. Antifungal resistance among Candida is growing, particularly for specific species such as Candida auris and Candida parapsilosis. These two species also spread more easily between patients in healthcare settings compared to other species of Candida. Awareness of this issue is essential for clinicians, as it can guide testing practices and clinical treatment decisions.

During this COCA Call, presenters will share current evidence demonstrating the increase in antifungal resistance among C. auris and C. parapsilosis and discuss recommendations for testing and treatment.

Webinar

Date: Thursday, September 18, 2025

Time: 2:00-3:00 P.M. ET

A few minutes before the webinar begins, please click here to join.

Presenters

Dallas Smith, PharmD, MAS
Epidemiologist
Mycotic Diseases Branch
Division of Foodborne Waterborne, and Environmental Diseases
National Center for Emerging and Zoonotic Infectious Diseases
Centers for Disease Control and Prevention

Meghan Lyman, MD
Acting Deputy Branch Chief
Mycotic Diseases Branch
Division of Foodborne Waterborne, and Environmental Diseases
National Center for Emerging and Zoonotic Infectious Diseases
Centers for Disease Control and Prevention

Call Objectives

COCA Call Objectives

At the conclusion of the session, the participant will be able to accomplish the following:

1. Cite background information on the topic covered during the presentation.
2. Discuss CDC’s role in the topic covered during the presentation.
3. Describe the topic’s implications for clinicians.
4. Discuss concerns and/or issues related to preparedness for and/or response to urgent public health threats.
5. Promote health improvement, wellness, and disease prevention in cooperation with patients, communities, populations at higher risk, and other members of an interprofessional team of healthcare providers.

Activity-specific Objectives

1. Describe the increasing prevalence of resistant Candida species.
2. Explain the epidemiology of emerging resistant Candida.
3. Outline appropriate testing including species identification, antifungal susceptibility testing, and whole genome sequencing.
4. Summarize treatment options and resources for resistant Candida species.

Continuing Education

Instructions for Obtaining Continuing Education (CE)

To receive continuing education (CE) for WC4520R-091825—The Path of Yeast Resistance: Drug-resistant Candida on the Rise, please visit CDC TRAIN and search for the course in the Course Catalog using WC4520R-091825. Follow the steps below by October 20, 2025. The registration code is COCA091825.

To receive continuing education (CE) for WD4520R-091825—The Path of Yeast Resistance: Drug-resistant Candida on the Rise, please visit CDC TRAIN and search for the course in the Course Catalog using WD4520R-091825. Follow the steps below between October 21, 2025, and October 21, 2027.

1. Register for and complete the course.
2. Pass the post-assessment at 75%.
3. Complete the evaluation.
4. Visit Your Learning to access your certificates and transcript.

Accreditation Statements

CPE: The Centers for Disease Control and Prevention designated this Knowledge-based event for pharmacists to receive 0.1 CEUs in pharmacy education. The Universal Activity Number is JA4008229-0000-25-050-L04-P and enduring JA4008229-0000-25-051-H04-P.

CME: The Centers for Disease Control and Prevention designates this live activity for a maximum of 1 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

AAPA CME: Credit Designation Statement – Live The Centers for Disease Control and Prevention has been authorized by the American Academy of PAs (AAPA) to award AAPA Category 1 CME credit for activities planned in accordance with AAPA CME Criteria. This activity is designated for 1 AAPA Category 1 CME credits. PAs should only claim credit commensurate with the extent of their participation.

CNE: The Centers for Disease Control and Prevention designates this activity for 1 nursing contact hours.

CEU: The Centers for Disease Control and Prevention is authorized by IACET to offer 0.1 CEUs for this program.

CECH: Sponsored by the Centers for Disease Control and Prevention, a designated provider of continuing education contact hours (CECH) in health education by the National Commission for Health Education Credentialing, Inc. This program is designated for Certified Health Education Specialists (CHES^®) and/or Master Certified Health Education Specialists (MCHES^®) to receive up to 1 total Category I continuing education contact hours. Maximum advanced level continuing education contact hours available are 1. Continuing Competency credits available are 1. CDC provider number 98614.

AAVSB/RACE: This program has been submitted (but not yet approved) for 1 hours of continuing education credit in jurisdictions which recognize AAVSB RACE approval; however, participants should be aware that some boards have limitations on the number of hours accepted in certain categories or restrictions on certain methods of delivery of continuing education.

For Certified Public Health Professionals (CPH): The Centers for Disease Control and Prevention is a pre-approved provider of Certified in Public Health (CPH) recertification credits and is authorized to offer 1 CPH recertification credits for this program.

DISCLOSURE: In compliance with continuing education requirements, all planners and presenters/moderators must disclose all financial relationships, in any amount, with ineligible companies over the previous 24 months as well as any use of unlabeled product(s) or products under investigational use.

CDC, our planners, and presenters/moderators wish to disclose they have no financial relationship(s) with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

Content will not include any discussion of the unlabeled use of a product or a product under investigational use with the exception of Dr. Meghan Lyman’s discussion of several antifungal medications in clinical trials for C. auris and availability of use under expanded access programs.

CDC did not accept financial or in-kind support from ineligible companies for this continuing education activity.

CDC complies with applicable Federal civil rights laws and does not discriminate based on race, color, national origin, age, disability, religion, or sex. To learn more visit: https://www.hhs.gov/civil-rights/for-individuals/nondiscrimination/index.html

Just a few weeks ago, a 44-year-old woman walked into my clinic with unusual vaginal bleeding. My examination findings were strongly suggestive of advanced cervical cancer. My worst fears were confirmed after further investigations.

The painful truth was that, as a gynaecologist, this was not the first piece of cervical cancer–related bad news I had to deliver in my career. What makes it even more difficult to accept that cervical cancer is a largely preventable disease, yet countless women in Pakistan continue to face it in silence and without timely intervention.

Globally, cervical cancer remains one of the leading causes of death among women. According to the World Health Organisation, there were an estimated 604,000 new cases and 342,000 deaths in 2020, making it the third most common malignancy among women. Human Papillomavirus (HPV), the primary cause of cervical cancer, is the most common sexually transmitted infection, with a 50 per cent lifetime risk of infection for both men and women.

In Pakistan, the picture is even more concerning. With over 73 million women aged 15 years and older at risk. More than 5,000 new cases are reported annually, and 64 per cent of these women die due to late diagnosis and inadequate screening. According to a study, the true burden is much greater due to the absence of a national cancer registry and extremely low screening rates.

Against this backdrop, Pakistan’s first nationwide HPV vaccine campaign, supported by Unicef and WHO, will run from September 15 to 27 (2025) and marks a historic landmark. The programme aims to reach 13 million girls aged 9 to 14 across Punjab, Sindh, the Islamabad Capital Territory and Azad Jammu and Kashmir. Even more promising is the planned inclusion of the HPV vaccine in the Expanded Programme on Immunisation (EPI), ensuring long-term sustainability. The phased launch, expanding to Khyber Pakhtunkhwa in 2026 and Balochistan and Gilgit-Baltistan in 2027, will strengthen routine immunisation and move Pakistan closer to global elimination goals.

The campaign advances the WHO goal to eliminate cervical cancer by 2030, which aims for 90 per cent of girls vaccinated by the age 15; 70 per cent of women screened; and 90 per cent of women with pre-cancer or invasive cancer receiving timely treatment. The WHO views this campaign as a revolutionary step towards a future where every girl in Pakistan is protected from cervical cancer.

Yet, the road ahead is not without challenges. About 36 per cent of Pakistani girls between the ages of 9 and 14 are out of school, making it difficult to reach them through school-based vaccination. In addition, Pakistan’s cervical cancer screening is purely opportunistic, with only 1.5–2 per cent of the women’s population ever screened. Without a national screening programme, most cases are diagnosed late, when treatment options are limited.

When I began my training as a gynaecologist ten years ago, I joined community outreach teams in Islamabad, performing simple visual inspections and referring women for cervical screening to the tertiary care unit. I recall that women flocked to the basic health units for their assessments. Even back then, I believed that if women were given the chance, they would step forward to protect their health. That potential remains, but it will take unwavering commitment to make this HPV vaccine campaign a life-changing reality.

To promote greater acceptance of HPV vaccination in communities across Pakistan, a multifaceted approach is essential, emphasising both health education and cultural sensitivity. The HPV vaccine should be presented not simply as a means of protection against a sexually transmitted infection, but as a proven shield against cervical cancer, which claims thousands of Pakistani women every year. Engaging the Council of Islamic Ideology and securing religious endorsements could be pivotal in Pakistan’s HPV vaccine rollout.

Providing parental consent forms and pre-vaccination counselling sessions can further address concerns around vaccine safety and efficacy. Engaging doctors and influencers to spread clear content in Urdu and regional languages, while showcasing success stories from Muslim and developing countries to prove HPV vaccination is compatible with Islamic values and acceptable globally.

Internationally, cervical cancer is responsible for one in four cancer orphans. It is a social tragedy, where a preventable disease claims the lives of women who leave behind devastated families. In Pakistan, women already face multiple barriers to healthcare, where lower value for women’s health, delayed diagnoses, and lack of empowerment often force them to suffer without seeking medical help. The HPV vaccine offers a rare chance to rewrite this story, but only if prevention is embraced as a shared responsibility

Pakistan’s HPV vaccine campaign is more than a health promotion campaign. It is a lifesaving opportunity for millions of girls. For the first time, we have the tools to stop a deadly cancer before it takes root. The challenge now is to ensure that every girl, whether in school or out, in cities or in villages, can access this vital vaccine.

As a gynaecologist who has witnessed the devastating consequences of cervical cancer firsthand, I urge parents, teachers, healthcare providers, policymakers, and community leaders to rally behind this campaign. If we combine vaccination, awareness, screening, and empowerment, we can make cervical cancer a disease of the past in Pakistan. Our will to act is all that stands between despair and hope.

The writer is a consultant obstetrician and gynaecologist.