Effects of current smoking on treatment outcomes in metastatic and locally advanced pancreatic carcinoma: a retrospective cohort study using the international PURPLE pancreas cancer registry

Introduction

Tobacco smoking is identified as a contributing factor in over 16,000 cancer diagnoses in Australia every year, making it the primary preventable cause of cancer and accounting for 50% of preventable cancer-related deaths in the country (1). It is estimated that 21.7% of the future pancreatic cancer burden in Australia will be attributable to current and recent smoking (2). There is sufficient evidence to infer that smoking cessation reduces the risk of developing lung, head and neck, gastroesophageal, pancreatic, liver, colorectal, renal, and cervical cancers (3). Smoking also contributes to an increased symptom burden in patients undergoing chemotherapy or radiation therapy. Conversely, patients with cancer who quit smoking prior to commencing treatment have a total symptom burden similar to non-smokers (4). Metastatic pancreatic cancer carries a poor prognosis with a median survival of less than 12 months and is the third leading cause of cancer-related deaths in Australia despite accounting for only 3% of all new cancer cases (5).

In a previous retrospective analysis of the Health Professionals Follow-Up Study and the Nurses’ Health Study, patients with pancreatic cancer at all stages who currently smoked had a 40% increased risk of death compared with non-smokers (6). A recent analysis has shown that patients undergoing neoadjuvant FOLFIRINOX (folinic acid, 5-fluorouracil, irinotecan, oxaliplatin) for pancreatic cancer had worse survival outcomes with continued smoking (7). On the contrary, a retrospective analysis from Princess Margaret Cancer Centre, smoking status and pack-years were not significantly associated with stage at diagnosis or overall survival (OS) in all stages of pancreatic cancer patients, even after adjusting for key clinical variables (8). Another retrospective analysis found no statistically significant difference between current smokers and non-smokers with metastatic pancreatic cancer receiving chemotherapy, though a trend towards worse outcomes in younger smokers was observed (9). These findings suggest that in aggressive, late-stage disease, the prognostic impact of smoking may be diminished by the overwhelming effect of tumour biology and disease burden (10). The conflicting evidence may be attributable to the heterogeneity in study populations, limitations of smoking data collection, variable adjustment for confounding factors, and methodological limitations such as retrospective design, missing data, and reliance on self-reported smoking behaviour. Given these uncertainties, there remains no clear consensus on whether continued smoking independently influences survival outcomes in advanced pancreatic carcinoma.

The emphasis on smoking cessation in oncology clinics is sub-optimal overall (11), with data suggesting that more than one-third of patients do not receive any smoking cessation counselling (12) and the majority of those who do receive counselling continue to smoke (13).

The aim of our research was to compare the impact of current smoking at the time of diagnosis of metastatic or locally advanced pancreatic cancer on OS, cancer-specific survival (CSS), and progression-free survival (PFS) on first-line palliative systemic treatment. We hypothesized that current smoking is associated with poorer outcomes in locally advanced or metastatic pancreatic carcinoma. By demonstrating an association between continued smoking and worse treatment outcomes, we may develop more effective strategies for discussing smoking cessation with newly diagnosed pancreatic cancer patients. The data may also be informative in directing health services resources to smoking cessation support. We present this article in accordance with the STROBE reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2025-186/rc).

Methods

This retrospective cohort study utilized prospectively collected data from the Pancreatic Cancer: Understanding Routine Practice & Lifting End Results (PURPLE) Translational Registry, a web-based database that records longitudinal information on consecutive patients with pancreatic cancer across more than 27 cancer centres in Australasia and Singapore. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of all participating hospitals (HREC/16/MH/216), with overarching ethics approval from the Melbourne Health Human Research Ethics Committee (EC00243, approval No. 2016.200). Individual consent for this retrospective analysis was waived.

Eligible patients were adults (aged 18 years or older) diagnosed with locally advanced or metastatic pancreatic carcinoma, who were enrolled in the registry between 2015 and June 2022. Inclusion criteria required both documentation of smoking status at the time of registry enrolment and receipt of palliative systemic therapy. Patients were excluded if they were managed with curative intent or if their smoking status was not recorded at enrolment. All eligibility criteria were applied prior to data analysis to ensure a well-defined study cohort.

Smoking status was classified at diagnosis, based on data collected at enrolment into the registry. Current smokers were defined as patients actively smoking at diagnosis, while non-smokers included both ex-smokers and never smokers as determined by the treating clinician at the initial oncology consultation. Baseline covariates were recorded at registry enrolment and included age, sex, comorbidity as measured by the Charlson index, disease stage (locally advanced or metastatic), socioeconomic status [measured by the Index of Relative Socio-Economic Advantage and Disadvantage (IRSAD)], presence of liver metastases, number of metastatic sites, and hospital location (metropolitan or regional).

The primary outcome was OS, defined as the time from diagnosis to death from any cause. Secondary outcomes included CSS (from diagnosis to death due to pancreatic cancer) and PFS (from diagnosis to disease progression or death). Patients were censored at the date of last recorded follow-up if alive and without disease progression. Survival outcomes and key clinical events were derived from prospectively updated registry data and clinical record review. The median duration of follow-up is reported in the Results.

Statistical analysis

Patients with missing smoking status or incomplete baseline data required for propensity modelling were excluded from the primary analysis. To account for potential bias due to missing data and confounding, inverse probability of treatment weighting (IPTW) using propensity scores was applied. Logistic regression models were used to generate propensity scores, with predictor variables including age, sex, disease stage, Charlson comorbidity index, IRSAD score, presence of liver metastases, number of metastatic sites, and hospital location. Separate propensity models were constructed for both smoking status and missingness, and the combined inverse probability weights were used in the analysis. No multiple imputation was performed due to the high proportion of missingness for some variables. The number and proportion of patients excluded due to missing data are detailed in the Results section.

As this was a registry-based observational study, no formal sample size calculation was performed; all eligible consecutive patients during the study period were included to maximize generalizability and statistical power. Categorical variables were summarized as frequencies and percentages and compared using Chi-squared tests. Continuous variables were summarized as mean (standard deviation) or median (interquartile range) and compared using independent t-tests or Kruskal-Wallis tests, as appropriate. Survival outcomes were analysed using Cox proportional hazards regression. Three models were constructed: an unweighted complete-case analysis, an IPTW analysis, and a weighted analysis with further adjustment for predefined confounders. Hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated and compared using Wald tests, with a two-tailed P value of <0.05 considered statistically significant. All analyses were conducted using SAS v9.4.

Potential survival bias was considered, recognizing that patients with more aggressive disease or heavier smoking histories may have died before registry enrolment, and that surviving smokers may represent a healthier subgroup. This limitation was taken into account when interpreting the results. Further details on the PURPLE Translational Registry are available at https://purple.wehi.edu.au (ACTRN12617001474347).

Results

Between 2015 and 2022, a total of 1,454 patients with advanced pancreatic cancer were enrolled in the PURPLE Translational Registry. Of these, 1,047 patients (72%) had smoking status recorded and were included in the analysis; 407 patients (28%) were excluded due to missing smoking status. Among the included cohort, 202 patients (19.3%) were current smokers at diagnosis, while 845 (80.7%) were classified as non-smokers (including ex- and never smokers).

All patients in this analysis had locally advanced or metastatic disease and received palliative systemic chemotherapy as their primary treatment modality, in line with standard management for advanced pancreatic cancer. Detailed data on previous treatments, such as prior surgical resection, adjuvant therapies, or the use of radiotherapy before developing advanced disease, were not included in this analysis. Similarly, information on specific chemotherapy regimens administered in the advanced setting was not included as a confounding variable.

Clinical and demographic characteristics are summarized in Table 1. Compared to non-smokers, current smokers were more likely to be male (61% vs. 52%, P=0.047), present with liver metastases (57% vs. 48%, P=0.03), be diagnosed at a younger age (median 64 vs. 70 years, P<0.001), have a lower Charlson comorbidity index (P<0.001), and reside in areas with lower socioeconomic status as indicated by IRSAD score (P=0.001). The number of metastatic sites and lines of systemic treatment received were similar between groups.

Survival outcomes are detailed in Tables 2,3 and illustrated in Figures 1-3. In the fully adjusted, inverse probability-weighted model, there was no statistically significant difference in OS between current smokers and non-smokers (median OS 6.87 vs. 6.93 months; HR =0.92, 95% CI: 0.84–1.01, P=0.09). Similarly, there were no significant differences in CSS (HR =0.93, 95% CI: 0.85–1.02, P=0.13) or PFS (HR =0.98, 95% CI: 0.90–1.16, P=0.72) between the two groups. Adjusted survival curves for all three outcomes are shown in Figures 1-3 and demonstrate no significant separation between current smokers and non-smokers.

Figure 1 Progression-free survival (adjusted).

Figure 2 Overall survival (adjusted).

Figure 3 Cancer-specific survival (adjusted).

A summary of missing data for baseline covariates and missing smoking status is also provided in Table 1. As noted, patients with missing smoking status were excluded from the analysis. The proportion of missing data for included covariates was low and is unlikely to have affected the study results.

Discussion

Our study did not reveal any significant associations between current smoking and adverse treatment outcomes, such as reduced OS, CSS, or PFS, in patients with locally advanced or metastatic pancreatic cancer. We used three distinct models: an initial model that conducted a complete case analysis, a second model that employed inverse probability weighting to account for missing smoking status and balance confounders between smokers and non-smokers, and a third model that incorporated adjustments for potential confounding variables within the weighted model. All three models failed to identify any statistically significant survival disparities between current smokers and non-smokers.

Our results align with Dandona et al. (14), who found no discernible impact of smoking, obesity, family history of pancreatic cancer, and type 2 diabetes mellitus on OS in patients (n=355) with resectable pancreatic cancer undergoing pancreaticoduodenectomy. Similarly, two other studies also reported no impact of smoking on survival outcomes in pancreatic cancer patients (15,16). Park et al. (15) analysed data from Korean male Government employees and teachers who participated in a national health examination. Participants were classified as current, former or never smokers based on the response to a single baseline question of “do you smoke cigarettes now?”. Among 382 patients with all stages of pancreatic cancer, smoking was not associated with reduced OS. Similarly, Olson and colleagues (16) reported similar results with no negative association between smoking, obesity, family history, and diabetes and survival among 475 patients in a single institution with all stages of pancreatic cancer.

Potential mechanisms by which smoking may influence the pathogenesis of pancreatic cancer are (I) initiation and progression of KRAS-induced pancreatic cancers by nicotine (17); and (II) cancer acceleration via promotion of an immune suppressive myeloid-derived stem cell (MDSC) predominant tumour microenvironment that may be associated with poorer outcomes (18). However, in established malignancies with aggressive disease biology, like pancreatic cancer, smoking may not independently influence patient survival time. In contrast, in other malignancies with better prognoses, such as renal cell carcinoma and metastatic non-small cell lung carcinoma, ongoing smoking does negatively impact survival as reported by Kroeger et al. (19) and Wang et al. (20). Both studies showed that quitting smoking around the time of diagnosis was associated with improved outcomes.

It is important to note that our study did find an association between current smoking and the diagnosis of pancreatic cancer at a significantly younger age, consistent with the results of Brand et al. (21). With the rising incidence, mortality, and burden of disease related to pancreatic cancer globally (22), interventions that reduce the incidence of pancreatic cancer should be strongly encouraged. Our study also found that current smokers were more likely to be men and from areas with lower IRSAD scores, consistent with existing data on smoking disparities (23-25), highlighting the importance of improved smoking cessation education and access to resources in these groups.

To address bias in advanced pancreatic cancer, we employed IPTW but excluded carbohydrate antigen 19-9 (CA19-9) as a confounder due to high missing data. As an elevated CA19-9 level is associated with poor prognosis (26,27), its exclusion may have introduced confounding. As with all retrospective studies, unmeasured patient or tumour characteristics may also have influenced our results. Using the PURPLE translational registry, we aimed to reflect real-world outcomes, though limitations (28) such as missing data (e.g., smoking data for 28% of patients) and under-representation of regional patients were observed. Increased registry participation from regional centres (29) since our analysis should improve future data generalizability. Smoking histories were limited to a single, patient-reported dichotomous categorisation of current smokers versus non-smokers, without accounting for past smoking or recent quitters, who are prone to relapse (30,31). This may have impacted findings as self-reported smoking often diverges from biochemical verification (32,33). Notably, studies like Yuan et al. (6) report worse outcomes for biochemically-verified smokers diagnosed with pancreatic cancer, emphasizing the importance of accurate smoking data.

Another limitation of our study was the exclusion of 28% of patients from the registry due to missing smoking status, and while the inverse probability weighting was employed, it may have led to residual bias. Survival bias may have also influenced our findings, as patients with very high burden disease or the highest smoking exposure may have died before registry enrolment and thus were not captured in our analysis. Moreover, smokers in our cohort were diagnosed at a younger age, which may have made them more likely to receive or tolerate more intensive chemotherapy regimens, leading to treatment selection bias. Despite the results of this study, there is an ample body of evidence emphasizing the need for best-practice smoking cessation care in oncology practice (34). Data from the general population shows that smoking cessation has a positive impact on anxiety, depression, and health-related quality of life (35,36). We recommend that smoking cessation counselling is offered to all patients in oncology clinics, as it may improve their quality of life via multiple mechanisms (4,37), reduce comorbid illness (38) and the incidence of second malignancies (39,40). The Australian Care to Quit stepped wedge cluster randomised controlled clinical trial is testing a comprehensive implementation intervention at nine cancer centres with the aim of improving smoking cessation support and the 6-month abstinence rate among oncology outpatients with all tumour types (41).

Conclusions

In conclusion, this retrospective cohort study did not demonstrate worse survival outcomes for current smokers with locally advanced or metastatic pancreatic cancer, compared with non-smokers. Smoking cessation care remains recommended for all patients with cancer per international guidelines (42), with ongoing research efforts focussed on the most effective method of delivering this.

Acknowledgments

We would like to acknowledge A/Prof. James Lynam, Director of Medical Oncology at Calvary Mater Newcastle, NSW, Australia for supporting this work.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2025-186/rc

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2025-186/prf

Funding: This project was supported by the Medical Oncology Department of Calvary Mater Newcastle, NSW Australia and was completed as part of Fellowship of Royal Australasian College of Physicians research project.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2025-186/coif). R.Z. has received research grant of 50,000 AUD from Roche, BMS, and AstraZeneca to perform a clinical trial on IO education, consulting fees from Janssen, BMS and Merck, and travel support from Merck. These have no conflict with the work performed in this publication. Z.W.W. has received honoraria for speaking engagements from Bristol Myers Squibb and MSD. C.U. received consulting fees from Merck Serono and AstraZeneca, and declared that the consulting roles are not relevant to this manuscript. D.G. has received modest consulting fees (all < AUD 5,000) from MSD, Taiho, Boehringer Ingelheim, BioNTech, Panbela Therapeutics, and Duo Therapeutics, and serves on Data Safety Monitoring Boards for ANZUP, OMICO, Monash Trial, and one biotech company, and received a grant from Bayer for a clinical trial to the AGITG. F.D. declares serving on an advisory board for Amgen, speakers fees from AstraZeneca, travel support from Merck and AstraZeneca, and provision of investigational medical product for clinical trials from Bristol Myers Squibb and AstraZeneca. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional review board of all participating hospitals (HREC/16/MH/216), with overarching ethics approval from the Melbourne Health Human Research Ethics Committee (EC00243, approval 2016.200). Individual consent for this retrospective analysis was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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