An evaluation of a palliative care outreach programme for children with Burkitt lymphoma in rural Cameroon.

BACKGROUND: Palliative care (PC) is the most appropriate treatment for patients with life-limiting, incurable diseases, but it is a relatively new concept in sub-Saharan Africa (SSA). A lack of curative treatment options for some conditions creates a great need for PC, but such services are rarely provided in SSA. More research into PC in SSA is urgently needed to create an evidence base to confirm the importance of appropriate PC services. OBJECTIVES: To gain a better understanding of the needs of patients and their families visited by a children's PC nurse in Cameroon and to identify aspects of the service that can be improved. METHODOLOGY: A qualitative study design with semi-structured interviews was used. Tape-recorded interviews were transcribed and thematically analysed. RESULTS: Twelve interviews were conducted with patients, carers and nurses. Financial aid, general disease improvement and prayers were the directly expressed needs of service recipients. Specialist training in children's PC was the main need expressed by the nurses. Open communication about clinical status and treatment failure, more detailed counselling, more distraction for patients and respite for carers were identified as underlying needs. CONCLUSION: It is possible to provide an effective children's PC service that meets the most urgent needs of recipients in a rural setting in SSA. Recommendations include improved counselling, specialist education for staff, expansion of local support networks and more frequent home visits. More studies are needed to help define the need for PC in children with life-limiting diseases.

MSF Paediatric Days: a step forward in operationalising 'Humanitarian Paediatrics'.

Around the world, one in four children live in a country affected by conflict, political insecurity and disaster. Healthcare in humanitarian and fragile settings is challenging and complex to provide, particularly for children. Furthermore, there is a distinct lack of medical literature from humanitarian settings to guide best practice in such specific and resource-limited contexts. In light of these challenges, Médecins Sans Frontières (MSF), an international medical humanitarian organisation, created the MSF Paediatric Days with the aim of uniting field staff, policymakers and academia to exchange ideas, align efforts, inspire and share frontline research and experiences to advance humanitarian paediatric and neonatal care. This 2-day event takes place regularly since 2016. The fourth edition of the MSF Paediatric Days in April 2021 covered five main topics: essential newborn care, community-based models of care, paediatric tuberculosis, antimicrobial resistance in neonatal and paediatric care and the collateral damage of COVID-19 on child health. In addition, eight virtual stands from internal MSF initiatives and external MSF collaborating partners were available, and 49 poster communications and five inspiring short talks referred to as 'PAEDTalks' were presented. In conclusion, the MSF Paediatric Days serves as a unique forum to advance knowledge on humanitarian paediatrics and creates opportunities for individual and collective learning, as well as networking spaces for interaction and exchange of ideas.

The inhibitor of growth 1 (ING1) is involved in trichostatin A-induced apoptosis and caspase 3 signaling in p53-deficient glioblastoma cells.

Prognosis for patients with glioblastoma multiforme (GBM) is poor. Inhibitors of histone deacetylases (HDACi) like trichostatin A (TSA) are promising alternatives to conventional treatment. Deficient tumor suppressor functions, such as TP53 mutations and p14(ARF)/p16(INK4a) deletions, are characteristic for GBM and can cause resistance to DNA damaging agents such as cisplatin and to HDACi like TSA. The type II tumor suppressor Inhibitor of growth 1 (ING1) is involved in DNA damage response and histone modification. We have previously shown that ING1 is downregulated in GBM and involved in glioma-induced angiogenesis and in cisplatin-induced apoptosis in malignant glioma cells. Hence, the goal of our present study was to investigate whether TSA affects ING1 protein expression and also whether modulating ING1 levels affects TSA-induced apoptosis in malignant glioma cells that contain deficient p53 function and inactive pl4(ARF)/p16(INK4a) signaling. If so, we asked, which apoptotic pathway might be the major mediator beyond this interaction. To test whether ING1 proteins function in TSA-induced apoptosis in GBM, we analyzed TSA effects in LN229 GBM cells, which harbor TP53 mutations and INK4a deletion, following ING1 knockdown by siRNA. Expression of ING1, acetylated core histones H3 and H4, and the proapoptotic proteins caspase 3 and Fas-associated death domain (FADD) was determined by Western blotting. Percentages of apoptotic cells were obtained by flow cytometry. TSA induced the major ING1 isoform p33(ING1b) and increased levels of both histone acetylation and apoptosis in LN229 cells. ING1 knockdown cells revealed marked resistance to TSA-induced apoptosis, impairment of caspase 3 activation, and suppression of FADD. The data suggest that ING1 contributes to TSA-induced apoptosis in GBM cells with deficient p53 and p14(ARF)/p16(INK4a) functions, possibly by regulating FADD/caspase 3 signaling.

The inhibitor of growth 1 (ING1) proteins suppress angiogenesis and differentially regulate angiopoietin expression in glioblastoma cells.

The inhibitor of growth 1 (ING1) homologue ING4 has previously been implicated as a negative regulator of angiogenesis in a murine glioma and a multiple myeloma model. An association between ING1 and angiogenesis has not been reported yet. Our previous studies using tumor samples from patients have shown that ING1 levels are downregulated in glioblastoma multiforme (GBM), one of the most highly vascularized malignancies. Based on this background, the goal of this study was to test the effects of the major ING1 splicing isoforms, p47ING1a and p33ING1b, on pathological angiogenesis induced by human GBM cells. We used a chorioallantoic membrane (CAM) assay to examine whether LN229 human GBM cells can induce angiogenesis and whether alterations in ING1 expression, such as ING1 knockdown by siRNA or ectopic ING1 overexpression using ING1a and ING1b expression constructs, can affect this process. Increased ING1 protein expression significantly suppressed LN229 cell-induced angiogenesis in the CAM assay. While no effects on the proangiogenic factors VEGF or IL-8 were noted, the expression of angiopoietins (Ang) 1 and 4 were increased by the p47ING1a, but not by the p33ING1b isoform. Levels of Ang-2 were not sensitive to altered ING1 levels. Our data are the first to suggest that ING1 proteins suppress neoangiogenesis in GBM. Moreover, our results may support the idea that ING1 proteins regulate the expression of proteins that are critical for angiogenesis in GBM such as the angiopoietins.