PURPOSE: Stigma is an understudied barrier to health care acceptance in pediatric oncology. We sought to explore the stigma experience, including its impact on cancer treatment decision making, and identify strategies to mitigate stigma for patients with osteosarcoma and retinoblastoma in Guatemala, Jordan, and Zimbabwe. METHODS: Participants included caregivers, adolescent patients (age 12-19 years), and health care clinicians. A semistructured interview guide based on The Health Stigma and Discrimination Framework (HSDF) was adapted for use at each site. Interviews were conducted in English, Spanish, Arabic, or Shona, audio-recorded, translated, and transcribed. Thematic analysis focused on stigma practices, experiences, outcomes, drivers, mitigators, and interventions. RESULTS: We conducted 56 interviews (28 caregivers, 19 health care clinicians, nine patients; 20 in Guatemala, 21 in Jordan, 15 in Zimbabwe). Major themes were organized into categories used to adapt the HSDF to global pediatric cancer care. Themes were described similarly across all sites, ages, and diagnoses, with specific cultural nuances noted. Pediatric cancer stigma was depicted as an isolating and emotional experience beginning at diagnosis and including internalized and associative stigma. Stigma affected decision making and contributed to negative outcomes including delayed diagnosis, treatment abandonment, regret, and psychosocial fragility. Overcoming stigma led to positive outcomes including resilience, treatment adherence, pride, and advocacy. Identified stigma drivers and mitigators were linked to potential interventions. CONCLUSION: Participants describe a shared stigma experience that transcends geography, cultural context, age, and diagnosis. Stigma manifestations have the potential to impact medical decision making and affect long-term psychological outcomes. Stigma assessment tools and interventions aimed at stigma mitigation including educational initiatives and support groups specific to pediatric cancer should be the focus of future research.

PURPOSE: Stigma contributes to fear and shame, resulting in delays in care-seeking behavior among individuals with cancer. As a social construct, stigma is affected by language, religion, culture, and local norms. This study explored pediatric cancer stigma at the time of diagnosis across diverse settings through the adaptation of two stigma measures. METHODS: This study was conducted with adolescents and caregivers of children with osteosarcoma and retinoblastoma at three centers in Jordan, Guatemala, and Zimbabwe. The Stigma-related Social Problems (SSP) and the eight-item Stigma Scale for Chronic Illness (SSCI-8) measures were translated into Arabic, Spanish, and Shona and contextually adapted for use with adolescents and caregiver proxies. Adapted measures were pilot-tested and iteratively revised. RESULTS: Extensive adaptations were made to both measures to make them relevant to the local pediatric contexts. The final measures were used in nine patients and 28 caregivers. The exploratory analysis found that domain-specific and overall scale scores for both measures indicate a higher level of stigma than those found in previous studies (SSP: patient [51.23], caregiver [40.74]; SSCI-8: patient [50.41], caregiver [49.78]). Paired, patient-caregiver proxy responses were analyzed, with disagreement between the pairs for both scales. CONCLUSION: Adapted measures detected high levels of stigma among patients with pediatric cancer and their caregiver proxies and demonstrated a lack of concordance in the reports. This suggests the importance of studying stigma in this population and the need to ask patients about their stigma without using proxy measures. The required adaptations suggest a need for stigma measures developed specifically for pediatric cancer.

Background: Globally, over 2 million new cases of lung cancer are diagnosed annually, representing about 11% of all cancers

Capecitabine is an oral prodrug that is converted to 5-FU via three enzyme-catalysed steps: carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TYMS). Approximately 80–90% of 5-FU, whether from capecitabine or direct administration, is quickly inactivated by dihydropyrimidine dehydrogenase (DPD), encoded by DPYD. Preemptive testing for four pathogenic DPYD variants that reduce DPD activity is advised; however, currently, no evidence for CES, CDA, or TYMS has necessitated a similar recommendation despite polymorphisms in these genes potentially causing treatment toxicity. The current preemptive testing guidelines for 5-FU and capecitabine are similar. A 74-year-old black woman with a caecal adenocarcinoma diagnosis of pT_4bG₁N₀M₀ was prescribed adjuvant oxaliplatin and capecitabine post-hemicolectomy. On day 16 of the first cycle, she presented with severe gastrointestinal, myelosuppressive, hand and foot side effects and enterocolitis infection. She underwent a pharmacogenomic workup with whole-exome sequencing and was noted to be genetically DPD non-deficient (DPYD *1/*9A). She was found to express CDA rs3215400 (c.-33delC) and CDA rs1048977, both of which are associated with an increased risk of toxicity from capecitabine. CDA rs3215400 has been specifically described as an ultrametabolizer variant with an observation to increase enzyme activity by 3–7 fold and the occurrence of adverse drug events in capecitabine. After recovery and follow-up, she continued to receive 5-FU, leucovorin, and oxaliplatin therapy which she tolerated well and completed six months of therapy. This case shows that the severe adverse effects of capecitabine therapy in a patient with a CDA ultrametabolizer profile can be successfully switched to 5-FU-based therapy at a normal dose and tolerate this alternative fluoropyrimidine.

Background: Infection with HIV increases the risk of developing hepatocellular carcinoma, and the albumin–bilirubin grade assesses liver function and has been shown to be prognostic. We evaluated the albumin–bilirubin score/grade and the HIV status of hepatocellular carcinoma patients in Zimbabwe and explored the impact on median survival. Methods: A 10-year retrospective observational study of hepatocellular carcinoma patients was conducted at a single tertiary-level cancer center in Harare, Zimbabwe. Survival probabilities were estimated using the Kaplan–Meier method, and differences between groups were compared using the log-rank test and Cox proportional hazards regression. Results: A total of 95 participants were evaluated, of whom 72.6% were male. Most HCC cases were diagnosed using imaging and serum alpha-fetoprotein, with 59% presenting at Barcelona Clinic Liver Cancer stage C or D. Compared with patients who were HIV-negative, patients who were HIV-positive (OR 2.2; 95% CI 1.54–5.26, p = 0.0008) or had an unknown HIV status (OR 4.2; 95% CI 2.2–8; p < 0.0001) had higher odds of being at ALBI grade 3 at the time of HCC diagnosis. ALBI grade 1 patients had better median survival compared to grade 2 and 3 patients, though this result was statistically insignificant (grade 2: HR = 1.45, 95% CI: 0.30–7.13; grade 3: HR = 1.47, 95% CI: 0.28–7.60). Regarding HIV status, median survival was 2.4 months for HIV-positive patients and 2.6 months for HIV-negative patients (p = 0.51); HIV positivity was not significantly associated with median survival (HR = 1.50, 95% CI: 0.46–4.91). Only 30.5% of patients received cancer therapy, all of which was palliative, with no observed survival benefit. Conclusions: The majority of hepatocellular carcinoma patients in Zimbabwe were diagnosed at an advanced stage, with hepatitis B or C viral infections and alcohol consumption identified as primary risk factors. Median survival rates were low. Neither HIV infection nor ALBI score grading had a significant impact on median survival.