Summary
Background
Infectious agents are an important preventable cause of cancer globally. To inform prevention efforts, we provide a comprehensive picture of cancer burden attributable to infections, including newly established, carcinogenic infectious agents and latest global cancer incidence estimates.
Methods
In this worldwide incidence analysis, we used data from the Global Cancer Observatory's Cancer Today (GLOBOCAN) database of cancer incidence in 2024 to estimate population-attributable fractions (PAFs), absolute numbers, and age-standardised incidence rates (ASIRs) of new cancer cases attributable to 12 infectious agents classified as Group 1 carcinogens by the IARC Monographs Programme: Helicobacter pylori, human papillomavirus (HPV), hepatitis B (HBV) and hepatitis C viruses (HCV), Epstein–Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus, Schistosoma haematobium, human T-cell lymphotropic virus, Opisthorchis viverrini, Clonorchis sinensis, Merkel cell polyomavirus, and HIV. Estimates stratified by sex, country, and age group were aggregated by UN geographical subregion and World Bank income group.
Findings
An estimated 2·3 million new cancer cases were attributable to infections globally in 2024, which is equivalent to 12% of all cancer cases. The largest number of cases was attributable to H pylori (n=760 000, PAF 4%), followed by HPV (n=750 000, 4%), HBV (n=360 000, 2%), EBV (n=260 000, 1%), and HCV (n=160 000, <1%). The largest burden of infection-attributable cancer was in eastern Asia, with 990 000 cases (42% of the global total, ASIR 31·9 per 100 000 cases). ASIRs were also higher than the global average (22·7) in sub-Saharan Africa (28·5), central and eastern Europe (24·3), and southeastern Asia (23·1). Focused analysis of EBV-attributable cancers revealed regional variation in the distribution of cancer types.
Interpretation
Our findings highlight the importance of infection control to achieve cancer prevention. Scientifically proven, but often underused, approaches include HPV and HBV vaccination; testing and treatment of HIV, H pylori, HBV, and HCV; safe injection practices; access to condoms and pre-exposure prophylaxis to prevent HIV transmission; and screening of precancerous lesions for HPV-driven cervical and anal cancer. Our findings also inform the investment cases for research and development for new prevention tools, most notably for EBV.
Funding
None.
Introduction
The global burden of cancer is predicted to grow from 20 million new cases in 2024, to 35 million in 2050, due to population ageing alone.1 Considering the overwhelming economic and social costs of cancer,2 investment in prevention is crucial. Infectious agents are a major preventable cause of cancer globally and are estimated to be the leading modifiable risk factor for cancer among women in 141 countries and men in 58 countries.3 Importantly, many carcinogenic infectious agents have existing or potential preventive interventions, including vaccines, diagnostics, treatments, and safe-injection practices.
The International Agency for Research on Cancer (IARC) Monographs Programme has classified 13 infectious agents (including nine viruses, one bacterium, and three parasites) as Group 1 carcinogens with sufficient evidence of causing cancer in humans.4, 5 Previous global estimates indicated that, in 2018, around 13% of all cancer cases (or 2·2 million cases) were due to infection.6 Since then, evidence has strengthened on carcinogenicity for additional infectious agents—notably HIV7 and Merkel cell polyomavirus (MCV)5—as well as on causal associations between established Group 1 infectious agents and additional cancer types, such as Epstein–Barr virus (EBV) and gastric cancer.8
Research in context.
Evidence before this study
The IARC Monographs programme has classified 13 infectious agents as Group 1 carcinogens with sufficient evidence of causing cancer in humans. We searched PubMed from Jan 1, 2019, to Feb 19, 2026, for studies quantifying national and global burden of cancer attributable to infectious agents using the search terms (“infection”[tiab]) AND (“cancer” OR “neoplasm” OR “carcinoma”) AND “attribut*”. There were no language restrictions. Previous global estimates indicated that approximately 2·2 million cancers worldwide were attributable to infections in 2018, with the highest burden in eastern Asia and sub-Saharan Africa. These estimates have informed prevention strategies but, since then, evidence has strengthened on carcinogenicity for additional infectious agents not previously considered (notably HIV and Merkel cell polyomavirus [MCV]) and on causal associations between established Group 1 infectious agents and additional cancer types, such as Epstein–Barr virus (EBV) and gastric cancer.
Added value of this study
This study brings together the latest evidence to provide an updated picture of cancer burden attributable to infections, considering advances in knowledge of cancer causality and expanded and up-to-date data on global cancer incidence, using updated GLOBOCAN 2024 incidence data and refined attributable fraction estimates. A major strength of our study is the incorporation of 16 additional causal infection–cancer type pairs compared with our previous 2018 global estimates, including cancers caused by HIV and MCV, as well as an expanded set of cancer sites caused by EBV, hepatitis B virus (HBV), hepatitis C virus (HCV), and Kaposi's sarcoma-associated herpesvirus.
Implications of all the available evidence
Our updated estimates highlight the continued importance of infection control in global cancer prevention strategies. Despite progress in vaccination and screening, infection-related cancers remain a major challenge globally, with persistent inequities especially impacting low-income and middle-income countries. Our findings emphasise the need to invest in new prevention tools, such as EBV vaccines, and also reinforce the need to scale-up proven interventions, such as HPV and HBV vaccination; testing and treatment of HIV, Helicobacter pylori, HBV, and HCV; safe injection practices; access to condoms and pre-exposure prophylaxis to prevent HIV transmission; and screening of precancerous lesions for HPV-driven cervical and anal cancers. Many of these strategies are cost-effective and well established, yet remain underutilised due to societal, financial, and political barriers, particularly in settings with the greatest need. Tackling infection-related cancers requires coordinated and equity-based strategies within global and local cancer prevention frameworks.
In this global study, we provide an updated overview of the cancer burden attributable to infections, considering recent advances in knowledge of cancer causality, as well as expanded and up-to-date data on global cancer incidence. We use population-attributable fractions (PAFs) and the number of attributable cases to provide goals for primary and secondary prevention. In addition, we provide age-standardised incidence rates (ASIRs) of cancer attributable to infections for international comparisons. These estimates are highly relevant for policy and can be used to advocate for resources for cancer prevention.
Methods
Study design and data sources
In this analysis of global incidence, we estimated the proportion, absolute numbers, and ASIRs of new cases of cancer for people of any age attributable to 12 infectious agents classified as Group 1 carcinogens by the IARC Monographs Programme: Helicobacter pylori, hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), EBV, Kaposi's sarcoma-associated herpesvirus (KSHV; also referred to as human herpesvirus 8), human T-cell lymphotropic virus type 1 (HTLV-1), Opisthorchis viverrini, Clonorchis sinensis, Schistosoma haematobium, MCV, and HIV.4, 5
We calculated PAFs according to specific methodologies for each of the 37 causal infection–cancer pairs, as detailed in the appendix (pp 2–6). For 21 (57%) of the 37 infection–cancer pairs, PAFs had been addressed previously6 and either remained unchanged (n=14; HPV for cancer of the cervix uteri and squamous cell carcinoma of the anus, penis, vulva, vagina, oral cavity, and larynx; H pylori for gastric non-Hodgkin lymphoma; EBV for cancer of the nasopharynx; HCV for non-Hodgkin lymphoma; KSHV for Kaposi's sarcoma; S haematobium for squamous cell carcinoma of the bladder; HTLV-1 for adult T-cell leukaemia and lymphoma; and O viverrini or C sinensis for intrahepatic cholangiocarcinoma), or were updated with newly available data (n=7; HPV for oropharyngeal cancer, H pylori for cardia and non-cardia gastric cancer sites, HBV and HCV for hepatocellular carcinoma, and EBV for Burkitt lymphoma and Hodgkin lymphoma). For 16 new infection–cancer pairs, PAFs came from published methodology (n=14; EBV for gastric cancer, diffuse large B-cell lymphoma, and extranodal natural killer cell or T-cell lymphoma [nasal type]; KSHV for primary effusion lymphoma; MCV for Merkel cell carcinoma; and HIV for cervical cancer, Kaposi's sarcoma, squamous cell carcinoma of the anus, penis, vulva, vagina, Hodgkin lymphoma, non-Hodgkin lymphoma, and squamous cell carcinoma of the conjunctiva), or were developed specifically for this study (n=2; HBV and HCV for intrahepatic cholangiocarcinoma), as detailed in the appendix (pp 2–3, 7). As previously described,6 PAFs were primarily estimated from the prevalence of infection in people with cancer, with the exception of HIV, for which population-based prevalence was used (appendix pp 2–7).7
National estimates of new cases of cancer in 2024 were extracted directly from the Global Cancer Observatory's Cancer Today (GLOBOCAN) database for cancers of the nasopharynx (ICD-10; C11), larynx (C32), vulva (C51), vagina (C52), cervix uteri (C53), and penis (C60), gastric cancer (C16), Kaposi's sarcoma (C46), Hodgkin lymphoma (C81), non-Hodgkin lymphoma (C82–86 and C96), and all cancers combined excluding non-melanoma skin cancer (C00–97 excluding C44). For squamous cell carcinoma of the conjunctiva and Merkel cell carcinoma, cases were obtained by applying published incidence rates to the 2024 population (appendix pp 3, 8). As in previous work,6 cancers of the oropharynx, tonsils, and base of tongue (C01 and C09–10), oral cavity (C02–06), cardia (C16.0) and non-cardia gastric cancer (C16.1–16.9), anal squamous cell carcinoma (C21), hepatocellular carcinoma (C22.0), intrahepatic cholangiocarcinoma (C22.1), non-Hodgkin lymphoma of gastric topography (ICD-O-3 C16, 9591), squamous cell carcinoma of the bladder (ICD-10 C67, ICD-O-3 8051–8078, 8083–8084), Burkitt lymphoma (C83.7), and adult T-cell leukaemia and lymphoma (C91.5) were obtained by applying proportions of these subtypes within the wider three-digit ICD-10 code based on Cancer Incidence in Five Continents Volumes 10–12 registry data—supplemented by the African Cancer Registry Network—to the wider cancer type group in GLOBOCAN (appendix pp 3, 8). This approach was newly expanded for specific subtypes of lymphoma (diffuse large B-cell lymphoma, extranodal natural killer cell or T-cell lymphoma, and primary effusion lymphoma).
Statistical analysis
For each infection–cancer pair, we calculated the number of attributable cases independent of other infectious agents by multiplying cancer-specific PAFs (appendix pp 2–6) by the number of new cancer cases in 2024, stratified by country, sex, and age group. Overall PAFs for infectious agents, both individually and combined, were calculated by summing attributable cases and dividing by all new cancer cases. ASIRs of infection-attributable cancers per 100 000 person-years were calculated using the Segi–Doll 1966 World Standard. We aggregated data by 14 UN geographical subregions and further grouped them into nine regions and four World Bank country income groups for 2022. Numbers of cancer cases are reported to two significant figures.
Uncertainty intervals were not estimated for cases, ASIR, or PAF because we did not identify a reliable approach to adequately incorporate the heterogeneity of data sources and methods underlying the cancer incidence and PAF estimates.
All analyses were done with R (version 4.3.2).
Role of the funding source
There was no funding source for this study.
Results
Table 1 shows the total number of new cases and PAFs of cancers attributable to infection globally in 2024 by cancer type. Table 2 presents the number, PAF, and ASIR of infection-attributable cancer cases broken down by infectious agent, UN geographical subregion, and income group. Globally, an estimated 2·3 million new cancer cases were attributable to infections in 2024, which was equivalent to a PAF of 12% of all cancer cases. The largest number of cases was attributable to H pylori (n=760 000; PAF 4%), followed by HPV (n=750 000, 4%), HBV (n=360 000, 2%), EBV (n=260 000, 1%), HCV (n=160 000, <1%), and KSHV (n=35 000, <1%). Other infections, including HTLV-1, MCV, HIV (counting conjunctiva cancer only so that other cancers due to HPV, EBV, or KSHV are not counted twice), and three parasites, were responsible for 19 000 cancer cases. The ASIR for all infections combined was 22·7 cancer cases per 100 000 person-years. HPV had the highest ASIR for infection-attributable cases (7·7), followed by H pylori (6·9), HBV (3·4), EBV (2·6), HCV (1·5), and KSHV (0·4).
Table 2.
ASIR per 100 000 person-years, number of cases, and PAFs of cancers attributable to infection in 2024 by infectious agent, UN geographical subregion, and World Bank income group
| Helicobacter pylori |
Human papillomavirus |
Hepatitis B virus |
Epstein–Barr virus |
Hepatitis C virus |
Kaposi's sarcoma-associated herpesvirus |
All infectious agents |
||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ASIR | Number of attributable cases | PAF | ||
| Global | 6·9 | 760 000 | 4% | 7·7 | 750 000 | 4% | 3·4 | 360 000 | 2% | 2·6 | 260 000 | 1% | 1·5 | 160 000 | <1% | 0·4 | 35 000 | <1% | 22·7 | 2 300 000 | 12% | |
| Asia | ||||||||||||||||||||||
| Eastern Asia | 11·9 | 410 000 | 6% | 6·8 | 180 000 | 3% | 8·4 | 260 000 | 4% | 3·4 | 98 000 | 2% | 1·2 | 42 000 | <1% | 0·0 | 560 | <1% | 31·9 | 990 000 | 15% | |
| South-central Asia | 3·9 | 82 000 | 4% | 6·3 | 130 000 | 6% | 0·7 | 15 000 | <1% | 1·7 | 36 000 | 2% | 0·6 | 13 000 | <1% | 0·0 | 440 | <1% | 13·3 | 280 000 | 12% | |
| Southeastern Asia | 3·6 | 29 000 | 3% | 8·6 | 70 000 | 6% | 4·9 | 40 000 | 3% | 4·2 | 34 000 | 3% | 1·5 | 12 000 | 1% | 0·0 | 340 | <1% | 23·1 | 190 000 | 16% | |
| Western Asia | 5·8 | 16 000 | 3% | 2·6 | 7700 | 2% | 1·1 | 3000 | <1% | 3·0 | 9100 | 2% | 1·2 | 3500 | <1% | 0·3 | 990 | <1% | 14·1 | 41 000 | 9% | |
| Africa | ||||||||||||||||||||||
| Northern Africa | 3·2 | 7700 | 2% | 3·6 | 8700 | 3% | 1·0 | 2300 | <1% | 3·5 | 9000 | 3% | 9·3 | 22 000 | 7% | 0·2 | 490 | <1% | 21·8 | 53 000 | 16% | |
| Sub-Saharan Africa | 3·1 | 21 000 | 2% | 16·6 | 130 000 | 14% | 2·8 | 21 000 | 2% | 1·8 | 16 000 | 2% | 1·0 | 7500 | <1% | 2·2 | 22 000 | 3% | 28·5 | 220 000 | 25% | |
| Europe | ||||||||||||||||||||||
| Central and eastern Europe | 9·2 | 54 000 | 4% | 10·5 | 46 000 | 4% | 0·8 | 4600 | <1% | 2·2 | 9800 | <1% | 1·5 | 8200 | <1% | 0·1 | 740 | <1% | 24·3 | 120 000 | 10% | |
| Northern Europe | 2·9 | 7500 | 1% | 7·2 | 12 000 | 2% | 0·4 | 1100 | <1% | 2·1 | 3800 | <1% | 1·1 | 2800 | <1% | 0·2 | 340 | <1% | 14·1 | 28 000 | 4% | |
| Southern Europe | 5·8 | 24 000 | 3% | 5·3 | 15 000 | 2% | 1·0 | 4100 | <1% | 2·6 | 6700 | <1% | 2·9 | 11 000 | 1% | 0·5 | 1600 | <1% | 18·2 | 63 000 | 7% | |
| Western Europe | 3·7 | 18 000 | 1% | 6·8 | 24 000 | 2% | 0·8 | 4000 | <1% | 2·1 | 7300 | <1% | 1·4 | 7200 | <1% | 0·1 | 500 | <1% | 15·0 | 62 000 | 5% | |
| America | ||||||||||||||||||||||
| Caribbean and Central America | 5·9 | 16 000 | 4% | 9·3 | 24 000 | 6% | 0·3 | 740 | <1% | 2·0 | 5100 | 1% | 0·9 | 2400 | <1% | 0·5 | 1200 | <1% | 19·2 | 50 000 | 13% | |
| North America | 2·8 | 21 000 | <1% | 7·6 | 47 000 | 2% | 0·6 | 4400 | <1% | 2·1 | 13 000 | <1% | 2·2 | 18 000 | <1% | 0·2 | 1200 | <1% | 15·8 | 110 000 | 5% | |
| South America | 8·3 | 51 000 | 5% | 9·9 | 55 000 | 5% | 0·3 | 1900 | <1% | 2·1 | 12 000 | 1% | 1·1 | 6900 | <1% | 0·7 | 4100 | <1% | 22·4 | 130 000 | 12% | |
| Oceania | 3·0 | 2400 | 1% | 7·8 | 4700 | 2% | 0·9 | 580 | <1% | 2·5 | 1500 | <1% | 2·3 | 1600 | <1% | 0·1 | <100 | <1% | 16·7 | 11 000 | 5% | |
| World Bank income group | ||||||||||||||||||||||
| Low income | 4·6 | 19 000 | 3% | 13·9 | 65 000 | 12% | 3·6 | 16 000 | 3% | 2·2 | 12 000 | 2% | 1·6 | 6800 | 1% | 2·3 | 14 000 | 3% | 29·1 | 140 000 | 25% | |
| Lower-middle income | 4·1 | 120 000 | 4% | 7·4 | 230 000 | 6% | 1·5 | 46 000 | 1% | 2·0 | 62 000 | 2% | 1·5 | 44 000 | 1% | 0·2 | 7100 | <1% | 16·9 | 520 000 | 15% | |
| Upper-middle income | 8·1 | 380 000 | 5% | 7·9 | 310 000 | 4% | 5·9 | 260 000 | 3% | 3·2 | 130 000 | 2% | 0·9 | 40 000 | <1% | 0·2 | 8800 | <1% | 26·4 | 1 100 000 | 14% | |
| High income | 7·8 | 240 000 | 3% | 6·6 | 140 000 | 2% | 1·1 | 33 000 | <1% | 2·6 | 57 000 | <1% | 2·3 | 67 000 | <1% | 0·2 | 4300 | <1% | 20·8 | 540 000 | 8% | |
The numbers of cases have been rounded to two significant figures. Total cases therefore might not equal sums due to rounding. ASIR=age-standardised incidence rate. PAF=population-attributable fraction.
Cases attributable to H pylori were mostly non-cardia gastric cancer (700 000 cases, cancer-specific PAF 85%; table 1). HPV-attributable cases were predominantly cervix uteri carcinoma (600 000, 100% of cervical cancer cases). Hepatocellular carcinoma made up most of HBV-attributable (330 000) and HCV-attributable (130 000) cancer cases, with cancer-specific PAFs of 52% for HBV and 20% for HCV. For EBV, nasopharyngeal cancers (110 000, 88%) were the main driver. Kaposi's sarcoma (34 000, 100%) made up most KSHV-attributable cancer cases. All 3900 cases of adult T-cell leukaemia and lymphoma were attributable to HTLV-1. An estimated 5900 cases of squamous cell carcinoma of the bladder were attributable to S haematobium (33%) and 3800 cases of intrahepatic cholangiocarcinoma were attributable to O viverrini and C sinensis (2%). Of HIV-attributable cancers, 2300 were squamous cell carcinoma of the conjunctiva (34%) and the remaining 79 000 were cancer types already accounted for in our approach due to coinfection with HPV, EBV, or KSHV.
Table 1.
Numbers of all new cases of infection-attributable cancer in 2024, by infectious agent, cancer type, and sex
|
Males |
Females |
Total |
||||||
|---|---|---|---|---|---|---|---|---|
| All new cases | New cases attributable to infectious agents | All new cases | New cases attributable to infectious agents | All new cases | New cases attributable to infectious agents | PAF | ||
| Helicobacter pylori | .. | .. | .. | .. | .. | .. | .. | |
| Non-cardia gastric cancer* | 520 000 | 450 000 | 300 000 | 260 000 | 830 000 | 700 000 | 85% | |
| Cardia gastric cancer* | 110 000 | 32 000 | 41 000 | 10 000 | 150 000 | 42 000 | 27% | |
| Non-Hodgkin lymphoma of gastric location† | 13 000 | 9900 | 11 000 | 8000 | 24 000 | 18 000 | 74% | |
| Human papillomavirus | .. | .. | .. | .. | .. | .. | .. | |
| Cervix uteri carcinoma† | NA | NA | 600 000 | 600 000 | 600 000 | 600 000 | 100% | |
| Oropharynx, tonsils, and base of tongue* | 120 000 | 47 000 | 29 000 | 11 000 | 150 000 | 58 000 | 38% | |
| Anal squamous cell carcinoma† | 11 000 | 12 000 | 21 000 | 21 000 | 32 000 | 32 000 | 100% | |
| Penis† | 35 000 | 18 000 | NA | NA | 35 000 | 18 000 | 51% | |
| Vagina† | NA | NA | 18 000 | 14 000 | 18 000 | 14 000 | 78% | |
| Vulva† | NA | NA | 49 000 | 12 000 | 49 000 | 12 000 | 25% | |
| Oral cavity† | 260 000 | 5000 | 110 000 | 2500 | 370 000 | 7500 | 2% | |
| Larynx† | 170 000 | 3800 | 24 000 | 560 | 190 000 | 4400 | 2% | |
| Hepatitis B virus | .. | .. | .. | .. | .. | .. | .. | |
| Hepatocellular carcinoma* | 470 000 | 250 000 | 170 000 | 84 000 | 640 000 | 330 000 | 52% | |
| Intrahepatic cholangiocarcinoma‡ | 87 000 | 16 000 | 72 000 | 12 000 | 160 000 | 27 000 | 17% | |
| Epstein-Barr virus | .. | .. | .. | .. | .. | .. | .. | |
| Nasopharynx† | 85 000 | 75 000 | 35 000 | 31 000 | 120 000 | 110 000 | 88% | |
| Gastric§ | 640 000 | 65 000 | 340 000 | 13 000 | 980 000 | 78 000 | 8% | |
| Hodgkin lymphoma* | 49 000 | 28 000 | 35 000 | 19 000 | 84 000 | 47 000 | 56% | |
| Diffuse large B-cell lymphoma§ | 100 000 | 11 000 | 80 000 | 8800 | 180 000 | 20 000 | 11% | |
| Burkitt lymphoma* | 8200 | 4100 | 3900 | 2100 | 12 000 | 6200 | 51% | |
| Extranodal natural killer cell or T cell lymphoma (nasal type)§ | 2500 | 2400 | 1300 | 1300 | 3800 | 3600 | 96% | |
| Hepatitis C virus | ||||||||
| Hepatocellular carcinoma* | 470 000 | 94 000 | 170 000 | 36 000 | 640 000 | 130 000 | 20% | |
| Non-Hodgkin lymphoma† | 300 000 | 9700 | 230 000 | 7600 | 530 000 | 17 000 | 3% | |
| Intrahepatic cholangiocarcinoma‡ | 87 000 | 5800 | 72 000 | 5100 | 160 000 | 11 000 | 7% | |
| Kaposi's sarcoma-associated herpesvirus | ||||||||
| Kaposi's sarcoma† | 25 000 | 25 000 | 9400 | 9400 | 34 000 | 34 000 | 100% | |
| Primary effusion lymphoma§ | 290 | 290 | 160 | 160 | 450 | 450 | 100% | |
| Schistosoma haematobium | .. | .. | .. | .. | .. | .. | .. | |
| Bladder squamous cell carcinoma† | 10 000 | 2900 | 7700 | 3000 | 18 000 | 5900 | 33% | |
| Human T-cell lymphotropic virus type 1 | ||||||||
| Adult T-cell leukaemia and lymphoma† | 2100 | 2100 | 1900 | 1900 | 3900 | 3900 | 100% | |
| Opisthorchis viverrini and Clonorchis sinensis | .. | .. | .. | .. | .. | .. | .. | |
| Intrahepatic cholangiocarcinoma† | 87 000 | 2400 | 72 000 | 1400 | 160 000 | 3800 | 2% | |
| Merkel cell polyomavirus | .. | .. | .. | .. | .. | .. | .. | |
| Merkel cell carcinoma§ | 2600 | 1800 | 1900 | 1300 | 4600 | 3200 | 70% | |
| HIV | .. | .. | .. | .. | .. | .. | .. | |
| Squamous cell carcinoma of the conjunctiva§ | 3000 | 880 | 3700 | 1400 | 6700 | 2300 | 34% | |
| Other cancer types§¶ | 420 000 | 30 000 | 1 000 000 | 49 000 | 1 400 000 | 79 000 | 6% | |
| All cancer types related to infection | .. | 1 200 000 | .. | 1 200 000 | .. | 2 300 000 | 12% | |
The numbers of cases have been rounded to two significant figures but total case numbers were calculated using unrounded numbers and total numbers therefore might not equal sums due to rounding. PAF=population-attributable fraction.
The infection–cancer pair for the PAF and burden calculation was addressed previously6 and the PAFs were derived from newly published methodology (appendix pp 2–6).
The infection–cancer pair for the PAF and burden calculation was addressed previously6 and the methodology remains unchanged.
The infection–cancer pair for the PAF and burden calculation was not addressed previously and methodology was developed specifically for this study (appendix pp 2–3, 7).
The infection–cancer pair for the PAF and burden calculation was not addressed previously and the PAFs were derived from newly published methodology (appendix pp 2–6).
Cervix uteri, vulva, vagina, penis, Kaposi's sarcoma, non-Hodgkin lymphoma, and Hodgkin lymphoma are also considered attributable to the above-mentioned carcinogenic agents and are not counted twice in the overall number of attributable cases.
ASIRs of infection-attributable cancer cases in 2024 per country for each infectious agent are shown in figure 1, with all infectious agents combined presented in the appendix (p 17). The largest number of infection-attributable cancer cases was in eastern Asia with 990 000 cases (42% of global total), equating to a PAF of 15% and an ASIR of 31·9 per 100 000 person-years in the region (table 2). PAFs and ASIRs were also higher than the global average (PAF 12%, ASIR 22·7) in sub-Saharan Africa (25%, 28·5), central and eastern Europe (10%, 24·3), and southeastern Asia (16%, 23·1). Regions with the lowest ASIRs were western Asia (14·1), northern Europe (14·1), western Europe (15·0), south-central Asia (13·3), and northern America (15·8), whereas PAFs were lowest in northern Europe (4%), western Europe (5%), North America (5%), Oceania (5%), and southern Europe (7%). Low-income and middle-income countries accounted for 77% of all infection-attributable cancer cases.
Figure 1.
ASIR of infection-attributable cancers per 100 000 person-years in 2024 for the six infectious agents with the most attributable cases
Number of cases displayed in parentheses. ASIR=age-standardised incidence rate.
The infection-attributable cancer burden in eastern Asia was largely driven by H pylori (410 000 cases, ASIR 11·9), and HBV (260 000 cases, 8·4; table 2). Within eastern Asia, Mongolia had consistently higher ASIRs than the regional average for HBV (33·3 vs 8·4), H pylori (26·8 vs 11·9), HCV (19·2 vs 1·2), HPV (8·0 vs 6·8), and EBV (4·1 vs 3·4; figure 1; table 2; appendix pp 9–16). For H pylori, the ASIRs in Japan (27·7) and South Korea (21·0) were also substantially higher than the regional average (11·9; table 2) and China had the highest number globally of cases of HBV (230 000) and H pylori-attributable cancer (260 000 cases; appendix pp 9–16).
Within south-central Asia, India had 77% of HPV-attributable cancer cases (100 000 cases; appendix pp 9–16), with a similar ASIR (6·8) to the regional average (6·3; table 2). In south-central Asia, infection-attributable cancer burden was also partly driven by H pylori (82 000 cases, ASIR 3·9). In southeastern Asia, burden was more evenly shared between HPV (ASIR 8·6), HBV (4·9), EBV (4·2), and H pylori (3·6).
Sub-Saharan Africa had the highest proportional burden of cancer attributable to HPV (PAF 14%), corresponding to an ASIR of 16·6 and based on 130 000 HPV-attributable cases (table 2). The region also had a substantial ASIR for KSHV (ASIR 2·2; 22 000 cases) compared with other regions (ASIRs for all other regions <0·7).
Within Europe, most of the infection-attributable cancer burden was due to H pylori (ASIRs from 2·9 in northern Europe [7500 cases] to 9·2 in central and eastern Europe [54 000 cases]) and HPV (ASIR from 5·3 in southern Europe [15 000 cases] to 10·5 in central and eastern Europe [46 000 cases]; table 2). Across the Americas, HPV and H pylori were also the main drivers of the infection-attributable cancer burden, with ASIRs for HPV ranging from 7·6 in North America (47 000 cases) to 9·9 in South America (55 000 cases), and for H pylori ranging from 2·8 in northern America (21 000 cases) to 8·3 in South America (51 000 cases). The ASIR for HCV-attributable cancer was higher in North America (2·2; 18 000 cases) than other regions in the Americas and higher than the global average. In Oceania, HPV was the main driver of infection-attributable cancer (7·8; 4700 cases; table 2), with higher ASIRs in Fiji (20·2) and Papua New Guinea (17·7) compared with New Zealand (5·0) and Australia (6·3; appendix pp 9–16).
Infection-attributable cancer burden in northern Africa was largely driven by HCV (ASIR 9·3; 22 000 cases, of which 21 000 were in Egypt; appendix pp 9–16) and in western Asia it was mainly driven by H pylori (5·8; 16 000 cases; table 2).
ASIRs of infection-attributable cancer cases by infectious agent, sex, and UN geographical subregion are shown in figure 2. For all infectious agents other than HPV, ASIRs were higher among males than females in all regions (figure 2). The ASIR of HPV-attributable cancer reached 30·8 in females compared with 0·9 in males in sub-Saharan Africa, whereas in North America, it was 9·5 in females compared with 5·9 in males.
Figure 2.
ASIR of infection-attributable cancers per 100 000 person-years in 2024 by infectious agent, UN geographical subregion, and sex
Data were aggregated by UN geographical subregion and further grouped into nine regions. ASIRs of cancer cases attributed to Helicobacter pylori (A), human papillomavirus (B), hepatitis B virus (C), Epstein–Barr virus (D), hepatitis C virus (E), and Kaposi's sarcoma-associated herpesvirus and other infectious agents (Schistosoma haematobium, human T-cell lymphotropic virus type 1, Opisthorchis viverrini, Clonorchis sinensis, Merkel cell polyomavirus, and HIV [F]). ASIR=age-standardised incidence rate.
We found the highest ASIR of EBV-attributable cancers in southeastern Asia (4·2), northern Africa (3·5), eastern Asia (3·4), and western Asia (3·0; table 2). The absolute and relative number of cancer cases attributable to EBV in 2024, according to UN geographical subregion and cancer type are shown in figure 3. For the distribution of the total EBV-attributable cancer burden, 65% of the burden was present in eastern Asia (98 000 cases [38%]), south-central Asia (36 000 cases [14%]), and southeastern Asia (34 000 cases [13%]; table 2, figure 3). Nasopharyngeal cancer accounted for 80% of all EBV-attributable cancer (27 000 of 34 000 cases) in southeastern Asia (figure 3), whereas in eastern Asia, nasopharyngeal (45 000 cases [46%]) and gastric cancers (43 000 cases [44%]) were almost equal drivers of EBV-attributable cancer (figure 3). Nasopharyngeal cancer was also the most common EBV-associated cancer type by attributable cases in south-central Asia and sub-Saharan Africa, with notable contributions of Hodgkin lymphoma and gastric cancer in south-central Asia and of Hodgkin lymphoma and Burkitt lymphoma in sub-Saharan Africa; in other world regions, gastric cancer and lymphomas (Hodgkin lymphoma and diffuse large B-cell lymphoma) were the most common EBV-attributable cancer types (figure 3).
Figure 3.
Absolute numbers and proportion of cancer cases attributable to EBV in 2024 by UN geographical subregion and cancer type
Data were aggregated by UN geographical subregion and further grouped into nine regions. EBV=Epstein–Barr virus.
Discussion
An estimated 2·3 million new cancer cases were attributable to infections globally in 2024. Low-income and middle-income countries harboured three-quarters of this burden, particularly those in eastern Asia, sub-Saharan Africa, and southeastern Asia. The main agents driving attributable cancer burden were H pylori, HPV, HBV, EBV, and HCV. However, each agent had distinct geographical patterns of attributable cancer incidence, with specific implications for infection control to reduce the burden of cancer.
H pylori remains a major cause of cancer globally. Although improved sanitation and reduced intrafamilial transmission correspond with observed declines in ASIRs of gastric cancer, numbers of H pylori-attributable gastric cancer cases are still projected to increase due to population ageing and growth,9 including in regions traditionally considered to have a low incidence (eg, sub-Saharan Africa).9 Most of the H pylori-attributable cancer cases and the highest ASIR were in eastern Asia. To tackle the local gastric cancer burden, Japan, South Korea, and China have implemented population-based gastric cancer screening programmes using endoscopy; in Japan, screening also includes barium meal.10 However, endoscopy is invasive and costly, limiting its broader applicability. Several countries in Europe are piloting H pylori screen-and-treat programmes.10 Global guidance on best practices for these population-based programmes has been developed for gastric cancer prevention, highlighting key considerations for implementation and urging greater global investment in prevention efforts.10 So far, there has been little progress in developing H pylori vaccines or highly effective H pylori therapies that can minimise ineffective antibiotic exposure, which would be highly impactful for controlling gastric cancer globally.
HPV is also a major infectious cause of cancer globally, especially impacting countries in sub-Saharan Africa, where the ASIR was more than double the global average. We considered 100% of cervical cancer to be attributable to HPV, of which 17 genotypes are classified as carcinogenic.11 However, the genotypes differ substantially in their carcinogenic potential and genotype-specific PAF: HPV16 and 18 alone account for nearly three-quarters of all cervical cancer cases globally and eight types (HPV16, 18, 31, 33, 35, 45, 52, and 58) account for 95%.11 Targeting high-risk HPV genotypes via vaccination and HPV testing in cervical screening are at the core of WHO's global strategy for cervical cancer elimination.12 Single-dose HPV vaccination programmes are expected to improve global HPV vaccine uptake, given their equivalent efficacy to two-dose or three-dose schedules13 and the availability of additional licensed HPV vaccines. However, greatly improved HPV vaccine coverage in low-income and middle-income countries is still needed if increasing inequalities in future cervical cancer burden are to be avoided.14 HPV-attributable cancers also occur in men, including oropharyngeal, anal, and penile cancer; thus gender-neutral vaccination is recommended in countries with sufficient resources.12 Men who have sex with men, in particular, do not benefit from herd immunity from female-only HPV vaccination and they, especially men who have sex with men living with HIV, are also among the groups at highest risk of HPV-related anal cancer15 and are at the highest priority for anal cancer screening.16 Lastly, blood-based markers are promising for early detection of HPV-related cancers, particularly oropharyngeal cancer.17
We estimated that the burden of hepatocellular carcinoma and intrahepatic cholangiocarcinoma attributable to HBV and HCV was highest in eastern Asia, southeastern Asia, and northern Africa, with Mongolia and Egypt particularly affected. To tackle the ongoing burden of viral hepatitis and liver cirrhosis,18 WHO launched an initiative to eliminate viral hepatitis,19 including objectives for scaling up neonatal HBV immunisation, promoting safe injection practices to prevent transmission, and improving access to testing and antiviral treatment for HBV and HCV,19 particularly for groups at high-risk.20 Of note, our analysis does not yet include hepatitis D virus (HDV), which was classified by the IARC Monographs programme as a Group 1 carcinogen in 2025, due to increased liver cancer risk in people co-infected with HBV.5 However, because HDV-attributable liver cancers are a subset of those attributable to HBV, they would not result in additional infection-attributable cancers in our approach, and prevention measures targeting HBV are expected to control the HDV-attributable cancer burden.
EBV ranked as the fourth highest infectious cause of cancer globally, ahead of HCV in attributable cases, constituting an important shift since our last global estimates.6 This change is due to the expanded evidence on the causal role of EBV in additional cancer sites, including some gastric cancers8 and specific non-Hodgkin lymphoma types other than Burkitt lymphoma.21 Although infection with EBV is almost ubiquitous in humans, the absolute burden and relative distribution of different EBV-related cancers vary considerably worldwide, which might suggest the influence of important co-factors, such as host genetics, environmental and dietary exposures, co-infection, and immunosuppression. The highest rates of EBV-attributable cancers are in southeastern Asia, comprising of mostly nasopharyngeal cancer, whereas gastric cancer and lymphomas are greater contributors in other regions. Some gastric adenocarcinomas are driven by EBV,8, 22 but it is unclear whether EBV acts independently, as assumed in our analysis, or acts in synergy with H pylori. As there are currently no efficient strategies to control infection, EBV should be considered an important target for investment in primary and secondary prevention. Several clinical trials on EBV vaccines are ongoing23 and testing blood for EBV antibodies and DNA is recommended to improve early detection and prognosis of nasopharyngeal cancer in high-incidence regions.24
To our knowledge, this is the first global analysis to incorporate HIV into overall estimates of cancer burden due to infections, integrating methodology published in the past year.7 HIV-attributable cancer burden is concentrated in southern and eastern Africa, where it is represented mainly by cervical cancer and Kaposi's sarcoma; in lower-burden settings, anal cancer and non-Hodgkin lymphoma are more prevalent.7 The 2025 WHO approval for global use of highly effective, long-acting, injectable pre-exposure prophylaxis holds great potential for primary prevention by reducing HIV transmission and HIV-attributable cancers if integrated into a comprehensive combination approach spanning condom promotion, HIV testing, and harm reduction services for people who inject drugs.25 Regarding secondary prevention, specific recommendations exist for cervical cancer screening for females with HIV,26 and people living with HIV are also primary targets for anal cancer screening.16 Yet, HIV prevention and control is at risk due to disinvestment of foreign aid funding over the past few years. Of note, because HIV increases the risk of cancers caused by other carcinogenic infections (ie, HPV, KSHV, and EBV) through immunosuppression, we did not count HIV in overall infection-related cancer estimates, except for conjunctiva cancer.27
Global prevention of Kaposi's sarcoma is also closely entwined with HIV control, being 71% co-attributable to HIV.7 An effective KSHV vaccine would be the ultimate solution to Kaposi's sarcoma prevention but has had little investment to date. Secondary prevention approaches for early detection of Kaposi's sarcoma are needed and are especially relevant in sub-Saharan Africa, which harbours most of the global burden. Regarding strategies to reduce the burden of cancer due to Schistosoma haematobium, which is primarily found in sub-Saharan Africa, available interventions include preventive chemotherapy with praziquantel—particularly through mass drug administration in endemic areas—combined with improved water, sanitation, and hygiene measures and snail-control strategies to reduce transmission.28
A major strength of our study is the incorporation of 16 additional infection–cancer type pairs beyond the 21 existing pairs in estimates for 2018, including those cancers caused by HIV and MCV,5 and an expanded set of cancer types caused by EBV, HBV, HCV, and KSHV. In line with other studies,29 we considered the causal associations between gastric cancer and EBV, and between intrahepatic cholangiocarcinoma and HBV and HCV, to have been well established since they were last evaluated by the IARC Monographs programme in 2009.4 We therefore believe we have addressed all cancer types with a strong epidemiological signature for having an underlying infectious cause.30 However, molecular epidemiological approaches for identifying bacterial and parasitic carcinogens are less well standardised than for viruses and the list of future infection–cancer pairs could include possible links between Plasmodium falciparum, which is the most common malaria parasite, and Burkitt lymphoma (currently IARC Monographs Group 2A).31
We updated previous PAF estimates for H pylori and gastric cancer,9 for HBV and HCV and hepatocellular carcinoma, for HPV and oropharyngeal cancer, and for EBV and Hodgkin lymphoma and Burkitt lymphoma,21 obtained from larger and more contemporary systematic analyses. HPV and oropharyngeal cancer PAF estimates were additionally improved by including the concept of p16-positivity as necessary to establish HPV causality. Estimates of EBV-attributable nasopharyngeal cancer burden were improved by accounting for regional variability in nasopharyngeal cancer incidence in China. In the absence of global PAF studies of HBV, HCV, and intrahepatic cholangiocarcinoma, we obtained prevalences from published meta-analyses. For specific subtypes of cancer not available in GLOBOCAN, we produced global burden estimates using the latest volume of the IARC Cancer Incidence in Five Continents (volume 12), which included many more population-based cancer registries (n=460) than previous volumes (343 in volume 11 and 290 in volume 10). Furthermore, for all cancer types, the latest GLOBOCAN estimates were used, which had higher coverage from cancer registries than previous releases,1 meaning that comparisons with previous results are not possible because of changes in data sources and data quality over time. The GLOBOCAN estimates used in this study are derived primarily from national data obtained from population-based cancer registries and vital registration systems wherever such data are available. Although these estimates rely on well established and validated modelling approaches, they remain constrained by substantial gaps in underlying data and representativeness, particularly in low-income settings. For instance, approximately 19% of the global population and only 2% of the population in Africa were covered by the high-quality population-based registries included in Cancer Incidence in Five Continents (volume 12). As our analyses rely on GLOBOCAN estimates, these limitations in coverage and data quality could lead to an underestimation or overestimation of the cancer burden attributable to infections, particularly in under-represented regions.
We must consider other limitations to our analysis. Firstly, we do not present burden by age because GLOBOCAN should not be considered robust at an age-specific level and we rarely had the necessary data on age-specific PAF, which we have shown can be higher in younger individuals (eg, HPV and vulva cancer6 or HIV and cervical or anal cancer).7 Similarly, we did not retrieve sex-specific PAFs from meta-analyses; instead, we applied the overall average PAF to both sexes, acknowledging that it might overlook sex-related differences. Also, in a few instances, odds ratios were used as approximations of relative risks, which is generally appropriate under the rare disease assumption in cancer epidemiology, especially when, as in our case, exposure is largely based on assessment from cancer cases and not population prevalence.32 Finally, we did not identify a method to reliably estimate uncertainty intervals given the diverse data sources and methodologies used to calculate global cancer burden and cancer-specific PAFs, instead favouring an approach that avoids the impression of precision.
It is also worth noting that the impact of these infectious agents extends to other non-cancer outcomes that could theoretically be avoidable through primary prevention of these agents. These conditions include liver cirrhosis for HBV and HCV;18 multiple sclerosis, mononucleosis, and systemic lupus erythematosus for EBV;23 and peptic ulcer, dyspepsia, and gastrointestinal bleeding for H pylori.33
To conclude, our findings underscore the importance of accelerating control of infectious agents to achieve cancer prevention goals. Although investment in the development of new preventive vaccinations for EBV, H pylori, and Kaposi's sarcoma is key, many prevention strategies are known to be cost-effective. Unfortunately, such strategies are often underused due to societal, financial, and political barriers, often in the settings that need them most. Global and local prevention efforts are thus a question of equity and should be considered in the promotion of universal prevention strategies. These efforts include key public health measures, such as vaccination for HPV and HBV; testing and treatment of H pylori, HIV, HBV, and HCV; safe injection practices; access to condoms and pre-exposure prophylaxis to prevent HIV transmission, and screening and treatment of precancerous lesions of HPV-driven cervical and anal cancer.
Contributors
Data sharing
The population-attributable fractions used in this study were collected from published meta-analyses, global studies, or were developed according to new methodology, as detailed in the appendix (pp 2–7). The cancer incidence data used in this study are available to the public from the Global Cancer Observatory and Cancer Incidence in Five Continents websites. All results from this study are available to the public through the dedicated cancers attributable to infections tool in the Global Cancer Observatory.
Declaration of interests
We declare no competing interests.
Acknowledgments
We thank all population-based cancer registries and their staff who have contributed to sharing the cancer incidence data used to build the estimates used in this study, including those of the African Cancer Registry Network. We also thank Murielle Colombet for processing the data used for subtype estimation, Jacques Ferlay and Max Parkin for providing incidence rates of Merkel cell carcinoma and squamous cell carcinoma of the conjunctiva, and Nadia Akel for proofreading and formatting the final manuscript. Where authors are identified as personnel of the International Agency for Research on Cancer and WHO, the authors alone are responsible for the views expressed in this Article and they do not necessarily represent the decisions, policy, or views of the International Agency for Research on Cancer and WHO. The designations used and the presentation of the material in this Article do not imply the expression of any opinion whatsoever on the part of WHO and the IARC about the legal status of any country, territory, city, or area, or of its authorities, or concerning the delimitation of its frontiers or boundaries.
Editorial note: The Lancet Group takes a neutral position with respect to territorial claims in published maps.
Acknowledgments
GMC conceived and designed the study. HR, DG, YH, MH, RS, CdM, JYP, IS, and GMC collected the data, analysed the data, or both. HR and DG accessed and verified the underlying data. All authors had full access to all the data in the study. HR and GMC drafted the manuscript. All authors contributed to the interpretation of data and approved the final manuscript.
Supplementary Material
References
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The population-attributable fractions used in this study were collected from published meta-analyses, global studies, or were developed according to new methodology, as detailed in the appendix (pp 2–7). The cancer incidence data used in this study are available to the public from the Global Cancer Observatory and Cancer Incidence in Five Continents websites. All results from this study are available to the public through the dedicated cancers attributable to infections tool in the Global Cancer Observatory.
