Risks of second primary cancer among patients with major histological types of lung cancers in both men and women.
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ABSTRACT: Background
Patterns of second primary cancers (SPCs) following first primary lung cancers (FPLCs) may provide aetiological insights into FPLC.Methods
Cases of FPLCs in 13 cancer registries in Europe, Australia, Canada, and Singapore were followed up from the date of FPLC diagnosis to the date of SPC diagnosis, date of death, or end of follow-up. Standardised incidence ratios (SIRs) were calculated to estimate the magnitude of SPC development following squamous cell carcinoma (SCC), small cell lung carcinoma (SCLC), and adenocarcinoma (ADC).Results
Among SCC patients, male SIR=1.58 (95% confidence interval (CI)=1.50-1.66) and female SIR=2.31 (1.94-2.72) for smoking-related SPC. Among SCLC patients, the respective ratios were 1.39 (1.20-1.60) and 2.28 (1.73-2.95), and among ADC patients, they were 1.73 (1.57-1.90) and 2.24 (1.91-2.61). We also observed associations between first primary lung ADC and second primary breast cancer in women (SIR=1.25, 95% CI=1.05-1.48) and prostate cancer (1.56, 1.39-1.79) in men.Conclusion
The FPLC patients carried excess risks of smoking-related SPCs. An association between first primary lung ADC and second primary breast and ovarian cancer in women at younger age and prostate cancers in men may reflect an aetiological role of hormones in lung ADC.
SUBMITTER: Chuang SC
PROVIDER: S-EPMC2853101 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ImportanceIn the last 4 decades, survival among patients with human papillomavirus (HPV)-associated cancers has improved, while the incidence of these cancers has increased among younger cohorts. Among survivors of HPV-associated cancers, persistent HPV infection may remain a risk factor for preventable HPV-associated second primary cancers (HPV-SPCs).ObjectivesTo investigate the risk of HPV-SPCs among survivors of HPV-associated index cancers and to test the hypothesis that the HPV-SPC risk among these persons has increased over the last 4 decades.Design, setting, and participantsA retrospective cohort study of 9 cancer registries of the Surveillance, Epidemiology, and End Results (SEER) database was conducted to identify patients with HPV-associated (cervical, vaginal, vulvar, oropharyngeal, anal, and penile) cancers diagnosed from January 1, 1973, through December 31, 2014. The dates of analysis were July 1, 2017, to January 31, 2018.Main outcomes and measuresThe HPV-SPC risk was quantified by calculating standard incidence ratios (SIRs) and excess absolute risks (EARs) per 10 000 person-years at risk (PYR). The HPV-SPC risk by time was estimated using Poisson regression.ResultsFrom 113 272 (73 085 female and 40 187 male) survivors of HPV-associated cancers, 1397 women and 1098 men developed HPV-SPCs. The SIRs for HPV-SPCs were 6.2 (95% CI, 5.9-6.6) among women and 15.8 (95% CI, 14.9-16.8) among men. The EARs were 18.2 per 10 000 PYR for women and 53.5 per 10 000 PYR for men. Among both women and men, those who had index oropharyngeal cancers had the highest HPV-SPC risk (SIR, 19.8 [95% CI, 18.4-21.4] and EAR, 80.6 per 10 000 PYR among women; SIR, 18.0 [95% CI, 16.9-19.1] and EAR, 61.5 per 10 000 PYR among men). Women who had index cervical cancers and men who had index anal cancers had the lowest HPV-SPC risk (SIR, 2.4 [95% CI, 2.2-2.7] and EAR, 4.5 per 10 000 PYR among women; SIR, 6.5 [95% CI, 4.7-8.8] and EAR, 18.5 per 10 000 PYR among men). Both women and men who had index HPV-associated cancers of any kind had a significantly higher risk of oropharyngeal HPV-SPCs. Over the last 4 decades, the risk of developing most types of HPV-SPCs after index cervical, vaginal, and vulvar cancers increased.Conclusions and relevanceAccording to this study, the HPV-SPC risk among survivors of HPV-associated cancers is significant, implying that persistent HPV infection at multiple sites may be associated with HPV-SPCs. These findings have the potential to inform surveillance recommendations for survivors of HPV-associated cancers.
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Project description:BackgroundSecond primary cancers (SPCs) are increasing due to improving survival in first primary cancers. Previous studies on SPCs in renal cell carcinoma (RCC) have focused on treatment and other risk factors, but data of RCC as an SPC are scarce.ObjectiveIn this study, we want to elucidate the risk for any SPC after RCC, and in reverse order, for RCC as an SPC after any cancer. We additionally consider how family histories influence the risks.Design setting and participantsPatient data were obtained from the Swedish Cancer Registry from years 1990 through 2015, and family data were obtained from the Multigeneration Register.Outcome measurements and statistical analysisWe employed standardized incidence ratios to estimate bidirectional relative risks of subsequent cancer associated with RCC.Results and limitationsWe identified 17 587 RCCs (60% in male patients). The highest increases for SPCs were observed for nervous system hemangioblastoma (HB; 26.8), adrenal (12.09) tumors, and renal pelvic cancer (6.32). In the reverse order, RCC as an SPC, nervous system HB (17.01), and adrenal tumors (15.34) were associated with the highest risks. Risks for many other sites (12 sites and subsites) were increased bidirectionally. For women, a total of seven sites and subsites were increased bidirectionally, and many were shared with men. The only significant sex difference in SPCs was the higher lung cancer risk in women (2.41) than in men (1.28). Patients with a family history of HBs or of prostate, colorectal and lung cancers showed high risks of these cancers as SPCs after RCC. Family history accounted for 30% of prostate cancers after RCC.ConclusionsThe bidirectional study design was able to suggest risk factors for SPCs and offered a clinical take-home message urging to consider strategies for early detection and prevention of SPCs. Readily available information on lifestyle (eg, smoking) and family history (eg, prostate cancer) may reveal targets for risk reduction with prognostic benefits.Patient summaryClose to 10% of kidney cancer patients develop another cancer. The cause for these other cancers may not depend on kidney cancer.
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Project description:BACKGROUND: This study examined the risk of third cancer of non-breast origin (TNBC) among women with bilateral breast cancer (BBC; either synchronous or metachronous), focussing on the relation with breast cancer treatment. METHODS: Risk was assessed, among 8752 Dutch women diagnosed with BBC between 1989 and 2008, using standardised incidence ratios (SIR) and Cox regression analyses to estimate the hazard ratio (HR) of TNBC for different treatment modalities. RESULTS: Significant increased SIRs were observed for all TNBCs combined, haematological malignancies, stomach, colorectal, non-melanoma skin, lung, head and neck, endometrial, and ovarian cancer. A 10-fold increased risk was found for ovarian cancer among women younger than 50 years (SIR=10.0, 95% confidence interval (CI)=5.3-17.4). Radiotherapy was associated with increased risks of all TNBCs combined (HR=1.3; 95%CI=1.1-1.6, respectively). Endocrine therapy was associated with increased risks of all TNBCs combined (HR=1.2; 95%CI=1.0-1.5), haematological malignancies (HR=2.0; 95%CI=1.1-3.9), and head and neck cancer (HR=3.3; 95%CI=1.1-10.4). After chemotherapy decreased risks were found for all TNBCs combined (HR=0.63; 95%CI=0.5-0.87). CONCLUSION: Increased risk of TNBC could be influenced by genetic factors (ovarian cancer) or an effect of treatment (radiotherapy and endocrine therapy). More insight in the TNBC risk should further optimise and individualise treatment and surveillance protocols in (young) women with BBC.
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Project description:We report a comprehensive proteogenomics analysis, including whole-genome sequencing, RNA sequencing, and proteomics and phosphoproteomics profiling, of 218 tumors across 7 histological types of childhood brain cancer: low-grade glioma (n = 93), ependymoma (32), high-grade glioma (25), medulloblastoma (22), ganglioglioma (18), craniopharyngioma (16), and atypical teratoid rhabdoid tumor (12). Proteomics data identify common biological themes that span histological boundaries, suggesting that treatments used for one histological type may be applied effectively to other tumors sharing similar proteomics features. Immune landscape characterization reveals diverse tumor microenvironments across and within diagnoses. Proteomics data further reveal functional effects of somatic mutations and copy number variations (CNVs) not evident in transcriptomics data. Kinase-substrate association and co-expression network analysis identify important biological mechanisms of tumorigenesis. This is the first large-scale proteogenomics analysis across traditional histological boundaries to uncover foundational pediatric brain tumor biology and inform rational treatment selection.
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Project description:BackgroundThe differential occurrence of second primary cancers by race following ovarian cancer is poorly understood. Our objective was to determine the incidence of second primary gynecologic cancers (SPGC) following definitive therapy for ovarian cancer. Specifically, we aimed to determine differences in SPGC incidence by Asian ethnic subgroups.MethodsWe identified 27,602 women ages 20 years and older and diagnosed with first primary epithelial ovarian cancer between 2000 and 2016 who received surgery and chemotherapy in 18 population-based Surveillance, Epidemiology and End Results Program registries. We compared the incidence of SPGC with expected incidence rates in the general population of women using estimated standardized incidence ratios (SIR) and 95% confidence intervals (CI).ResultsThe incidence of SPGC was lower among White women (SIR = 0.73; 95% CI, 0.59-0.89), and higher among Black (SIR = 1.80; 95% CI, 0.96-3.08) and Asian/Pacific Islander (API) women (SIR = 1.83; 95% CI, 1.07-2.93). Increased risk of vaginal cancers was observed among all women, although risk estimates were highest among API women (SIR = 26.76; 95% CI, 5.52-78.2) and were also significant for risk of uterine cancers (SIR = 2.53; 95% CI, 1.35-4.33). Among API women, only Filipinas had significantly increased incidence of SPGC overall including both uterine and vaginal cancers.ConclusionsRisk of SPGC following treatment of ovarian cancer differs by race and ethnicity, with Filipina women having the highest rates of second gynecologic cancers among Asian women.ImpactEnsuring access and adherence to surveillance may mitigate ethnic differences in the early detection and incidence of second gynecologic cancers.
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2022-10-17 | PXD031467 |
Project description:<p>Francesca Petralia,Nicole Tignor,Boris Reva, et al., (2020) <a href="https://www.cell.com/cell/fulltext/S0092-8674(20)31451-3" target="_blank">Cell 183, 1962-1985</a></p><p>We report a comprehensive proteogenomics analysis, including whole-genome sequencing, RNA sequencing, and proteomics and phosphoproteomics profiling, of 218 tumors across 7 histological types of childhood brain cancer: low-grade glioma (n = 93), ependymoma (32), high-grade glioma (25), medulloblastoma (22), ganglioglioma (18), craniopharyngioma (16), and atypical teratoid rhabdoid tumor (12). Proteomics data identify common biological themes that span histological boundaries, suggesting that treatments used for one histological type may be applied effectively to other tumors sharing similar proteomics features. Immune landscape characterization reveals diverse tumor microenvironments across and within diagnoses. Proteomics data further reveal functional effects of somatic mutations and copy number variations (CNVs) not evident in transcriptomics data. Kinase-substrate association and co-expression network analysis identify important biological mechanisms of tumorigenesis. This is the first large-scale proteogenomics analysis across traditional histological boundaries to uncover foundational pediatric brain tumor biology and inform rational treatment selection.</p><p>The Children's Brain Tumor Network (CBTN) and the Pacific Pediatric Neuro-Oncology Consortia (PNOC) are collaborative research consortia focused on identifying therapies for children with brain tumors (<a href="https://cbttc.org" target="_blank">https://cbttc.org</a>). The consortia have contributed a <a href="https://kidsfirstdrc.org/support/studies-and-access/#SD_BHJXBDQK" target="_blank">Pediatric Brain Tumor Atlas (PBTA) dataset</a>, a cohort of 991 brain tumor subject clinical data, with associated whole genome sequencing and RNAseq hosted by the Gabriella Miller Kids First Data Resource (<a href="https://kidsfirstdrc.org/" target="_blank">kidsfirstdrc.org</a>) as part of the Gabriella Miller Kids First Pediatric Research Program (Kids First). Kids First is a Pan NIH Common Fund program dedicated to the development of large-scale data resources to help researchers uncover new insights into the biology of childhood cancer and structural birth defects (<a href="https://commonfund.nih.gov/KidsFirst" target="_blank">https://commonfund.nih.gov/KidsFirst</a>).</p><p>Mass Spectrometry raw data generation along with preliminary analyses were performed at the <a href="https://tcmp.hms.harvard.edu/" target="_blank">Thermo Fisher Scientific Center for Multiplexed Proteomics (TCMP)</a>, Harvard Medical School (HMS) under the direction of <a href="https://cellbio.med.harvard.edu/people/faculty/gygi" target="_blank">Prof. Steven Gygi</a>. Samples were prepared using the streamline (SL)-TMT protocol (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5994137/" target="_blank">Navarrete-Perea et al., 2018</a>) and MS analysis was performed using the SPS-MS3 strategy (<a href="https://www.nature.com/articles/nmeth.1714" target="_blank">Ting et al., 2011</a>) developed in the <a href="https://gygi.med.harvard.edu/" target="_blank">Gygi lab</a>. Additional data analyses from the CPTAC Common Data Analysis Pipeline (<a href="https://www.ncbi.nlm.nih.gov/pubmed/26860878" target="_blank">Rudnick et al., 2016</a>) and from the University of Michigan Proteomics and Integrative Bioinformatics Laboratory (<a href="https://github.com/Nesvilab" target="_blank">https://github.com/Nesvilab</a>) are also provided. All raw and processed genomic data, as well as pathology reports, radiology reports, MRIs, histology slide images are accessible via the <a href="https://portal.kidsfirstdrc.org/dashboard" target="_blank">Kids First DRC (Data Resource Center)</a>.</p>
2021-02-04 | MSV000086810 | MassIVE
Project description:BackgroundPrevious population-based studies on second primary cancers (SPCs) in urothelial cancers have focused on known risk factors in bladder cancer patients without data on other urothelial sites of the renal pelvis or ureter.AimsTo estimate sex-specific risks for any SPCs after urothelial cancers, and in reverse order, for urothelial cancers as SPCs after any cancer. Such two-way analysis may help interpret the results.MethodsWe employed standardized incidence ratios (SIRs) to estimate bidirectional relative risks of subsequent cancer associated with urothelial cancers. Patient data were obtained from the Swedish Cancer Registry from years 1990 through 2015.ResultsWe identified 46 234 urinary bladder cancers (75% male), 940 ureteral cancers (60% male), and 2410 renal pelvic cancers (57% male). After male bladder cancer, SIRs significantly increased for 9 SPCs, most for ureteral (SIR 41.9) and renal pelvic (17.2) cancers. In the reversed order (bladder cancer as SPC), 10 individual FPCs were associated with an increased risk; highest associations were noted after renal pelvic (21.0) and ureteral (20.9) cancers. After female bladder cancer, SIRs of four SPCs were significantly increased, most for ureteral (87.8) and pelvic (35.7) cancers. Female bladder, ureteral, and pelvic cancers associated are with endometrial cancer.ConclusionsThe risks of recurrent urothelial cancers were very high, and, at most sites, female risks were twice over the male risks. Risks persisted often to follow-up periods of >5 years, motivating an extended patient follow-up. Lynch syndrome-related cancers were associated with particularly female urothelial cancers, calling for clinical vigilance.
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Project description:BackgroundDue to its rarity and high heterogeneity, neither established guidelines nor prospective data are currently available for using chemotherapy in the treatment of appendiceal cancer. This study was to determine the use of chemotherapy and its potential associations with survival in patients with different histological types of the cancer.MethodsPatients with histologically different appendiceal cancers diagnosed during 1998-2016 were selected from the Surveillance, Epidemiology, and End Results (SEER) database. The role and effect of chemotherapy were examined in the treatment of the disease. The Kaplan-Meier method was applied to construct survival curves and significance was examined by Log-rank test. Cox proportional hazard models were used to analyze the impact of chemotherapy and other variables on survival in these patients.ResultsA total of 8733 appendiceal cancer patients were identified from the database. Chemotherapy was administrated at highly variable rates in different histological types of appendiceal cancer. As high as 64.0% signet ring cell carcinoma (SRCC), 46.4% of mucinous adenocarcinomas (MAC), 40.6% of non-mucinous adenocarcinoma (NMAC) and 43.9% of mixed neuroendocrine non-neuroendocrine neoplasms (MiNENs) were treated with chemotherapy, whereas only 14.7% of goblet cell carcinoma (GCC), 5% neuroendocrine tumors (NETs) and 1.6% carcinomas (NEC) received chemotherapy. In all patients combined, chemotherapy significantly improved overall survival during the entire study period and cancer-specific survival was improved during in cases from 2012-2016. Further multivariate analysis showed that both cancer-specific and overall survival was significantly improved with chemotherapy in patients with MAC, NMAC and SRCC, but not for patients with GCC, MiNENs, NETs and NECs. Number (> 12) of lymph node sampled was associated with survival of patients with most histological types of cancer under study. Other prognostic factors related to individual histological types were identified.ConclusionsChemotherapy is administrated at highly variable rates in different histological types of appendiceal cancer. Efficacy of chemotherapy in the treatment of these cancers has been improved in recent years and is significantly associated with better survival for patients with NMAC, MAC, and SRCC. Adequate lymph node sampling may result in a survival benefit for most of these patients.
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