A critical review and analysis of the context, current burden, and application of policy to improve cancer equity in Ghana.

BACKGROUND: Cancer causes a major disease burden worldwide. This is increasingly being realised in low and middle-income countries, which account disproportionately for preventable cancer deaths. Despite the World Health Organization calling for governments to develop policies to address this and alleviate cancer inequality, numerous challenges in executing effective cancer policies remain, which require consideration of the country-specific context. As this has not yet been considered in Ghana, the aim of this review was to bring together and critique the social-environmental, health policy and system factors to identifying opportunities for future health policies to reduce cancer burden in the Ghanian context. A critical policy-focused review was conducted to bring together and critique the current health systems context relating to cancer in Ghana, considering the unmet policy need, health system and social factors contributing to the burden and policy advances related to cancer. CONCLUSION: The findings highlight the changing burden of cancer in Ghana and the contextual factors within the socio-ecosystem that contribute to this. Policies around expanding access to and coverage of services, as well as the harmonization with medical pluralism have potential to improve outcomes and increase equity but their implementation and robust data to monitor their impact pose significant barriers.

Medical pluralism, healthcare utilization and patient wellbeing: The case of Akan cancer patients in Ghana.

PURPOSE: As cancers increase in Ghana and in many low-and middle-income countries, healthcare utilization has become critical for disease management and patients' wellbeing. There is evidence that medical pluralism is common among cancer patients in Ghana and many other African countries, which results in lack of adherence to and absconding from hospital treatments. The objective of this study was to examine ways in which beliefs in disease causation influence medical pluralism among Akan cancer patients in Ghana. METHODS: A qualitative research approach was employed in this study. In-depth interviews were conducted for thirty (30) cancer patients who were purposively recruited from Komfo Anokye Teaching Hospital in Ghana. Thematic content analysis was used in analysing data. RESULTS: Our findings revealed that cancer patients ascribed both physical and spiritual causality to their illness. As such, they combined orthodox treatment with spiritual healing and herbal medicine. Regarding the order of therapeutic search, patients reported to herbal and spiritual centres before going to the hospital, a phenomenon which contributes to the late reporting and diagnosis as well as bad prognosis of cancers in Ghana. CONCLUSION: The findings of this research elucidate the relationship between culture and health care choices of cancer patients in Ghana. Increased awareness creation is crucial in eradicating myths surrounding cancers in Ghana.

What influences cancer treatment service access in Ghana? A critical interpretive synthesis.

OBJECTIVES: Multiple social-cultural and contextual factors influence access to and acceptance of cancer treatment in Ghana. The aim of this research was to assess existing literature on how these factors interplay and could be susceptible to local and national policy changes. DESIGN: This study uses a critical interpretive synthesis approach to review qualitative and quantitative evidence about access to adult cancer treatment services in Ghana, applying the socioecological model and candidacy framework. RESULTS: Our findings highlighted barriers to accessing cancer services within each level of the socioecological model (intrapersonal, interpersonal community, organisational and policy levels), which are dynamic and interacting, for example, community level factors influenced individual perceptions and how they managed financial barriers. Evidence was lacking in relation to determinants of treatment non-acceptance across all cancers and in the most vulnerable societal groups due to methodological limitations. CONCLUSIONS: Future policy should prioritise multilevel approaches, for example, improving the quality and affordability of medical care while also providing collaboration with traditional and complementary care systems to refer patients. Research should seek to overcome methodological limitations to understand the determinants of accessing treatment in the most vulnerable populations.

Publisher Correction: A DHODH inhibitor increases p53 synthesis and enhances tumor cell killing by p53 degradation blockage.

The original PDF version of this Article listed the authors as "Marcus J.G.W. Ladds," where it should have read "Marcus J. G. W. Ladds, Ingeborg M. M. van Leeuwen, Catherine J. Drummond et al.#".Also in the PDF version, it was incorrectly stated that "Correspondence and requests for materials should be addressed to S. Lín.", instead of the correct "Correspondence and requests for materials should be addressed to S. Laín."This has been corrected in the PDF version of the Article. The HTML version was correct from the time of publication.

A DHODH inhibitor increases p53 synthesis and enhances tumor cell killing by p53 degradation blockage.

The development of non-genotoxic therapies that activate wild-type p53 in tumors is of great interest since the discovery of p53 as a tumor suppressor. Here we report the identification of over 100 small-molecules activating p53 in cells. We elucidate the mechanism of action of a chiral tetrahydroindazole (HZ00), and through target deconvolution, we deduce that its active enantiomer (R)-HZ00, inhibits dihydroorotate dehydrogenase (DHODH). The chiral specificity of HZ05, a more potent analog, is revealed by the crystal structure of the (R)-HZ05/DHODH complex. Twelve other DHODH inhibitor chemotypes are detailed among the p53 activators, which identifies DHODH as a frequent target for structurally diverse compounds. We observe that HZ compounds accumulate cancer cells in S-phase, increase p53 synthesis, and synergize with an inhibitor of p53 degradation to reduce tumor growth in vivo. We, therefore, propose a strategy to promote cancer cell killing by p53 instead of its reversible cell cycle arresting effect.