The WHO's New Cancer Projections: What NPs Need to Know

 

NP CHRONICLES

Clinical Education for NP Students & New Graduates

The WHO's New Cancer Projections: What NPs Need to Know

Global Health  |  Oncology Prevention  |  Health Equity

A new World Health Organization report, released this month, offers a sobering long-range forecast: global cancer cases are projected to climb from roughly 20.6 million in 2024 to as many as 35 million a year by 2050 — a jump of about 67 percent. The report, covered by the Washington Post's Daniel Wu, is not primarily a story about medical failure. It's a story about demographics, risk factor exposure, and above all, deep inequity in who gets access to prevention, early detection, and treatment.

For nurse practitioners, this report lands close to home. Whether you're doing primary care screening, managing chronic disease risk factors, or counseling patients on tobacco and alcohol use, you are already working the levers this report identifies as most fixable. Here's what's in the WHO's findings and why it matters for day-to-day practice.

The Headline Numbers

Metric	2024	2050 (projected)
Global annual cancer cases	~20.6 million	~35 million
Global cancer deaths (2024)	9.7 million	—
Breast cancer 5-yr survival, high-income countries	~85–90%	—
Breast cancer 5-yr survival, low-income countries	<30%	—

 

The report projects that cancer incidence will rise in every region of the world, but unevenly — the steepest increases are expected in Africa and the Eastern Mediterranean region, areas with the least infrastructure to absorb that growth. By contrast, the rate of new cancer cases in the United States has been relatively stable in recent years, according to the National Institutes of Health, even as global numbers climb.

Why Cases Are Rising: It's Not Just “More Cancer”

The WHO report is careful to separate several distinct drivers, and the distinction matters for how we talk to patients and communities about it:

•     Aging populations. As life expectancy rises worldwide, more people live long enough to develop cancers that are fundamentally diseases of accumulated cellular damage and age.

•     Known, modifiable risk factors — principally tobacco, alcohol use, and rising obesity rates. These are the factors the report repeatedly flags as both a major driver of the projected increase and the most addressable lever available.

•     Improved surveillance and diagnostic capacity, which sounds paradoxical but is genuinely part of the story: better screening and imaging catch cancers that would previously have gone undiagnosed or been attributed to another cause of death.

Emil Lou, MD, an oncologist at the University of Minnesota quoted in the Post's coverage, framed the tension well: treatments like immunotherapy have measurably improved survivability for many patients, but the rising global case count is a reminder that better treatment alone doesn't solve a prevention and access problem.

The Equity Gap Is the Real Story

The single most striking figure in the report is the gap in outcomes by income level. In high-income countries, five-year net survival for breast and prostate cancer sits around 80 to 90 percent. In low-income countries, breast cancer survival drops below 30 percent — not because the biology of the disease is different, but because access to timely diagnosis and treatment is.

Cervical cancer tells a similarly stark story in the other direction. Isabelle Soerjomataram, an epidemiologist with the International Agency for Research on Cancer, noted that cervical cancer has been pushed to “almost elimination” in parts of Europe and North America, driven largely by HPV vaccination and screening infrastructure — while it remains the leading cancer diagnosis in much of sub-Saharan Africa.

CLINICAL BOTTOM LINE The WHO projects a 67% rise in global cancer incidence by 2050, driven mainly by aging populations and modifiable risk factors — tobacco, alcohol, and especially obesity. Survival gaps between high- and low-income countries remain enormous (breast cancer 5-year survival: >85% vs. <30%), underscoring that access to prevention and early detection, not just treatment innovation, determines outcomes. An estimated 4 in 10 cancer cases worldwide are linked to risk factors we already know how to address.

Where the Report Sees Progress — and Where It Doesn't

Encouraging trends

•     Global tobacco use has dropped 27 percent since 2010, a meaningful public health win the report explicitly credits.

•     HPV vaccination has expanded significantly: 85 percent of countries now include the HPV vaccine in national immunization programs, and an estimated 31 percent of girls globally have received their first dose, up from 17 percent in 2019.

The stalled trend: obesity

The report's most alarming finding may be the near-universal failure to curb rising obesity rates. Obesity is linked to more than a dozen cancers, including liver, pancreatic, and colorectal cancer. WHO cancer control lead André Ilbawi was blunt about the trajectory: obesity-associated cancers are on track to become the norm in a significant number of countries within the next two to three decades.

NUANCE TO FLAG It's tempting to read a 67% projected increase in cases as purely bad news, but the report's authors are explicit that rising case counts partly reflect success — aging populations are, in large part, a product of improved life expectancy and reduced deaths from other causes earlier in life. The real alarm in this report isn't that people are living long enough to get cancer; it's that so much of the projected increase is preventable and that survival outcomes remain so unevenly distributed by income. Framing this accurately matters when discussing the report with patients, who may otherwise hear only “cancer is getting worse” without the context of what's actually driving it.

What This Means for Your Practice

Four in 10 new cancer cases worldwide are linked to risk factors we already know how to address, according to Soerjomataram. For NPs in primary care, that statistic is essentially a job description. The interventions with the clearest evidence of impact at the population level are ones most NPs are already positioned to deliver at the individual level:

•     Tobacco cessation counseling and pharmacotherapy at every applicable visit, not just annual wellness exams.

•     HPV vaccination counseling and catch-up dosing for eligible patients and their children — particularly relevant given how much of the global cervical cancer gap traces back to vaccination access.

•     Alcohol use screening using a validated tool (AUDIT-C or similar) integrated into routine visits, not reserved for patients who volunteer a concern.

•     Weight management conversations framed around cancer risk specifically — many patients are unaware that obesity is linked to liver, pancreatic, and colorectal cancers, and hearing that connection directly from a clinician can shift motivation.

•     Appropriate screening referrals (breast, cervical, colorectal) without assuming access barriers that may not apply to your specific patient — and proactively addressing the ones that do, such as cost, transportation, or health literacy.

Global Numbers, Local Relevance

It's easy to read a WHO global report and file it under “not my patient population.” But the same risk factors driving the global projection — tobacco, alcohol, obesity, and inconsistent access to screening — are exactly the factors that predict outcome disparities within the U.S. as well, across income levels, rural versus urban geography, and insurance status. The global report is, in a real sense, a magnified version of disparities many NPs already see in their own patient panels.

The encouraging half of this report is worth holding onto: unlike many of medicine's hardest problems, the biggest driver of preventable cancer burden identified here isn't a scientific unknown. It's an access and behavior-change problem — the kind NPs address in exam rooms every day.

 

Reference

Wu, D. (2026, July 8). Cancer cases worldwide are expected to soar in the coming decades, a report finds. Here's why. The Washington Post.

Creatine and the Immune System: What a New Dendritic Cell Study Means for Cancer Care

 

NP CHRONICLES

Clinical Education for NP Students & New Graduates

Creatine and the Immune System: What a New Dendritic Cell Study Means for Cancer Care

Research Spotlight  |  Oncology & Immunology  |  Board-Relevant Physiology

Ask most people what creatine is for, and you'll get the same answer: bigger lifts, more muscle, better gym performance. That reputation is well earned — creatine is one of the most studied and safest performance supplements available. But a growing body of research is pointing to a second life for this humble metabolite, one that has nothing to do with the squat rack and everything to do with how the immune system fights cancer.

A study published in iScience in April 2026 by Kang, Elsten-Brown, Wang, and colleagues at UCLA adds an important piece to that story. The researchers show that dendritic cells — the immune system's professional “antigen presenters” — rely on creatine to power their activation, and that supplementing creatine can make dendritic cells better at rallying T cells against tumors. For NPs working in oncology, primary care, or integrative settings, this is worth understanding, both for the mechanism and for the practical conversations it's likely to generate with patients.

A Quick Refresher: What Dendritic Cells Actually Do

Dendritic cells (DCs) are the immune system's scouts and messengers. They sit in tissues — including tumors — waiting to detect danger signals. Once activated, they capture antigens, migrate to lymph nodes, and present those antigens to T cells, essentially teaching the adaptive immune system what to attack. Without well-activated DCs, T cells never get the briefing they need to mount an effective antitumor response.

Tumors know this, and part of how cancers evade the immune system is by starving or disabling the DCs sitting inside them. A tumor microenvironment that's short on nutrients and long on metabolic stress tends to produce sluggish, poorly activated DCs — and sluggish DCs mean an under-primed T cell army.

What the Study Found

The research team started by looking at gene expression in dendritic cells pulled from mouse melanoma tumors and compared them to DCs from the spleen. One gene stood out: the creatine transporter, CrT (also known as SLC6A8), was markedly upregulated in the tumor-dwelling DCs. The same transporter also increased sharply when lab-grown DCs were stimulated with a bacterial signal (LPS), the kind of “danger cue” that triggers DC activation.

That pattern — a transporter that goes up specifically when a cell is activated or under metabolic pressure — is a strong hint that creatine uptake matters for DC function. The team then tested that hint directly using three complementary approaches.

1. Knock out the creatine transporter, and DCs struggle.

•     Dendritic cells grown from CrT-knockout mice showed sharply reduced survival after activation.

•     They expressed lower levels of activation markers CD86 and MHC-II (I-Ab).

•     They produced less TNF-α and IL-6, and were markedly worse at driving proliferation and cytokine output in antigen-specific T cells co-cultured alongside them.

•     When these knockout DCs were injected into mice and the animals' T cell recall response was tested two weeks later, the response was measurably weaker — confirming the defect held up in a living animal, not just a dish.

2. Add creatine, and DCs do better.

•     Creatine supplementation improved survival of activated dendritic cells.

•     It increased expression of the same activation markers (CD86, MHC-II) and boosted proinflammatory cytokine output (IL-1β, IL-6, TNF-α).

•     The effect wasn't limited to one type of activation signal — it held up whether DCs were stimulated through TLR4 (LPS) or TLR3 (poly I:C) pathways, suggesting a fairly general effect on DC activation rather than a quirk of one signaling route.

3. The mechanism traces back to ATP.

Using mass spectrometry, the researchers showed that creatine-supplemented DCs held higher intracellular ATP and lower AMP/ADP — in other words, better-buffered energy reserves. That mattered because DC activation runs through energy-hungry signaling cascades, particularly NF-κB. When creatine (or ATP itself) was added, NF-κB signaling ramped up; when the creatine transporter was blocked or deleted, NF-κB signaling dropped off. The takeaway: creatine isn't acting as a magic immune signal on its own — it's topping off the ATP tank that inflammatory signaling pathways draw from.

From the Dish to the Mouse to (Possibly) the Clinic

The in vitro findings held up in living animals. In a mouse melanoma model, daily creatine injections slowed tumor growth and increased the number and activation of a particularly potent DC subset (cDC1s) inside the tumor. Single-cell sequencing of tumor-infiltrating immune cells showed creatine-treated dendritic cells turning up inflammatory and antigen-presentation genes while turning down glycolysis — a metabolic signature consistent with DCs shifting from “conserve energy” mode into “get to work” mode.

Encouragingly, the human data pointed the same direction. Monocyte-derived dendritic cells grown from healthy donor blood also upregulated the creatine transporter upon stimulation, and creatine supplementation boosted their inflammatory cytokine output and their ability to activate antigen-specific T cells targeting NY-ESO-1, a tumor antigen expressed across many cancer types.

CLINICAL BOTTOM LINE Creatine appears to help fuel dendritic cell activation by preserving intracellular ATP, which in turn sustains the inflammatory signaling (chiefly NF-κB) that dendritic cells need to prime T cells against tumors. In mouse models, creatine supplementation slowed tumor growth and improved dendritic cell activity within tumors. This is preclinical, mechanistic work — not a clinical recommendation — but it strengthens a pattern already seen with creatine's effects on T cells and macrophages in cancer immunity.

Why This Fits a Bigger Pattern

This isn't creatine's first appearance in the cancer immunology literature. Earlier work from some of the same investigators found that creatine uptake directly boosts antitumor CD8 T cell responses, and separate research has linked creatine to proinflammatory (M1-like) polarization of tumor-associated macrophages. Taken together, three major arms of the antitumor immune response — T cells, macrophages, and now dendritic cells — all appear to lean on the same creatine/ATP buffering system when they're asked to do energetically demanding work.

There's also an epidemiologic thread worth mentioning: a retrospective analysis of NHANES data spanning roughly a decade found that higher dietary creatine intake was associated with a lower incidence of cancer. Association isn't causation, and dietary pattern data is notoriously confounded, but it's a data point that lines up directionally with the mechanistic work.

A nuance patients (and clinicians) should know

NUANCE TO FLAG Creatine's relationship with cancer is not one-directional. Several studies cited in this same paper note that malignant cells can co-opt creatine metabolism to fuel their own metastasis and progression, and that blocking creatine transport or creatine kinase has slowed tumor growth in some prostate and colon cancer models. In other words, the same energy-buffering trick that helps immune cells work harder may, in a different cellular context, help cancer cells work harder too. This is exactly why “creatine is good for the immune system” cannot be flattened into “patients with cancer should take creatine” without qualification.

What This Means for Practice — For Now

It's worth being precise about what this study does and doesn't support, especially given how often patients arrive already primed by supplement marketing and social media health claims.

•     This is preclinical (mouse and in vitro human cell) research. There is no clinical trial yet testing creatine supplementation as an adjunct cancer immunotherapy in patients.

•     The antitumor benefit was shown in a single mouse melanoma model. The authors themselves note this as a limitation and call for testing across more physiologically relevant tumor models.

•     Creatine's documented benefits in oncology so far are strongest for supportive care — there is existing evidence that creatine can help preserve muscle mass and body weight in cancer-associated cachexia, and some data suggesting it may blunt doxorubicin-related cardiotoxicity.

•     Creatine has a well-established long-term safety profile in the general population, which is part of why the authors argue it could move to clinical trials relatively quickly — but “could move to trials” is not the same as “is ready for clinical use” in oncology, particularly given the tumor-promoting data mentioned above.

•     Patients on active cancer treatment who ask about creatine supplementation should be directed to discuss it with their oncology team before starting, given the mixed tumor-intrinsic data and the lack of trials in this specific context.

The Physiology Worth Remembering

For board review and patient teaching alike, the core mechanism is a nice illustration of basic bioenergetics applied to immunology:

•     Creatine enters cells via the creatine transporter (CrT/SLC6A8).

•     Creatine kinase converts creatine to phosphocreatine, which acts as a rapidly mobilized energy reserve.

•     When ATP is consumed, phosphocreatine donates a phosphate group back to ADP, quickly regenerating ATP — the same creatine kinase/phosphocreatine shuttle that powers muscle during short bursts of intense activity.

•     Activated immune cells, it turns out, tap the same energy-buffering system to sustain the signaling cascades (like NF-κB) that drive inflammatory gene expression.

It's the same biochemistry bodybuilders have relied on for decades — just running inside a dendritic cell instead of a bicep.

Bottom Line for Your Next Patient Conversation

If a patient with cancer asks about creatine supplementation after reading about “immune-boosting” research, this is a reasonable framework: the mechanistic and preclinical case for creatine supporting antitumor immunity is real and growing, but it is not yet clinical evidence, and creatine's effects on tumor cells themselves are context-dependent and not uniformly favorable. Encourage patients to loop in their oncology team, and reserve enthusiasm for the supportive-care indications (cachexia, possibly cardioprotection during certain chemotherapy regimens) where the evidence base is more mature.

 

References

Kang, E., Elsten-Brown, J., Wang, Y.-C., et al. (2026). Creatine uptake promotes dendritic cell activation and enhances antitumor immunity. iScience, 29, 115436. https://doi.org/10.1016/j.isci.2026.115436

Di Biase, S., Ma, X., Wang, X., et al. (2019). Creatine uptake regulates CD8 T cell antitumor immunity. J Exp Med, 216, 2869–2882.

Peng, Z., & Saito, S. (2023). Creatine supplementation enhances anti-tumor immunity by promoting ATP production in macrophages. Front Immunol, 14, 1176956.

Jiang, J., Zhao, H., Chen, J., et al. (2024). The association between dietary creatine intake and cancer in U.S. adults: insights from NHANES 2007–2018. Front Nutr, 11, 1460057.

Wei, L., Wang, R., Lin, K., et al. (2022). Creatine modulates cellular energy metabolism and protects against cancer cachexia-associated muscle wasting. Front Pharmacol, 13, 1086662.