scholarly journals Determinants of survival in children with cancer in Johannesburg, South Africa

2021 ◽  
Vol 5 ◽  
Author(s):  
Nadia Beringer ◽  
Kate G. Bennett ◽  
Janet E. Poole ◽  
Jennifer A. Geel

Background: Childhood cancer, although rare, remains an important cause of death worldwide. The outcomes of children with all cancer types in South Africa are not well-documented.Aim: The aim of the article was to determine local childhood cancer survival rates and establish determinants of survival.Setting: The study was conducted at a state and a private hospital in South Africa.Methods: This retrospective cohort study consecutively included all children with a proven malignancy from 01 January 2012 to 31 December 2016. Univariable and multivariable analyses were used to establish which factors significantly impacted overall survival (OS).Results: Of a total of 677 study participants, 71% were black South Africans. The estimated 5-year overall survival (OS) was 57% (95% confidence interval [CI]: 53-61%) and significant determinants of OS on the multivariable analysis included: ethnicity, cancer-type and nutritional status. White and Indian patients had higher OS compared to black patients (hazard ration [HR] (95% CI) 0.46 (0.30-0.69) p = 0.0002 and HR (95%) 0.38 (0.19-0.78) p = 0.0087, respectively). Underweight patients had inferior survival (HR (95% CI) 1.78 (1.28-2.47)) p = 0.0006. Patients with neuroblastoma had an increased risk of dying compared to those with leukaemia (HR [95% CI] 1.78 [1.08-2.94]) p = 0.025. Progression of disease was the most common cause of death, followed by disease relapse.Conclusion: The childhood cancer survival rate obtained in this study can be used as a baseline to facilitate improvement. Non-modifiable prognostic factors included ethnicity and cancer-type whilst modifiable risk factors included undernutrition. Undernutrition should be addressed on a national and local level to improve survival.

2001 ◽  
Vol 37 (6) ◽  
pp. 810-816 ◽  
Author(s):  
B. Terracini ◽  
J.-W. Coebergh ◽  
G. Gatta ◽  
C. Magnani ◽  
C. Stiller ◽  
...  

2021 ◽  
Author(s):  
Silvia Ravera ◽  
Tiziana Vigliarolo ◽  
Silvia Bruno ◽  
Fabio Morandi ◽  
Danilo Marimpietri ◽  
...  

ABSTRACTPurposeSurvival rates of Childhood Cancer Patients have improved tremendously over the past four decades. However, cancer treatments are associated with an increased risk of developing an anticipated onset of chronic diseases typical of aging. Thus, we aimed to identify molecular/metabolic cellular alterations responsible for early aging in Childhood Cancer Survivors (CCS).Patients and MethodsBiochemical, proteomic and molecular biology analyses were conducted on mononuclear cells (MNCs) isolated from peripheral blood of 196 CCS, comparing the results with those obtained on MNCs of 154 healthy subjects.ResultsData demonstrate that CCS-MNCs show: i) inefficient oxidative phosphorylation associated with low energy status and a metabolic switch to lactate fermentation compared with age-matched normal controls; ii) increment of lipid peroxidation due to an unbalance among the oxidative stress production and the activation of the antioxidant defenses; (iii) significantly lower expression of genes and proteins involved in mitochondrial biogenesis and metabolism regulation, such as CLUH, PGC1-α, and SIRT6 in CCS, not observed in the age-matched healthy or elderly subjects. The application of a mathematical model based on biochemical parameters predicts that CCS have a biological age significantly increased by decades compared to the chronological age. Overall, the results show that the impact of chemo/chemoradiotherapy on mitochondria efficiency in 196 CCS was rather homogeneous, irrespective of cancer type, treatment protocols, and time elapsed from the end of the curative period.ConclusionsOur study identifies some biochemical and molecular alterations possibly contributing to the pathophysiology of anticipated aging and metabolic deficiency described in CCS. These results may be useful in identifying approaches to restore the mitochondrial function, slowing down the aging and the associated pathological conditions in CCS.


2020 ◽  
Vol 27 (1) ◽  
pp. 1-9
Author(s):  
Jelena Rascon ◽  
Giedrė Smailytė

Background. Population-based EUROCARE-5 studies demonstrated that childhood cancer survival rates in Lithuania were 10–20% lower than the European mean. We aimed to analyse the change in the outcome of treatment of paediatric malignancies in Lithuania over 30 years. Methods. A single-centre retrospective analysis of children below 18 years of age treated for cancer at Vilnius University Hospital Santaros Klinikos between 1982 and 2011 was carried out. The minimal requirement of 5-year follow-up after diagnosis was specified for survival estimation. The vital status was assessed using data from the population-based Lithuanian Cancer Registry. To evaluate changes over time, the entire cohort was split into three groups according to the time of diagnosis: 1982–1991, 1992–2001, and 2002–2011. Results. A total of 1268 children met the inclusion criteria. The shortest median follow-up was 8.9 (IQR 6.4–11.5) years for patients treated in the third decade. The 5-year overall survival of the entire cohort increased from 37.3% (95% CI 30.2–44.3) in 1982–1991 to 70.7% (95% CI 66.4–74.1) in 2002–2011 (p < 0.0001). The same trend was evident when calculated separately for leukaemia (p < 0.0001), lymphoma (p < 0.0005), and solid tumours (p < 0.004). The percentage of cure rose from zero in the early years of the period analysed to 80% in 2010 and 2011. The improvement in the treatment outcome was attributable to the reduction of treatment-related mortality from 45.8% in 1982–1991 to 12.4% in 2002–2011 and disease recurrence from 30.4% to 19.6% for the same periods, respectively. Conclusions. Significant progress in the cure rate of children treated for cancer at our institution was observed over 30 years. Collaborative national and international clinical and research efforts are crucial to ensure further advances in care and cure.


2019 ◽  
Vol 20 (7) ◽  
pp. 972-983 ◽  
Author(s):  
Zachary J Ward ◽  
Jennifer M Yeh ◽  
Nickhill Bhakta ◽  
A Lindsay Frazier ◽  
Fabio Girardi ◽  
...  

2020 ◽  
Vol 4 (5) ◽  
Author(s):  
Erin L Marcotte ◽  
Jeremy M Schraw ◽  
Tania A Desrosiers ◽  
Wendy N Nembhard ◽  
Peter H Langlois ◽  
...  

Abstract Background There is a persistent, unexplained disparity in sex ratio among childhood cancer cases, whereby males are more likely to develop most cancers. This male predominance is also seen for most birth defects, which are strongly associated with risk of childhood cancer. We conducted mediation analysis to estimate whether the increased risk of cancer among males is partially explained by birth defect status. Methods We used a population-based birth cohort with linked data from birth certificates, birth defects registries, and cancer registries from Arkansas, Michigan, North Carolina, and Texas. We conducted counterfactual mediation analysis to estimate the natural direct and indirect effects of sex on cancer risk, modeling birth defect status as mediator. State; birth year; plurality; and maternal race and ethnicity, age, and education were considered confounders. We conducted separate analyses limited to cancers diagnosed younger than 1 year of age. Results Our dataset included 10 181 074 children: 15 110 diagnosed with cancer, 539 567 diagnosed with birth defects, and 2124 co-occurring cases. Birth defect status mediated 38% of the association between sex and cancer overall. The proportion mediated varied by cancer type, including acute myeloid leukemia (93%), neuroblastoma (35%), and non-Hodgkin lymphoma (6%). Among children younger than 1 year of age at cancer diagnosis, the proportion mediated was substantially higher (82%). Conclusions Our results suggest that birth defects mediate a statistically significant proportion of the relationship between sex and childhood cancer. The proportion mediated varied by cancer type and diagnosis age. These findings improve our understanding of the causal pathway underlying male sex as a risk factor for childhood cancer.


Cancer ◽  
2002 ◽  
Vol 95 (8) ◽  
pp. 1767-1772 ◽  
Author(s):  
Gemma Gatta ◽  
Riccardo Capocaccia ◽  
Michel P. Coleman ◽  
Lynn A. Gloeckler Ries ◽  
Franco Berrino

2019 ◽  
Vol 37 (27_suppl) ◽  
pp. 143-143
Author(s):  
Jingxuan Zhao ◽  
Xuesong Han ◽  
Zhiyuan Zheng ◽  
Leticia Maciel Nogueira ◽  
Paul C. Nathan ◽  
...  

143 Background: Childhood cancer survival varies by race/ethnicity in the United States. This study evaluated the impact of potentially modifiable characteristics - health insurance and area-level social deprivation - on racial/ethnic disparities in childhood cancer survival nationwide. Methods: We identified 65,113 childhood cancer patients aged < 18 years newly diagnosed with any of 10 common cancer types (e.g. central nervous system (CNS) neoplasms, acute lymphoblastic leukemia (ALL), Hodgkin lymphoma) from the 2004-2014 National Cancer Database. Cox proportional hazard models were used to compare survival probabilities by race and ethnicity (non-Hispanic white (NHW) vs non-Hispanic black (NHB), Hispanic, and non-Hispanic other (NH other)) for each cancer type. We conducted mediation analyses by the mma R package to evaluate the racial/ethnic survival disparities mediated by health insurance (private, Medicaid, and uninsured) and social deprivation index (SDI) quartile. SDI is a composite measure of deprivation based on seven characteristics (e.g. income, education, employment). Results: Compared to NHW, worse survival were observed for NHB (HR (hazard ratio): 1.4, 95% CI: 1.3-1.5), Hispanic (HR: 1.2, 95% CI: 1.1-1.2), and NH other (HR: 1.2, 95% CI: 1.1-1.3) for all cancer sites combined after adjusting for sociodemographic characteristics other than health insurance and SDI. Health insurance explained 20% of the survival disparities and SDI explained 19% of the disparity between NHB vs NHW; health insurance explained 48% of the survival disparities and SDI explained 45% of the disparity between Hispanic vs NHW. For ALL, health insurance significantly explained 15% and 18% of the survival disparities between NHB and Hispanic vs NHW, respectively. SDI significantly explained 19% and 31% of the disparities, respectively. Conclusions: Health insurance and SDI mediated racial/ethnic survival disparities for several childhood cancers. Expanding insurance coverage and improving healthcare access in disadvantaged areas may effectively reduce disparities for these cancer sites.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e16781-e16781
Author(s):  
Jori Lee Kaplan ◽  
Benjamin Powers ◽  
Wenyi Fan ◽  
Michael J. Schell ◽  
Barbara Centeno ◽  
...  

e16781 Background: Borderline resectable pancreatic ductal adenocarcinoma (BR PDAC) is a subset of pancreatic cancer with unique prognostic implications. A multimodality, neoadjuvant therapy (NAT) approach has known benefits such as downstaging tumors, reducing the risk of a positive margin, and treating micrometastatic disease. Patient selection and therapy sequencing are controversial owing to the high risk of recurrence. Therefore, we aimed to identify factors predicting recurrence and overall survival (OS) in BR PDAC patients undergoing NAT. Methods: We identified BR PDAC patients treated with NAT followed by surgery at Moffitt Cancer Center between 2008-2015. We evaluated clinical, demographic, and perioperative factors to identify predictors of recurrence and OS. Statistical analyses were performed with univariate and multivariable Cox regression models. Results: 117 patients with BR PDAC who received NAT were evaluated; 53 (45%) were female and 64 (55%) were male. Of those, 91 (78%) received gemcitabine/xeloda/taxotere and the remainder received other gemcitabine or 5FU regimens. 107 (91%) patients received neoadjuvant radiation, mainly 5-day dose painted SBRT. Post- NAT CA 19-9 normalized in 39 (33%) and 11 (9%) additional patients normalized after surgery. Pathologic treatment effect was appreciated in 85 (73%) patients and pathologic complete response (pCR) was seen in 18 (15%). 95 (81%) patients initiated adjuvant therapy. In multivariable analysis, the strongest predictor of recurrence was higher log(10) post-operative CA 19-9 (HR 2.29; 95% CI, 1.40-3.75). Time from initiation of NAT to surgery ≥ 5 months also predicted recurrence (HR 2.08; 95% CI, 1.16-3.72). In OS analysis, 71 patients had recurrence after multimodality treatment; 61 (86%) died and 10 (14%) were alive. In multivariable analysis, the strongest predictors of prolonged OS from recurrence were female gender (HR 0.47; 95% CI, 0.26-0.84) and presence of a treatment effect (HR 0.37; 95% CI, 0.15-0.93). Conclusions: We observed treatment effects and pCR comparable to other institutions, supporting a multimodality approach to BR PDAC. Higher post-operative CA 19-9 and time to surgery ≥ 5 months from initiation of NAT were associated with an increased risk of recurrence. These data suggest that timely receipt of surgery after completion of NAT may impact recurrence and OS in BR PDAC.


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