Risk of cancer incidence and mortality in patients with chronic pain: A systematic review and meta-analysis.

There is abundant but discrepant scientific literature reporting an effect of opioids on the course of cancer. The International Agency for Research on Cancer monographs recently classified opium consumption as carcinogenic to humans in certain organs, raising concerns this may be due at least in part to the alkaloids opium contains (such as morphine and codeine). This systematic review investigated whether opioid exposure among cancer-free individuals is independently associated with the risk of future cancer incidence or cancer mortality. An electronic database search was conducted in PubMed, EMBASE, Web of Science, PsycINFO, International Pharmaceutical s, CINAHL and Scopus. Studies were included if they provided a statistical estimate of cancer mortality, cancer incidence, or cancer risk following opioid exposure. Study quality was assessed using the Newcastle–Ottawa Scale. Study characteristics and outcomes were extracted and analysed in a descriptive narrative synthesis. There were 27 studies that met the inclusion criteria, representing a total of 4,542,745 participants. Twelve of the 27 were rated as high quality according to the Newcastle–Ottawa Scale. The observed data is consistent with a small increase in the risk of cancer incidence or cancer mortality following opioid exposure, particularly in a subset of organs. There is, however, considerable uncertainty in the evidence given the substantial risk of bias in estimating the overall effect of opioid exposure on cancer outcomes in these studies. This review synthesises studies reporting cancer risk following opioid exposure and identifies the key methodological factors influencing ongoing uncertainty estimating the true effect. Rigorous epidemiological studies employing specific methods to minimize bias are warranted.

Tea is one of the most commonly consumed beverages worldwide. Teas from the plant Camellia sinensis can be grouped into green, black and oolong tea. Cross-culturally tea drinking habits vary. Camellia sinensis contains the active ingredient polyphenol, which has a subgroup known as catechins. Catechins are powerful antioxidants. It has been suggested that green tea polyphenol may inhibit cell proliferation and observational studies have suggested that green tea may have cancer-preventative effects. To critically assess any associations between green tea consumption and the risk of cancer incidence and mortality. We searched eligible studies up to January 2009 in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Amed, CancerLit, Psych INFO and Phytobase and reference lists of previous reviews and included studies. We included all prospective, controlled interventional studies and observational studies, which either assessed the associations between green tea consumption and risk of cancer incidence or that reported on cancer mortality. At least two review authors independently applied the study criteria, extracted data and assessed methodological quality of studies. Due to the nature of included studies, which were mainly epidemiological, results were summarised descriptively according to cancer diagnosis. Fifty-one studies with more than 1.6 million participants were included. Twenty-seven of them were case-control studies, 23 cohort studies and one randomised controlled trial (RCT).Twenty-seven studies tried to establish an association between green tea consumption and cancer of the digestive tract, mainly of the upper gastrointestinal tract, five with breast cancer, five with prostate cancer, three with lung cancer, two with ovarian cancer, two with urinary bladder cancer one with oral cancer, three further studies included patients with various cancer diagnoses.The methodological quality was measured with the Newcastle-Ottawa scale (NOS). The 9 nested case-control studies within prospective cohorts were of high methodological quality, 13 of medium, and 1 of low. One retrospective case-control study was of high methodological quality and 21 of medium and 5 of low.Results from studies assessing associations between green tea and risk of digestive tract cancer incidence were highly contradictory. There was limited evidence that green tea could reduce the incidence of liver cancer. The evidence for esophageal, gastric, colon, rectum, and pancreatic cancer was conflicting. In prostate cancer, observational studies with higher methodological quality and the only included RCT suggested a decreased risk in men consuming higher quantities green tea or green tea extracts. However, there was limited to moderate evidence that the consumption of green tea reduced the risk of lung cancer, especially in men, and urinary bladder cancer or that it could even increase the risk of the latter. There was moderate to strong evidence that green tea consumption does not decrease the risk of dying from gastric cancer. There was limited moderate to strong evidence for lung, pancreatic and colorectal cancer. There is insufficient and conflicting evidence to give any firm recommendations regarding green tea consumption for cancer prevention. The results of this review, including its trends of associations, need to be interpreted with caution and their generalisability is questionable, as the majority of included studies were carried out in Asia (n = 47) where the tea drinking culture is pronounced. Desirable green tea intake is 3 to 5 cups per day (up to 1200 ml/day), providing a minimum of 250 mg/day catechins. If not exceeding the daily recommended allowance, those who enjoy a cup of green tea should continue its consumption. Drinking green tea appears to be safe at moderate, regular and habitual use.

The purpose was to investigate the association between serum osteoprotegerin (OPG) and risk of incident cancer and cancer mortality in a general population. OPG was measured in serum collected from 6,279 subjects without prior cancer recruited from a general population. Incident cancer and cancer-related mortality were registered from inclusion in 1994-95 until end of follow-up December 31, 2008. Cox regression models were used to estimate crude and adjusted (for age, sex and other confounders) hazard ratios and 95% confidence intervals (HR 95% CI). There were 948 incident cancers and 387 deaths in the cohort during 71,902 person-years of follow up (median 13.5 years). Subjects with serum OPG in the upper tertile had 79% higher risk of incident gastrointestinal cancer than those in the lowest tertile (HR 1.79, 95% CI 1.19-2.67). In women <60 years, serum OPG (per SD 0.81 ng/ml) was associated with reduced risk of incident cancer (all cancers merged; 0.73; 0.57-0.94) and breast cancer (0.51; 0.31-0.83) after adjustment. Subjects in the upper tertile of OPG had higher risk of cancer-related mortality (1.63; 1.16-2.28), particularly mortality from cancer in the gastrointestinal system (2.28; 1.21-4.28) compared to those in the lowest OPG tertile. No significant association was detected between OPG and risk of death from cancer in the respiratory system or death from prostatic cancer. Our findings from a large population based cohort study suggest that serum OPG was associated with increased risk of incident gastrointestinal cancer, inversely associated with breast cancer, and predicts cancer-related mortality.

Background and AimsAssociations between soy intake and risk of cancer have been evaluated in prospective observational studies with inconsistent results. Whether the potential anticancer effects offered by soy were attributed to soy isoflavones and soy protein still needs to be elucidated. This study aimed to comprehensively quantify the association of soy, soy isoflavones and soy protein intake with risk of cancer incidence and cancer mortality by conducting a meta-analysis of all available studies.MethodsPubMed, Embase, Web of Science, and Cochrane Library databases were searched up to 16 September 2021. Prospective cohort studies that examined the effect of soy, soy isoflavones and soy protein on cancer incidence and cancer mortality were identified. Random-effects models were used to pool the multivariable-adjusted relative risks (RRs) and corresponding 95% confidence intervals (CIs). The potential dose-response relations were explored by using generalized least-squares trend estimation.ResultsEighty one prospective cohort studies were included in the meta-analysis. A higher intake of soy was significantly associated with a 10% reduced risk of cancer incidence (RR, 0.90; 95% CI, 0.83–0.96). Each additional 25 g/d soy intake decreased the risk of cancer incidence by 4%. Intake of soy isoflavones was inversely associated with risk of cancer incidence (RR, 0.94; 95% CI, 0.89–0.99), whereas no significant association was observed for soy protein. The risk of cancer incidence was reduced by 4% with each 10 mg/d increment of soy isoflavones intake. Similar inverse associations were also found for soy in relation to site-specific cancers, particularly lung cancer (RR, 0.67; 95%CI, 0.52–0.86) and prostate cancer (RR, 0.88; 95%CI, 0.78–0.99). However, high intake of soy, soy isoflavones and soy protein were not associated with cancer mortality.ConclusionsHigher intake of soy and soy isoflavones were inversely associated with risk of cancer incidence, which suggested that the beneficial role of soy against cancer might be primarily attributed to soy isoflavones. These findings support recommendations to include soy as part of a healthy dietary pattern for the prevention of cancer.

Joint association of biological aging and lifestyle with risks of cancer incidence and mortality: A cohort study in the UK Biobank

BackgroundThyroid hormone has been shown to be involved in carcinogenesis via its effects on cell proliferation pathways. The objective of this study is to determine the association between subclinical hypothyroidism (SCH) and the risk of incident cancer and cancer mortality via systematic review.MethodsA systematic search was performed on Medline and Pubmed to identify relevant studies. Randomized controlled trials, and observational studies assessing SCH or its treatment and the risk of incident cancer or cancer mortality were identified.ResultsA total of 7 cohort and 2 case-control studies met our inclusion criteria. In general, these studies were of medium to good quality. Overall, studies revealed no association between SCH and breast and prostate cancer. One study found that untreated SCH may be associated with an increased risk of colorectal cancer (adjusted odds ratio [OR]: 1.16; 95% confidence interval [CI]: 1.08–1.24). One study showed an increased risk in thyroid cancer incidence (adjusted OR: 3.38; 95% CI: 2.05–5.59) associated with elevation of a thyroid stimulating hormone (TSH) of > 1.64mIU/L. Two studies found an increase in cancer mortality among patients with SCH compared to euthyroid individuals; in contrast one study found no association between subclinical hypothyroidism and cancer mortality among aging men.ConclusionThe number of studies examining thyroid dysfunction and cancer risk and mortality is limited. Future studies assessing the association between thyroid dysfunction and cancer risk and mortality are needed, which will further address the need to treat subclinical hypothyroidism.

Sleep duration is emerging as an important modifiable risk factor for morbidity and mortality. We assessed the association between sleep duration and cancer incidence and mortality among Japanese adults using data from six population-based cohorts with 271 694 participants. During a total follow-up period of about 5.9 million person-years, we identified 40 751 incident cancer cases and 18 323 cancer deaths. We computed study-specific hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression models and pooled the estimates using random-effects meta-analysis. Sleep duration of ≥10hours (vs 7hours) was associated with increased risk of cancer incidence among women (HR 1.19, 95% CI 1.02-1.38), but not men, and increased risk of cancer mortality among men (HR 1.18, 95% CI 1.00-1.39) and women (HR 1.44, 95% CI 1.20-1.73). Sleep duration of ≤5hours (vs 7hours) was not associated with cancer incidence and mortality. However, among postmenopausal women, sleep durations of both ≤5 and ≥10hours (vs 7hours) were associated with an increased risk of cancer mortality. Among Japanese adults, sleep duration of ≥10hours is associated with increased risk of cancer incidence and mortality among women and cancer mortality among men.

BackgroundIn many developed countries, socioeconomic status is associated with cancer incidence and survival. However, research in Japan is sparse. We examined the association between neighborhood deprivation based on the Japanese Deprivation Index and the risk of incidence, mortality and survival from total and major cancers in the Japan Public Health Center-based Prospective Study.Methods86,112 participants were followed through the end of 2009. A total of 10,416 incident cases and 5,510 deaths from cancer were identified among 1,348,437 person-years of follow-up (mean follow-up: 15.7 years). The Japanese deprivation index was used to access neighborhood deprivation. Hazard ratios and 95% confidence intervals were calculated by Cox regression analysis.ResultsWe found no associations between neighborhood deprivation index and the incidence of total and major cancers. In some cancer risks or deaths, however, we found positive or inverse associations with a higher deprivation index, such as a decreased risk of colorectal cancer incidence and an increased risk of liver cancer incidence and deaths in women.ConclusionAlthough some positive or inverse associations were detected for specific sites, the neighborhood deprivation index has no substantial overall association with the risk of incidence, mortality and survival from cancer in the Japanese population.

Both baseline cardiorespiratory fitness and adiposity predict the risk of cancer mortality. However, the effects of changes in these two factors over time have not been evaluated thoroughly. The aim of this study was to examine the independent and joint associations of changes in cardiorespiratory fitness and body composition on cancer mortality. The cohort consisted of 13,930 men (initially cancer-free) with two or more medical examinations from 1974 to 2002. Cardiorespiratory fitness was assessed by a maximal treadmill exercise test, and body composition was expressed by body mass index (BMI) and percent body fat. Changes in cardiorespiratory fitness and body composition between the baseline and the last examination were classified into loss, stable, and gain groups. There were 386 deaths from cancer during an average of 12.5 yr of follow-up. After adjusting for possible confounders and BMI, change hazard ratios (95% confidence intervals) of cancer mortality were 0.74 (0.57-0.96) for stable fitness and 0.74 (0.56-0.98) for fitness gain. Inverse dose-response relationships were observed between changes in maximal METs and cancer mortality (P for linear trend = 0.05). Neither BMI change nor percent body fat change was associated with cancer mortality after adjusting for possible confounders and maximal METs change. In the joint analyses, men who became less fit had a higher risk of cancer mortality (P for linear trend = 0.03) compared with those who became more fit, regardless of BMI change levels. Being unfit or losing cardiorespiratory fitness over time was found to predict cancer mortality in men. Improving or maintaining adequate levels of cardiorespiratory fitness appears to be important for decreasing cancer mortality in men.

Risk of cancer incidence and mortality associated with diabetes: A systematic review with trend analysis of 203 cohorts

Epidemiological studies have suggested inconclusive associations between 25-hydroxyvitamin D and total cancer incidence and mortality. The aim of this study was to quantitatively assess these associations by combining results from prospective cohort studies. A systematic literature search was implemented in PubMed and Scopus databases in April 2019. Comparing the highest with the lowest categories, the multivariate-adjusted relative risks (RRs) and the corresponding 95% confidence intervals (CIs) were pooled using a random-effects model. A trend estimation was performed using a two-stage, dose-response, meta-analysis method. Twenty-three independent prospective studies were included for data synthesis. Eight studies investigated the association between 25-hydroxyvitamin D and the risk of cancer incidence (7511 events and 70,018 participants), and the summary estimate showed that 25-hydroxyvitamin D is marginally associated with cancer risk (Summary RR = 0.86; 95% CI: 0.73, 1.02; I2 = 70.8%; p = 0.001). Sixteen studies investigated the association between 25-hydroxyvitamin D and the risk of cancer mortality (8729 events and 101,794 participants), and a higher 25-hydroxyvitamin D concentration was inversely associated with the risk of cancer mortality (Summary RR = 0.81; 95% CI: 0.71, 0.93; I2 = 48.8%, p = 0.012). Dose-response analysis indicated that the risk of cancer incidence was reduced by 7% (RRs = 0.93; 95% CI: 0.91, 0.96), and the risk of cancer mortality was reduced by 2% (RRs = 0.98; 95% CI: 0.97, 0.99), with each 20 nmol/L increment of 25-hydroxyvitamin D concentration. This meta-analysis provides evidence that a higher 25-hydroxyvitamin D concentration is associated with a lower cancer incidence and cancer mortality.

The risk of cancer developing in people with psoriasis has raised some concern, with little clarity regarding differentiation in risk according to psoriasis severity. To conduct a systematic review and meta-analysis of observational studies on the risk of cancer incidence and mortality in people with psoriasis. Six electronic databases (MEDLINE, Embase, MEDLINE in Process, Cochrane Central Register, Web of Science, and LILACS [Literatura Latino-Americana e do Caribe em Ciências da Saúde]) were searched from inception to November 15, 2017, for eligible studies. Cohort and case-control studies that provided estimates of the risk of cancer incidence or cancer mortality associated with psoriasis were included. Data were extracted relating to study design, study population, and risk estimates. Study-specific estimates of the relative risk (RR) were combined using a random-effects model. Heterogeneity was quantified using the I2 statistic. Data were analyzed from April 9, 2018, through February 22, 2019. Pooled RR estimates for cancer incidence and cancer mortality for psoriasis cohorts compared with people without psoriasis. A total of 58 unique studies were included, with quality varying for the incidence and the mortality studies. Severe psoriasis (RR, 1.22; 95% CI, 1.08-1.39 [9 studies]) and all severities of psoriasis (RR, 1.18; 95% CI, 1.06-1.31 [7 studies]) were associated with an increased risk of cancer (overall), and associations were found for a range of site-specific cancers, including colon (RR, 1.18 [95% CI, 1.03-1.35]), colorectal (RR, 1.34 [95% CI, 1.06-1.70]), kidney (RR, 1.58 [95% CI, 1.11-2.24]), laryngeal (RR, 1.79 [95% CI, 1.06-3.01]), liver (RR, 1.83 [95% CI, 1.28-2.61]), lymphoma (RR, 1.40 [95% CI, 1.24-1.57]), non-Hodgkin lymphoma (RR, 1.28 [95% CI, 1.15-1.43]), keratinocyte cancers (RR, 1.71 [95% CI, 1.08-2.71]), esophageal (RR, 2.05 [95% CI, 1.04-4.07]), oral cavity (RR, 2.80 [95% CI, 1.99-3.93]), and pancreatic (RR, 1.41 [95% CI, 1.16-1.73]). Overall cancer mortality risk was higher in patients with severe psoriasis (RR, 1.22; 95% CI, 1.08-1.38 [4 studies]). Specifically, liver (RR, 1.43 [95% CI, 1.09-1.88]), esophageal (RR, 2.53 [95% CI, 1.87-3.41]), and pancreatic (RR, 1.31 [95% CI, 1.02-1.69]) cancer mortality were found to be elevated in those with severe psoriasis. The heterogeneity of estimates was often very high despite stratification. Marked attenuation of risk was found in those studies that adjusted estimates for smoking, alcohol consumption, and obesity. In this study, people with psoriasis appeared to have an increased risk of cancer incidence and cancer-related mortality involving a range of site-specific cancers. Future research examining specific lifestyle factors, treatments, and the inflammatory processes that contribute to psoriasis may help provide additional information on the underlying mechanisms for the apparent increased cancer risk.

Blacks have been documented to have low vitamin D levels. We thus examined whether total cancer incidence and mortality rates differ between Blacks and Whites in a population of male health professionals, and particularly for digestive system cancers (oral, esophagus, stomach, pancreas, and colorectum), which have been most consistently linked to poor vitamin D status. Second, we examined whether Blacks might be more susceptible to these cancers if they concurrently had other risk factors for hypovitaminosis D. In the Health Professionals Follow-up Study, from 1986 to 2002, 99 of 481 Black men and 7,019 of 43,468 White men were diagnosed with cancer. Adjusting for multiple dietary, lifestyle, and medical risk factors, using Cox modeling, Black men were at higher risk of total cancer incidence [relative risk (RR), 1.32; 95% confidence interval (95% CI), 1.08-1.61; P = 0.007] and total cancer mortality (RR, 1.89; 95% CI, 1.40-2.56; P < 0.0001) and especially digestive system cancer mortality (RR, 2.24; 95% CI, 1.35-3.70). Compared with Whites with relatively few risk factors for hypovitaminosis D, Blacks also with few risk factors for hypovitaminosis D were not at appreciably higher risk of total cancer incidence (RR, 0.95; 95% CI, 0.60-1.51) or mortality (RR, 1.55; 95% CI, 0.91-2.62), but Black men with additional risk factors for poorer vitamin D status had a much higher cancer incidence (RR, 1.57; 95% CI, 1.16-2.11) and mortality risk (RR, 2.27; 95% CI, 1.57-3.28). This pattern was even more pronounced for digestive system cancer. Our results suggest that the high frequency of hypovitaminosis D in Blacks may be an important, and easily modifiable, contributor to their higher risk of cancer incidence and mortality.

Background: Previous studies have investigated the association between reproductive factors and lung cancer risk; however, findings have been inconsistent. This study aims to assess the association between reproductive factors with lung cancer incidence and mortality among Asian women. Methods: A total of 308,949 female participants with a mean age of 55.13 from 11 prospective cohorts and four Asian countries (Japan, Korea, China, and Singapore) in the Asia Cohort Consortium (ACC) were included. Cox proportional hazards regression models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CIs). Results: A total of 3,119 primary lung cancer cases and 2,247 lung cancer deaths were identified with a mean follow-up of 16.4 years. Parous women had a lower risk of lung cancer incidence and mortality as compared with nulliparous women, with HRs of 0.82 (95% CI = 0.70 - 0.96) and 0.78 (95% CI = 0.65 - 0.94). Corresponding HRs were lowest among women with 1-2 children, with HRs of 0.78 (95% CI = 0.66 - 0.93) and 0.72 (95% CI = 0.59 - 0.87) for lung cancer incidence and mortality. The protective association of parity and lung cancer incidence was greater among ever-smokers (HR=0.66, 95% CI = 0.49 - 0.87) than in never-smokers (HR=0.90, 95% CI = 0.74 - 1.09) (P-interaction = 0.029). Compared with age at first delivery ≤20 years, older age at first delivery (≥26 years) was associated with a lower risk of lung cancer incidence and mortality. Compared with age at menopause &amp;lt;45 years, older age at menopause (≥55 years) was associated with a decreased risk of lung cancer mortality (HR=0.75, 95% CI = 0.58 - 0.96). Women who ever used hormone replacements had a higher likelihood of developing non-small cell lung cancer (HR = 1.30, 95% CI = 1.01 - 1.67), compared to those who never used hormone replacements. Conclusions: Distinct from Western women, Asian parous women, especially those who have 1-2 children had a lower risk of lung cancer incidence and mortality compared with nulliparous women. Future studies are needed to assess the underlying mechanisms, the relationships within these female reproductive factors, and the potential changes in smoking habits over time. Citation Format: Xin Yin, Rie Kishida, Sarah Krull Abe, Md. Rashedul Islam, Md. Shafiur Rahman, Eiko Saito, Qing Lan, Batel Bletcher, Melissa Merritt, Ji-Yeob Choi, Aesun Shin, Ryoko Katagiri, Xiao-Ou Shu, Norie Sawada, Akiko Tamakoshi, Woon-Puay Koh, Ichiro Tsuji, Chisato Nagata, Sue K. Park, Sun-Seog Kweon, Yu-Tang Gao, Shoichiro Tsugane, Takashi Kimura, Jian-Min Yuan, Yukai Lu, Seiki Kanemura, Yumi Sugawara, Keiko Wada, Min-Ho Shin, Habibul Ahsan, Paolo Boffetta, Kee Seng Chia, Keitaro Matsuo, You-Lin Qiao, Nathaniel Rothman, Wei Zheng, Manami Inoue, Daehee Kang, Wei Jie Seow. Association between reproductive factors with lung cancer incidence and mortality: A pooled analysis of over 308,000 females in the Asia Cohort Consortium. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4200.

Studies have demonstrated an association between elevated levels of total white blood cell (WBC) count, within the clinically normal range, and an increased risk of overall cancer incidence and mortality. However, a paucity of data exists on the relationship between WBC subtypes and cancer outcomes. We hypothesize that chronic low-grade inflammation in healthy individuals, reflected by elevated neutrophil count, is associated with an increased risk of subsequent cancer incidence and mortality. To test this hypothesis, we prospectively evaluated the association between neutrophil count, cancer incidence, and mortality in the Atherosclerosis Risk in Communities (ARIC) study. Total neutrophil counts were measured at enrollment (1987-1989) and, in a subset, at visit 2. Participants with a neutrophil count more than two standard deviations from the mean and cancer at baseline were excluded. Cancer incidence and mortality data were available through 12/31/2006 and 12/31/2009, respectively. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models. Neutrophil count was modeled as tertiles, with separate cut-offs for whites and blacks to account for differences in their distribution. The analytic cohort consisted of 6,252 whites (51% female) and 3,400 blacks (62% female). The mean age at blood draw was 54 years and 53.5 years, respectively. The mean neutrophil count was 3.7 cu/mcL (range: 1.9-6.6) in whites and 2.7 cu/mcL (range: 1.0-5.7) in blacks. Among whites, 1,346 cancer cases developed over 102,541 person-years and, among blacks, 655 cancer cases developed over 53,308 person-years. In analyses of cancer mortality, 504 cancer deaths occurred over 125,744 person-years in whites and 301 over 63,592 person-years in blacks. The proportion of cancer subtypes did not differ by race for either outcome. Neutrophil count was not associated with cancer incidence in whites or blacks. However, in blacks, neutrophil count was associated with a significant but non-linear increase in cancer mortality in the highest tertile compared to the lowest (HR: 1.4, 95% CI: 1.0, 1.8) after adjusting for study center, age, sex, education level, body mass index, prior cardiovascular disease, diabetes, smoking, alcohol intake and aspirin use in the past two weeks. This association was modified by smoking status (p-interaction=0.04). Among never smokers, a linear increase in mortality was observed with a 2.1-fold (95% CI: 1.1, 3.7) increase in risk in the highest versus lowest tertile. This association remained when the average neutrophil count (baseline and visit 2) was used. A similar pattern was not observed in whites. Neutrophil count measured prior to diagnosis was associated with cancer mortality among non-smokers in blacks but not whites. This supports a relationship between chronic low-grade inflammation and cancer outcomes in blacks, the mechanism of which remains to be elucidated. Citation Format: Sarah A. Davidovics, Anna Prizment, Kumar Visvanathan, Kala Visvanathan. Neutrophil count, cancer incidence and cancer mortality: disparate relationships by race. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2525. doi:10.1158/1538-7445.AM2013-2525