Disparities in the treatment and outcomes of lung cancer among HIV-infected people in Texas.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 6070-6070
Author(s):  
Gita Suneja ◽  
Meredith S. Shiels ◽  
Sharon K. Melville ◽  
Melanie A. Williams ◽  
Ramesh Rengan ◽  
...  

6070 Background: HIV-infected (HIV+) people are at elevated risk for lung cancer and have higher mortality following lung cancer diagnosis than uninfected (HIV-) individuals. The disparity in survival is partly due to advanced stage at diagnosis, but it is unclear whether HIV+ people with lung cancer are less likely to receive cancer treatment, which could worsen survival. Methods: We included adults ≥ 18 years of age with lung cancer reported to the Texas cancer registry (N=156,930). HIV status was determined by linkage with the enhanced Texas HIV/AIDS Reporting System. We compared HIV+ and HIV- lung cancer cases with respect to demographic and clinical characteristics. For non-small cell lung cancer (NSCLC) cases, we identified predictors of cancer treatment (surgery, radiation, and chemotherapy) using logistic regression. We used Cox regression to evaluate the effects of HIV and treatment on lung cancer-specific mortality. Results: Compared with HIV- lung cancer cases (N=156,593), HIV+ lung cancer cases (N=337) were more likely to be young, non-Hispanic black, male, and to have distant stage disease (53.7% vs. 44.4%). HIV+ cases were less likely to receive cancer treatment than HIV- cases (60.3% vs. 77.5%; odds ratio 0.39, 95%CI 0.30-0.52 after adjustment for diagnosis year, age, sex, race, stage, and histologic subtype). In Cox models adjusted for these variables, both HIV infection (hazard ratio [HR] 1.34, 95%CI 1.15-1.56) and lack of cancer treatment (HR 1.69, 95%CI 1.66-1.72) were associated with higher lung cancer-specific mortality. After adjustment for cancer treatment, the association between HIV and lung cancer mortality was attenuated (HR 1.25, 95%CI 1.06-1.47). The association between HIV and lung cancer-specific mortality was stronger among untreated lung cancer cases (HR 1.32, 95%CI 1.01-1.72) than treated cases (adjusted HR 1.16, 95%CI 0.94-1.43; p-interaction=0.34). Conclusions: In this population-based study, HIV+ people with NSCLC were less likely to be treated for lung cancer than their HIV- counterparts. This lack of treatment may be partly responsible for higher cancer-related mortality in HIV+ cases. Further investigation is needed to understand disparities in cancer treatment for HIV+ people.

2015 ◽  
Vol 33 (21) ◽  
pp. 2376-2383 ◽  
Author(s):  
Anna E. Coghill ◽  
Meredith S. Shiels ◽  
Gita Suneja ◽  
Eric A. Engels

Purpose Despite advances in the treatment of HIV, HIV-infected people remain at increased risk for many cancers, and the number of non–AIDS-defining cancers is increasing with the aging of the HIV-infected population. No prior study has comprehensively evaluated the effect of HIV on cancer-specific mortality. Patients and Methods We identified cases of 14 common cancers occurring from 1996 to 2010 in six US states participating in a linkage of cancer and HIV/AIDS registries. We used Cox regression to examine the association between patient HIV status and death resulting from the presenting cancer (ascertained from death certificates), adjusting for age, sex, race/ethnicity, year of cancer diagnosis, and cancer stage. We included 1,816,461 patients with cancer, 6,459 (0.36%) of whom were HIV infected. Results Cancer-specific mortality was significantly elevated in HIV-infected compared with HIV-uninfected patients for many cancers: colorectum (adjusted hazard ratio [HR], 1.49; 95% CI, 1.21 to 1.84), pancreas (HR, 1.71; 95% CI, 1.35 to 2.18), larynx (HR, 1.62; 95% CI, 1.06 to 2.47), lung (HR, 1.28; 95% CI, 1.17 to 1.39), melanoma (HR, 1.72; 95% CI, 1.09 to 2.70), breast (HR, 2.61; 95% CI, 2.06 to 3.31), and prostate (HR, 1.57; 95% CI, 1.02 to 2.41). HIV was not associated with increased cancer-specific mortality for anal cancer, Hodgkin lymphoma, or diffuse large B-cell lymphoma. After further adjustment for cancer treatment, HIV remained associated with elevated cancer-specific mortality for common non–AIDS-defining cancers: colorectum (HR, 1.40; 95% CI, 1.09 to 1.80), lung (HR, 1.28; 95% CI, 1.14 to 1.44), melanoma (HR, 1.93; 95% CI, 1.14 to 3.27), and breast (HR, 2.64; 95% CI, 1.86 to 3.73). Conclusion HIV-infected patients with cancer experienced higher cancer-specific mortality than HIV-uninfected patients, independent of cancer stage or receipt of cancer treatment. The elevation in cancer-specific mortality among HIV-infected patients may be attributable to unmeasured stage or treatment differences as well as a direct relationship between immunosuppression and tumor progression.


Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2027
Author(s):  
Christoph Roderburg ◽  
Sven H. Loosen ◽  
Anselm Kunstein ◽  
Raphael Mohr ◽  
Markus S. Jördens ◽  
...  

Background: Cancer is the second leading cause of death worldwide and incidence rates for several tumor entities are rising. In addition to a high cancer-specific mortality rate, many cancer patients also suffer from additional comorbidities. Among these, several psychological morbidities have been extensively studied in the past, but findings on the association between cancer and dementia have remained conflicting. In the present study, we evaluated the possibility of an association between cancer and dementia. Methods: Based on data from the IQVIA Disease Analyzer database, a total of 92,868 cancer outpatients initially diagnosed between 2000 and 2018 were matched by age, gender, index year, and yearly consultation frequency to 92,868 individuals without cancer. Ten-year incidence rates of dementia were compared for the two cohorts. Results: The overall cumulative incidence of dementia was significantly higher in cancer patients (19.7%) than in non-cancer patients (16.7%, p < 0.001). Cox regression models confirmed that this association was significant for both male (HR: 1.35 [1.30–1.41], p < 0.001) and female (HR: 1.26 [1.21–1.31], p < 0.001) patients and was consistent among all age groups analyzed (65–70, 71–75, 76–80, 81–85, and >85 years). In addition, the association between cancer and dementia was significant for all cancer entities analyzed (skin, digestive organs, prostate, breast, urinary tract, lymphoid and hematopoietic tissue, and lung cancer) and most pronounced in patients with lung cancer (HR: 1.44 [1.28–1.62], p < 0.001). Conclusions: Our data provide strong evidence for an increased incidence of dementia in a large cohort of patients with different cancer entities, which should raise awareness of this important comorbidity in cancer patients.


2020 ◽  
Vol 18 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Carlotta Palumbo ◽  
Francesco A. Mistretta ◽  
Sophie Knipper ◽  
Angela Pecoraro ◽  
Zhe Tian ◽  
...  

Background: Conditional survival (CS) may reveal important differences in cancer-specific mortality (CSM) among patients with nonmetastatic renal cell carcinoma (nmRCC). This study assessed CS according to T and N stages in patients treated surgically for nmRCC. Patients and Methods: Within the SEER database (2001–2015), all patients with nmRCC treated with either partial or radical nephrectomy were identified. CSM-free estimates according to T and N stage and substage groupings (pT1aN0–pT4N0 and pTanyN1) and multivariable Cox regression models with adjustment for Fuhrman grade and histologic subtype were assessed. Results: According to T and N stage and substage groupings, the following patients were included in the study: 35,966 (46.2%) with pT1aN0 disease; 18,858 (24.2%) with pT1bN0; 5,977 (7.7%) with pT2aN0; 2,511 (3.2%) with pT2bN0; 11,839 (15.2%) with pT3aN0; 1,037 (1.3%) with pT3b–cN0; 402 (0.5%) with pT4N0; and 1,302 (1.7%) with pTanyN1. Conditional CSM-free survival estimates were 98.2% at 1 year versus 98.0% at 10 years of event-free follow-up for patients with pT1aN0 disease, relative to baseline. Conversely, pT4N0/pTanyN1 conditional CSM-free survival estimates were 55.8% at 1 year versus 77.9% at 8 years of event-free follow-up. Attrition due to mortality was highest in patients with pT4N0/pTanyN1 disease. In multivariable Cox regression analyses, T stage, tumor grade, and histologic subtype represented independent predictors, but no interactions were identified. Conclusions: Tumor stage and its substages represent extremely important determinants of prognosis after lengthy event-free follow-up. The recorded observations have critical importance for physicians regarding patient follow-up and counseling.


2019 ◽  
Vol 57 (1) ◽  
pp. 114-121 ◽  
Author(s):  
Yoshinori Handa ◽  
Yasuhiro Tsutani ◽  
Takahiro Mimae ◽  
Yoshihiro Miyata ◽  
Morihito Okada

AbstractOBJECTIVESAlthough segmentectomy for lung cancer has been widely accepted, complex segmentectomy, which creates several, intricate intersegmental planes, remains controversial. Potential arguments include risk of incurability and ‘failure of cancer control’. We compared the outcomes of complex segmentectomy versus lobectomy and evaluated its use in lung cancer treatment.METHODSWe retrospectively reviewed clinical stage IA lung cancer patients who underwent complex segmentectomy (n = 99) or location-adjusted lobectomy (n = 94) between April 2009 and December 2017. Clinicopathological and postoperative results were compared. Factors affecting survival were assessed by the Kaplan–Meier method and the Cox regression analysis.RESULTSNo significant differences were detected in 30-day mortality (0% vs 0%), overall complications (26.3% vs 21.3%) and prolonged air leakage (11.1% vs 9.6%) rates between the 2 groups, respectively. Comparable results were obtained for 5-year overall (93.5% vs 96.4%, respectively; P = 0.21) or recurrence-free (92.3% vs 88.5%, respectively; P = 0.82) survivals after complex segmentectomy or lobectomy. There were 2 (2.0%) recurrences after complex segmentectomy and 7 (7.5%) after lobectomy (P = 0.094), with 0 (0%) margin relapses in each group. Multivariable Cox regression analysis revealed that complex segmentectomy and lobectomy had a numerically similar impact on recurrence-free survival (hazard ratio 0.93, 95% confidence interval 0.32–2.69; P = 0.90).CONCLUSIONSComplex segmentectomy can provide acceptable short- and long-term outcomes in lung cancer treatment.


2020 ◽  
pp. tobaccocontrol-2019-055412
Author(s):  
Jae Jeong Yang ◽  
Danxia Yu ◽  
Xiao-Ou Shu ◽  
Neal D Freedman ◽  
Wanqing Wen ◽  
...  

BackgroundLittle is known about the health harms associated with low-intensity smoking in Asians who, on average, smoke fewer cigarettes and start smoking at a later age than their Western counterparts.MethodsIn this pooled analysis of 738 013 Asians from 16 prospective cohorts, we quantified the associations of low-intensity (<5 cigarettes/day) and late initiation (≥35 years) of smoking with mortality outcomes. HRs and 95% CIs were estimated for each cohort by Cox regression. Cohort-specific HRs were pooled using random-effects meta-analysis.FindingsDuring a mean follow-up of 11.3 years, 92 068 deaths were ascertained. Compared with never smokers, current smokers who consumed <5 cigarettes/day or started smoking after age 35 years had a 16%–41% increased risk of all-cause, cardiovascular disease (CVD), respiratory disease mortality and a >twofold risk of lung cancer mortality. Furthermore, current smokers who started smoking after age 35 and smoked <5 cigarettes/day had significantly elevated risks of all-cause (HRs (95% CIs)=1.14 (1.05 to 1.23)), CVD (1.27 (1.08 to 1.49)) and respiratory disease (1.54 (1.17 to 2.01)) mortality. Even smokers who smoked <5 cigarettes/day but quit smoking before the age of 45 years had a 16% elevated risk of all-cause mortality; however, the risk declined further with increasing duration of abstinence.ConclusionsOur study showed that smokers who smoked a small number of cigarettes or started smoking later in life also experienced significantly elevated all-cause and major cause-specific mortality but benefited from cessation. There is no safe way to smoke—not smoking is always the best choice.


2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 44-44
Author(s):  
M. Kohli ◽  
D. W. Mahoney ◽  
H. S. Chai ◽  
D. W. Hillman ◽  
D. R. Rider ◽  
...  

44 Background: We investigated the association of germline genetic variation in hormone biosynthesis and metabolism genes with prostate cancer specific mortality in a cohort of advanced prostate cancer patients. Methods: We successfully genotyped 852 single nucleotide polymorphisms (SNPs) from 97 genes in a cohort of 267 advanced prostate cancer patients at the time of progression to castration recurrence (CRPC) during on-going androgen ablation. Tagging SNPs with minor allele frequency (MAF) of >5% and r2 ≥0.8 were selected from HapMap, NIEHS and Seattle SNP databases. Medical records were queried for cause of death. The primary endpoint of time to prostate cancer specific mortality (PCSM), was pre-defined as time from development of CRPC to death from prostate cancer progression. Principle components analysis was used for gene-levels tests, and to account for multiple testing, we calculated the false discovery rate (FDR). For SNP level results, hazard ratios (HR) and 95% confidence intervals (CI) were estimated using cox regression. Results: The median age of the cohort was 72 years at CRPC. 43% had a Gleason score (GS)=8-10, 33% a GS=7, and 24% a GS<7. After a median follow-up of 1.8 years (IQ range: 0.8–3.3 years), 139 patients died, of which 107 were due to prostate cancer progression. In unadjusted gene level analyses, UGT1A7 (p=0.0059; FDR=0.19), UGT1A10 (p=0.0017; FDR=0.17) and UGT1A3 (p=0.0037; FDR=0.18) were associated with PCSM. After adjusting for age and GS, SNPs strongly associated with PCSM are listed in the Table . Conclusions: Variation in UGT genes involved in hormone metabolism yield prognostic information in CRPC. Further validation is needed to develop these as prognostic biomarkers. [Table: see text] No significant financial relationships to disclose.


Heart ◽  
2017 ◽  
Vol 104 (13) ◽  
pp. 1076-1085 ◽  
Author(s):  
Mathias Seviiri ◽  
Brigid M Lynch ◽  
Allison M Hodge ◽  
Yi Yang ◽  
Danny Liew ◽  
...  

ObjectiveMost studies investigating the association between resting heart rate (RHR) and mortality have focused on cardiovascular disease (CVD) mortality, and measured RHR at only one time point. We aimed to assess associations of RHR and changes in RHR over approximately a decade with overall and cause-specific mortality.MethodsWe used data from participants in the Melbourne Collaborative Cohort Study with RHR measures at baseline (1990–1994; n=41 386; 9846 deaths) and at follow-up (2003–2007; n=21 692; 2818 deaths). RHR measures were taken by trained staff, using Dinamap monitors. Cox models were used to estimate HR and 95% CI for the associations between RHR and mortality. Vital status and cause of death were ascertained until August 2015 and December 2013, respectively.ResultsAfter adjustment for confounders, including blood pressure and known medical conditions but not arrhythmias or atrial fibrillation, RHR was associated with a higher risk of death of similar magnitude for CVD (HR per 10 beats per minute (bpm)=1.11, 95% CI 1.07 to 1.16), cancer (HR=1.10, 95% CI 1.06 to 1.13) and other causes (HR=1.20, 95% CI 1.16 to 1.25). Higher mortality was observed for most cancer sites, including breast (HR=1.16, 95% CI 1.03 to 1.31), colorectal (HR=1.18, 95% CI 1.08 to 1.29), kidney (HR=1.27, 95% CI 1.03 to 1.57) and lung cancer (HR=1.19, 95% CI 1.10 to 1.29). Temporal increases in RHR were associated with higher mortality, particularly for individuals whose RHR increased by more than 15 bpm.ConclusionsRHR and changes in RHR over a decade are associated with mortality risk, including from causes other than CVD such as breast, colorectal or lung cancer. Monitoring of RHR may have utility in identifying individuals at higher mortality risk.


2020 ◽  
Vol 77 (11) ◽  
pp. 795-797
Author(s):  
Irina Guseva Canu ◽  
Alan Gaillen-Guedy ◽  
Pascal Wild ◽  
Kurt Straif ◽  
Danièle Luce

ObjectivesTitanium dioxide (TiO2) is widely used in construction, food, cosmetic and medical industry. The current evidence on TiO2 carcinogenicity in humans is considered inadequate. As French participants of the European cohort of TiO2 workers exhibited an increase in mortality from lung cancer, we aimed at investigating whether TiO2 exposure, co-exposures or smoking can explain this increase.MethodsWe reanalysed the data of 833 French male workers (follow-up period 1968–1997) and used multiple imputation to complete their smoking status. We considered respirable TiO2 dust as primary exposure of interest, estimated as continuous cumulative (mg/m3-year) and annual average (mg/m3) concentrations and binary and 4-class categorical variables, with cut-off values of 0.3 and 2.4 mg/m3 (the German and American occupational exposure limits, respectively). For each exposure metric, we estimated HRs and associated 95% CIs, using Cox regression models adjusted for calendar period, exposure duration and smoking.ResultsThe fully adjusted model yielded a HR=3.7 (95% CI=0.79 to 17.95) for TiO2-exposed workers vs unexposed and a HR=27.33 (95% CI=4.35 to 171.84) for those exposed to >2.4 mg/m3 as annual average concentration. Employment duration was negatively related with lung cancer mortality, therefore cumulative exposure had a small effect on mortality (HR=1.03 (95% CI=0.99 to 1.08) per mg/m3-year).ConclusionThis study suggests a positive relationship between TiO2 exposure and lung cancer mortality in TiO2 workers, whatever the exposure variable used, despite a limited statistical power in some models. The results question the current evidence on TiO2 carcinogenicity in humans but need to be confirmed in other cohorts, using different statistical approaches.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 7069-7069
Author(s):  
Raymond U Osarogiagbon ◽  
Xinhua Yu

7069 Background: Pathologic nodal stage is a key prognostic factor in resectable non-small cell lung cancer (NSCLC). Mediastinal lymph node (MLN) metastasis connotes a poor prognosis. Yet, some NSCLC resections in the US do not include MLN examination. Methods: We analyzed SEER data from 1998 to 2002 to quantify the long-term survival impact of failure to examine MLN in resected NSCLC. We used Kaplan-Meier methods to compare the unadjusted survival difference between patients with, and without, MLN examination. We used Cox proportional hazards and competing risk models to serially adjust for the impact of risk factors on survival differences. Results: Sixty-two percent of patients with pathologic N0 or N1 NSCLC had no MLN examined. Men, African-Americans, patients with more advanced stage, and those who had less than pneumonectomy were less likely to have MLN examination. Five-year all-cause mortality (46.9% v 51.7%, p<.001), and lung cancer-specific mortality (31.5% v 36%, p<.001), rates were higher in those without MLN examination. After adjustment for potential confounders, MLN examination was associated with a 6% reduction in all-cause mortality (HR, 0.94; CI, 0.89-0.99; p=.014), and 10% reduction in lung cancer-specific mortality (HR, 0.90; 95% CI, 0.84-0.96; p=.002) rates. The excess risk in 1 year’s cohort of U.S. lung resections was 2,700 lives over 5 years. Conclusions: Failure to examine MLN was a common practice in "MLN-negative" NSCLC resections, which significantly impaired long-term survival. Efforts to understand the etiology of this quality gap, and measures to eliminate it, are warranted.


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