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Association of lymphocyte-to-C-reactive protein ratio with all-cause and cause-specific mortality among US cancer survivors

European Journal of Medical Research volume 30, Article number: 312 (2025) Cite this article

Abstract

Background

Lymphocyte-to-C-reactive protein ratio (LCR) has been linked to survival in malignancies. However, most studies are from Asia. The knowledge about the link between LCR levels and risks of all-cause mortality and cause-specific mortality among cancer participants in the US is lacking.

Methods

Using multivariable Cox proportional hazards regression, we investigated the associations between LCR and mortalities in 1999 cancer participants from the National Health and Nutrition Examination Survey 1999–2008 with mortality follow-up through December 31, 2019.

Results

The median follow-up time was 156 months. Cancer participants with low LCR levels were associated with increased risks for all-cause and cancer mortality. Based on the full adjustment model, compared to the lowest LCR tertile, the hazard ratios and 95% confidence interval (HR, 95% CI) of all-cause mortality were 0.75 (0.66–0.87) in the second tertile, 0.60 (0.49–0.72) in the top tertile. The HR of cancer mortality was 0.71 (0.52–0.99) in the second tertile and 0.53 (0.35–0.79) in the top tertile. The link between LCR level and all-cause and cancer mortality remained significant when individuals who died within 2 years of follow-up were excluded.

Conclusions

This prospective study provided evidence of inverse associations between LCR levels and all-cause and cause-specific mortalities based on representative noninstitutional US cancer survivors. Integrating LCR assessment in the clinical routine of US cancer patients may aid in identifying cancer individuals at high risk of mortalities.

Introduction

Cancer is the second leading cause of death in the US and a serious public health problem globally [1]. Growing and ageing of the US population are projected to cause an increase of nearly 50% in cancer incident cases by 2050 [2]. Despite recent improvements in multidisciplinary approaches, there is still a poor prognosis for many cancer patients. Identifying more accurate, simple, and noninvasive screening markers associated with cancer prognosis is clinically valuable and could help improve prognosis prediction and individualised therapy.

Inflammation has been recognised as a cancer-enabling characteristic and a critical indicator of cancer progression [3]. It is crucial across different stages of cancer, from initiation through metastasis [4]. Inflammation response contributes to multiple hallmark capabilities of cancer. It fosters tumour progress since incipient neoplasias by supplying tumour microenvironments with bioactive molecules and chemicals, including reactive oxygen species, which accelerate tumour genetic evolution towards a heightened stage [4]. There is substantial interaction between local immune cell infiltration in the tumour microenvironment and the systemic inflammation responses, which contribute mutually to cancer development [5, 6]. The advantages of being noninvasive and easily detectable in the systemic circulation have given rise to intense investigation into the association between systemic inflammation response and malignancies.

A series of mediators of systemic inflammation, such as circulating immune cells, acute-phase proteins, and cytokines, or their combinations, particularly those reflecting innate inflammation response, has been developed and demonstrated independent prognostic or predictive power for cancer survival or treatment outcomes in multiple malignancies [7,8,9,10,11,12]. The lymphocyte-to-C-reactive protein ratio (LCR) is relatively less studied than the conventional ones among systemic inflammatory markers. LCR, combining lymphocyte counts and C-reactive protein (CRP), was newly developed for the first time to demonstrate a significant inverse link to disease-free survival and overall survival in gastric cancer by Okugawa et al. in 2019 [13]. Lymphocytes are crucial in the immune responses combating cancer in the circulation and in the tumour microenvironment [14]. A decreased lymphocyte count results in an insufficient and weak immunologic reaction to a tumour [15]. CRP, secreted by hepatocytes, may inhibit T effector cells directly and is associated with impaired outcomes of cancers as a surrogate marker of high interleukin-6 (IL-6) levels [16, 17]. LCR functions as a composite biomarker, integrating immune competence (via lymphocyte count) and inflammation-driven immunosuppression (via CRP levels). Decreased LCR has been suggested by increasing evidence to have predictive value for worse treatment outcomes and poorer survival in some solid malignancies as a novel systemic inflammation biomarker [18,19,20,21,22] and exhibited a superior power linking to cancer survival than other systemic inflammation-related parameters [18, 23,24,25]. These significant associations may arise mechanically from the fact that reduced LCR levels could reflect both inadequate antitumour immune responses and elevated systemic inflammatory state that potentially facilitates disease progression and is indicative of worse prognosis. However, most of the included patients come from Asia, especially Japan, and most studies were retrospectively designed and lacked detailed information on the causes of death. A lack of knowledge exists regarding the associations between LCR levels and risks of all-cause mortality and cause-specific mortality in the US cancer populations.

Herein, we examined prospectively the relationship between LCR levels and risks for all-cause, cancer, cardiovascular disease (CVD) mortalities based on a nationally representative noninstitutionalised US cancer population from five 2-year cycles of the National Health and Nutrition Examination Survey (NHANES) 1999–2008 linked to National Death Index (NDI) for 2019.

Materials and methods

Study population

This study used the NHANES data set of 1999–2000, 2001–2002, 2003–2004, 2005–2006, and 2007–2008 cycles. The NHANES data set includes a nationally representative sample of noninstitutionalised US civilians with an intricate, multistage, stratified, clustered probability design (https://www.cdc.gov/nchs/index.htm). The National Center for Health Statistics Research Ethics Review Board approved the NHANES and waived the informed consent for public data use. Upon enrollment, each participant provided written consent without receiving any compensation or incentive. The survey includes interviews and physical evaluations. The former occurs at the participant’s home, while the latter is conducted at mobile examination centres (MECs) travelling throughout the country. At recruitment, trained interviewers administered and collected standardised questionnaires on socioeconomic and demographic characteristics, health-related behaviours, and health conditions from study participants. Mobile examination centres provide physical measurements and lab tests by trained medical professionals. NHANES study procedures are described in more detail elsewhere. (https://www.cdc.gov/nchs/nhanes/index.htm) The cross-sectional study reporting was guided by STROBE (Strengthening the Reporting of Observational Studies in Epidemiology).

As shown in Fig. 1, 54,120 people participated in the NHANES (1999–2008). Mortality status was followed up until December 31, 2019. Adults eligible for the self-reported physician diagnosis cancer questionnaires were first enrolled [26]. 1999 cancer participants were enrolled in the final analysis after excluding those without CRP or circulating blood cell test results, those who were ineligible for mortality follow-up, and those who denied cancer or malignancy.

Fig. 1
figure 1

Study flow chart. NHANES, National Health and Nutrition Examination Survey

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Ascertainment of cancer

All participants in this study had a confirmed history of cancer at their enrollment in NHANES. The cancer ascertainment relied on self-reported data from NHANES medical condition questionnaires. Participants were asked at home via the Computer-Assisted Personal Interview system if a doctor or health professional had ever told them they had cancer or a malignancy. Those who answered “yes” were classified as cancer survivors and subsequently asked about the type of cancer and their age at initial diagnosis [27].

Laboratory measurements

Detailed descriptions of laboratory methods can be found at (https://wwwn.cdc.gov/nchs/nhanes/analyticguidelines.aspx). Blood samples were processed and stored under suitable conditions (−20 °C) until they were sent for testing. Lymphocyte counts were measured in the mobile examination centres with the Beckman Coulter MAXM haematology flow cytometer (Beckman Coulter, Fullerton, CA, USA) as part of a complete blood count. Latex-enhanced nephelometry on a Behring Nephelometer was used to quantify CRP. LCR was calculated by dividing lymphocyte count (1000 cells per microliter) by CRP level (milligrams per deciliter).

Ascertainment of mortality

The public-use linked mortality file (LMF) provides the mortality follow-up data through December 31, 2019, including mortality status and underlying causes of death. Death causes were coded according to the 10th International Classification of Diseases (ICD-10). The mortality outcomes included all-cause mortality referring to death from any cause, cancer mortality (codes C00–C97), and CVD mortality (codes I00–I09, I11, I13, I20–I51, and I60–I69).

Assessment of covariates

Demographic information and lifestyle factors, including age, sex, race/ethnicity, education level, family income-to-poverty ratio, and smoking history, were collected by the household interview. Age was referred to the participant’s age at NHANES enrollment. Race/ethnicity category consisted of Mexican American, other Hispanic, non-Hispanic White, non-Hispanic Black, and other races. A non-smoker is one who has never smoked or smoked less than 100 cigarettes in their lives [28, 29]. Body mass index (BMI) was calculated in the Mobile Examination Centre. Coronary heart disease (CHD) was diagnosed in the medical conditions section by the question, “Has a doctor or other health professional ever told you that you had coronary heart disease?” The interval since the first cancer diagnosis was calculated as the difference between the age at NHANES enrollment and the age at first cancer diagnosis [27]. Diabetes was defined according to the ADA’s diabetes diagnostic criteria: self-reported diagnosis, use of oral hypoglycemic medication, fasting blood glycose ≥ 126 mg/dL, or HbA1c ≥ 6.5% [30].

Statistical analysis

Due to the NHANES’ complex sampling design, the analysis in this study used the sampling weights for interviews (WTMEC2YR) and variables (SDMVPSU, SDMVSTRA) involved in the study design to obtain the appropriate weights (https://wwwn.cdc.gov/nchs/nhanes/tutorials/weighting.aspx). Baseline characteristics were divided into groups by LCR tertiles. The continuous variables were reported as the survey-weighted mean (SE); the categorical variables were reported as survey-weighted percentage [95% confidence intervals (CIs)]. We used the Kaplan–Meier curves to demonstrate the all-cause mortality. The competing risk models were employed to show the cumulative incidence functions (CIF) for cancer-specific and CVD-specific mortalities by LCR tertiles, with the competing risk category referred to as non-cancer mortality or non-CVD mortality, respectively. Multivariable Cox proportional hazards regression models were utilised to compute hazard ratios (HRs) and 95% CIs for the links between LCR tertiles and all-cause, cancer, and CVD mortality risks. Duration of follow-up was defined as the interval from the examination date of NHANES to the date of death or the end of follow-up (December 31, 2019) [27]. There were two multivariable models. Model 1 adjusted for age (continuous of years), sex (male or female), and race/ethnicity (Mexican American, other Hispanic, non-Hispanic Black, non-Hispanic White, or other races including multiracial). Model 2 additionally adjusted for educational level (12th grade or less, high school graduate, or some college or more), the family ratio of income to poverty (≤1.0, 1.1–3.0, >3.0), BMI (≤25.0, 25.1–30.0, >30.0), smoking history and CHD. Restricted cubic spline analysis examined the nonlinear associations between LCR and mortality with full adjustment for covariates in model 2. The likelihood ratio test was employed to test for nonlinearity. The LCR–mortality link was further explored using the stratified analyses by age (<60, ≥60), sex, race (non-Hispanic White, others), BMI (≤30, >30), smoking history (yes or no), and CHD (yes or no). A P value for the production terms estimated the interaction significance between LCR tertiles and stratified factors. The following sensitivity analyses were conducted: (1) we repeated the primary analyses according to the LCR quartiles. (2) Chronic bronchitis status was additionally adjusted. (3) The interval since the first cancer diagnosis was additionally adjusted. (4) Both diabetes and the interval since the first cancer diagnosis were additionally adjusted. (5) The impact of different LCR levels on cancer mortality and CVD mortality was investigated using competing risk models multiply adjusted for the covariates of model 2. R software version 4.4 (The R Foundation; http://www.R-project.org) and EmpowerStats (X&Y Solutions, Inc.; http://www.empowerstats.com) were used for statistical analysis. A significant difference was defined as P < 0.05 (two-sided).

Results

Baseline characteristics

Among the 1999 cancer participants in the final analysis, a median follow-up time of 156 months (interquartile range: 111.0–192.0) led to the identification of 1074 all-cause deaths, 307 cancer deaths, and 298 CVD deaths.

In Table 1, the baseline characteristics of cancer participants are presented by LCR tertiles. The mean (SE) age of all included participants was 61.5 (0.5) years; 953 (weighted 40.7%) were men. Cancer participants with higher levels of LCR tended to be younger, non-Hispanic white, with higher family income-to-poverty ratio, and less likely to be overweight/obese or have CHD.

Table 1 Cancer participants’ characteristics by LCR tertiles of NHANES 1999–2008
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LCR and mortality

Figure 2 illustrates the associations between LCR on a continuous scale and mortality. For all-cause mortality and cancer mortality, an L-shaped correlation was observed.

Fig. 2
figure 2

Associations of LCR on a continuous scale with mortalities. Restrict cubic spline analyses of A all-cause mortality, B cancer mortality, and C CVD mortality according to LCR levels on a continuous scale. Solid blue lines represent multivariate-adjusted hazard ratios and light-blue areas demonstrate the 95% confidence intervals; knots were placed at the 5th, 35th, 65th, and 95th percentiles. Adjusted for age, sex, race and ethnicity, educational level (12th grade or less, high school graduate, some college or more), family ratio of income to poverty (≤1.0, 1.1–3.0, >3.0), BMI (≤25.0, 25.1–30.0, >30), smoking history, and coronary heart disease

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Multiple adjusted Kaplan–Meier curves for all-cause mortality and the competing risk models estimating the CIF for cancer and CVD mortality are shown in Fig. 3. Table 2 summarises the Cox proportional hazard model results based on LCR tertiles. Based on multivariable adjustment, Cox proportional hazards analysis revealed that higher LCR tertiles were significantly linked to lower all-cause mortality and cancer mortality. In model 2, compared to the reference group (the lowest tertile), the HR (95% CI) for all-cause mortality was 0.75 (0.66–0.87) in the second tertile, 0.60 (0.49–0.72) in the top tertile. Similarly, compared to the reference group, the HR (95% CI) for cancer mortality was 0.71 (0.52–0.99) in the second tertile and 0.53 (0.35–0.79) in the top tertile. The link between LCR levels and CVD mortality was not significant, with multivariable-adjusted HRs (95% CI) across three tertiles of LCR levels were 1.0 (reference), 0.85 (0.61–1.18), and 0.80 (0.55–1.15).

Fig. 3
figure 3

Survival and cumulative incidence curves stratified by LCR levels. A Kaplan–Meier curves for all-cause mortality across LCR tertiles; B cumulative incidence curves for cancer-specific mortality stratified by LCR tertiles with the competing risk category referred to as non-cancer death; C cumulative incidence curves for CVD-specific mortality stratified by LCR tertiles with the competing risk category referred to non-CVD death. Adjusted for age, sex, race and ethnicity, educational level (12th grade or less, high school graduate, some college or more), family ratio of income to poverty (≤1.0, 1.1–3.0, >3.0), BMI (≤25.0, 25.1–30.0, >30), smoking history, and coronary heart disease

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Table 2 Cox regression of all-cause, cancer, and CVD mortality by LCR tertiles among cancer participants in NHANES 1999–2008
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We also investigate whether LCR levels are related to relative long-term outcomes. After excluding participants who died within the first 2 years (N = 133), we found that the top tertile of LCR was still significantly associated with lower all-cause and cancer mortality. The HR (95% CI) in model 2 across three tertiles of LCR levels was 1.0 (reference), 0.80 (0.69–0.93), and 0.61 (0.50–0.74) for all-cause mortality, and was 1.0 (reference), 0.90 (0.64–1.26), and 0.64 (0.42–0.99) for cancer mortality, respectively (Table 3). Supplementary Fig. 1 demonstrates the multiple adjusted Kaplan–Meier curves for all-cause mortality and the CIF for cancer and CVD mortality by competing risk models after excluding participants who died within the first 2 years.

Table 3 Cox regression of all-cause, cancer and CVD mortality with participants died within 2 years excluded
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Stratified analyses

In the stratified analyses, we found that the relationships between LCR tertiles and all-cause and cancer mortality risks were generally consistent across different subgroups after adjustment for multiple covariates, except that a significant interaction was detected between LCR tertiles and age for all-cause mortality risk (P for interaction = 0.002), indicating stronger protective effects of high LCR tertile in younger participants (age < 60). Higher LCR levels were associated with a reduced risk of CVD mortality in specific subgroups, including older individuals (≥60 years), males, non-Hispanic whites, individuals with BMI < 30, and non-smokers, but the interaction between LCR levels and stratification variables was insignificant (Table 4).

Table 4 Stratified analysis for the associations of LCR level and all-cause and cancer and CVD mortalities
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Sensitivity analyses

In general, sensitivity analyses yielded consistent results when repeating the main analysis based on quartiles of LCR levels (Supplementary Table 1) or further adjusting for additional covariates (Supplementary Table 2), including: further adjusting for chronic bronchitis status (Supplementary Table 3); further adjusting for the interval since the first cancer diagnosis (Supplementary Table 4); further adjusting for both diabetes and the interval since the first cancer diagnosis (Supplementary Table 5); or analysing the impact of different LCR levels on cancer and CVD mortality and the cause-specific mortalities after excluding participants who died within the first 2 years using competing risks models with multiple adjustments (Supplementary Table 6).

Discussion

This study examined the relationship between LCR and mortalities in 1999 cancer individuals from the NHANES 1999–2008. After a following-up of 156 months (median), multivariate-adjusted Cox proportional hazard models based on categories of LCR levels demonstrated that cancer participants with low LCR levels were linked to higher risks for all-cause, cancer-related mortality, and the mortalities when excluding participants who died within the first 2 years compared to higher LCR levels. Analyses based on stratification and sensitivity proved our findings robust without profound changes. Although there was no significant association between LCR levels and CVD mortality in the total population, the stratified analysis indicated an inverse association between LCR of the top tertile and CVD mortality in individuals aged ≥ 60, males, non-Hispanic whites, individuals with body mass index under 30, and non-smokers.

Our result demonstrated that cancer participants with lower LCR levels were linked to elevated risks for all-cause mortality and cancer mortality. Cancer patient outcomes are determined by multiple factors, such as immunological response, inflammation, and nutrition status. The lymphocytes play a crucial role in fighting against cancers and viral infections. While CRP, a relatively stable downstream indicator of inflammation than pro-inflammatory cytokines [31], is an established parameter in clinical practice to link with cancer mortality [16, 32], cancer risk, disease recurrence and treatment response in various solid malignancies [33, 34]. However, due to its nature as a non-specific marker, its rise alone could be influenced by various causes independent of the tumour. The combination of decreased lymphocyte count and elevated CRP may reflect both deficient immune response and increased systemic inflammation. Decreased LCR has been linked to higher mortality in both non-cancer and cancer populations. A retrospective study in a population with COVID-19 viral infection reported that lower LCR could effectively prognosticate the worse inpatient survival [35]. LCR has also been linked to survival in a spectrum of malignancies [36,37,38,39,40,41,42]. Most of the studies were conducted retrospectively in a single institute. The link between LCR and survival was reported in colorectal cancer patients with metastatic disease [24], resectable disease [18, 25], or Meta analyses [42]. In a Japanese retrospective study in gastric cancer patients after curative treatment, decreased LCR was associated with worse recurrence-free survival and overall survival [36]. The preoperative LCR was linked to postoperative survival of gallbladder cancer in a Chinese retrospective study [39]. In hepatocellular carcinoma, LCR has been shown to correlate inversely to survival [20, 43], including in patients treated with transarterial chemoembolization [41] or curative intention [44]. The associations between decreased LCR and worse survival in resectable oesophagal cancer [21, 40], early breast cancer [37, 45], or resected non-small cell lung cancer [38] were also reported. Our findings are also supported by some studies on institutional pan-cancer populations reporting that lower LCR levels are linked with worse survival of older age [12], obese or overweight [46], malnourished [7], advanced stage [47], or non-metastatic [48] populations. However, the included participants in previous studies were from East Asia, as CRP is routinely tested in most cases in Japan but has not been included in general clinical settings in many other countries, thus limiting the investigation for LCR in cancer mortality in non-Asia populations. In addition, there was little information on the actual causes of death in most studies. The combination of lymphocyte count and CRP has also been evaluated amongst a set of systemic inflammation-related parameters and exhibited a superior predictive value compared to other parameters in cancer survival [18, 23,24,25]. This study provides the first evidence based on a large representative non-institutional population of the US for a significant inverse link between LCR and risks for all-cause and cancer-specific mortalities, suggesting that such a combination is an effective and feasible tool that could be considered integrated into clinical routine setting to identify cancer individuals at higher mortality risks in non-Asia populations.

In this study, follow-up was calculated from the date of the NHANES examination, consistent with previous studies using NHANES cohorts [27, 49]. Given that differences in follow-up definitions calculated from recruitment dates versus from cancer diagnosis dates may affect the comparability of results across studies, we adjusted for the interval between age at first cancer diagnosis and age at NHANES examination as a covariate in sensitivity analyses to account for any temporal misalignment [27]. Notably, the results remained consistent with the primary findings, suggesting that the follow-up calculation method did not substantially affect our conclusions.

Decreased LCR could be merely a result of cancer development instead of a risk factor. To reduce the reverse-causality bias, we also explored the links between LCR and survival outcomes after excluding participants who died within the first 2 years. Our findings showed that lower LCR levels were still associated with increased risks for all-cause and cancer-related mortalities when excluding individuals who died in a short period. Our findings were supported by Zhang et al., reporting that higher LCR could predict better 5-year survival in cancer populations with malnutrition. However, Zhang et al. did not exclude patients with a shorter life span and lacked details for the causes of death [7]. Our results make the implication of a causal relationship between LCR level and mortalities of cancer patients more convincing, although due to the observational study design, that could not be inferred.

The association between LCR and CVD mortality in cancer patients has not been reported before. LCR levels were not significantly linked to CVD mortality in this study, either using Cox proportional hazards models or competing risk models with multiple adjustments. As the number of cancer survivors elevates as expected [2], the need for ongoing care for other chronic diseases increases. Among these, CVD is the dominant cause of non-cancer death deserving attention in cancer survivors [50]. Elevated CRP is a well-established cardiovascular risk factor [51, 52] that plays a crucial role in inducing vascular endothelial dysfunction and complement activation [53]. LCR is relatively less investigated in CVD. A single-centre study retrospectively explored preoperative LCR in patients with ST-segment elevation myocardial infarction and reported that lower LCR is linked to worse prognosis [54]. Another study showed that lower LCR was associated with left ventricular apical thrombus [55]. Inconsistent with the two studies, in the total population, the link between LCR and CVD mortality was not significant in this study. While the stratified analysis indicated higher LCR levels to be a prognostic marker for CVD mortality in specific populations aged ≥60, males, non-Hispanic whites, individuals with body mass index under 30, and non-smokers, the non-significant interaction analysis caution against overinterpreting subgroup differences without further validation. Future diverse cohort studies with adequate power are needed to elucidate the role of LCR in cardiovascular outcomes for informing personalised risk assessment.

The strengths of this study are as follows: we provide evidence for a link between lower LCR levels and higher mortality risks by a prospective study based on a large-scale nationally representative non-institutional U.S cancer sample, which complements prior findings from other populations, especially Asia, and enhances generalizability; we performed a cause-specific mortality analysis, offering additional insights into the relationship between LCR and specific causes of death, such as cancer and cardiovascular disease; During the statistical analysis, a complex survey-weighted design was considered, and detailed covariate data were also utilised to be adjusted as possible confounders; In the sensitive analysis, competing risks models for cause-specific mortalities with multiple adjustments were introduced, Which all strengthened the robustness of our findings.

Several limitations should be mentioned. First, lymphocyte count and CRP were derived from a single blood test, which is less informative than serial measurements. However, the lack of longitudinal biomarker data in NHANES prevents us from evaluating temporal changes in LCR. Future studies with repeated measurements are needed to provide a more comprehensive understanding of the prognostic capacity of LCR and confirm its stability over time. Second, self-reported cancer diagnoses, though collected via structured protocols to improve accuracy, remain susceptible to recall bias or misclassification without validation. Third, causes of death may not be accurately represented on death certificates in some cases. Fourth, although the significant association between LCR and mortalities after excluding participants who died within the first 2 years could reduce the reverse-causality bias, however, due to the nature of the observational study and potential oversight confounders, the causal relationships between LCR and mortalities in cancer survivors could not be inferred. Finally, this study used data from NHANES, which, as a convenient sample, has inherent limitations. In particular, the data set lacks detailed information on cancer types and treatments, which are crucial for understanding survival outcomes in cancer patients. Therefore, our findings may have missed some potential covariates that could influence the results. Future studies with more comprehensive, cancer-related records are needed to validate and extend these findings.

Conclusions

This study provided evidence of inverse associations between LCR levels and all-cause, cancer-specific, and mortalities in a large US cancer population. Integrating LCR assessment in the clinical routine of US cancer survivors may aid in identifying individuals at high risk of mortalities.

Availability of data and materials

The datasets in the study are from the Centers for Disease Control and Prevention (https://wwwn.cdc.gov/nchs/nhanes/Default.aspx) and are publicly available.

Abbreviations

LCR:

Lymphocyte-to-C-reactive protein ratio

NHANES:

The National Health and Nutrition Examination Survey

CI:

Confidence interval

NDI:

National Death Index

MECs:

Mobile examination centers

ICD-10:

The 10th International Classification of Diseases

CVD:

Cardiovascular disease

HR:

Hazard ratio

CHD:

Coronary heart disease

CRP:

C-reactive protein

BMI:

Body mass index

CIF:

Cumulative incidence function

FIPR:

Family income-to-poverty ration

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Funding

The study was supported by the Capital Health Research and Development of Special Fund (CN) (No.2022-2-2013).

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Authors and Affiliations

  1. Department of Thoracic Surgery, Xuanwu Hospital, Capital Medical University, Changchun Street 45#, Beijing, 100053, China

    Jingying Nong, Ruotian Wang & Yi Zhang

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  1. Jingying Nong
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  2. Ruotian Wang
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  3. Yi Zhang
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Contributions

YZ and JYN conceived the study. JYN and RTW analysed the data with the support of YZ. JYN wrote and revised the manuscript. All authors approved the final manuscript.

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Correspondence to Jingying Nong or Yi Zhang.

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The National Center for Health Statistics Research Ethics Review Board approved the NHANES, and consent from all participants was documented.

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Nong, J., Wang, R. & Zhang, Y. Association of lymphocyte-to-C-reactive protein ratio with all-cause and cause-specific mortality among US cancer survivors. Eur J Med Res 30, 312 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-025-02527-1

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-025-02527-1

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European Journal of Medical Research

ISSN: 2047-783X

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