ESMO / ASCO Recommendations for a Global Curriculum in Medical Oncology Edition 2016

The European Society for Medical Oncology (ESMO) and the American Society of Clinical Oncology (ASCO) are publishing a new edition of the ESMO/ASCO Global Curriculum (GC) thanks to contribution of 64 ESMO-appointed and 32 ASCO-appointed authors. First published in 2004 and updated in 2010, the GC edition 2016 answers to the need for updated recommendations for the training of physicians in medical oncology by defining the standard to be fulfilled to qualify as medical oncologists. At times of internationalisation of healthcare and increased mobility of patients and physicians, the GC aims to provide state-of-the-art cancer care to all patients wherever they live. Recent progress in the field of cancer research has indeed resulted in diagnostic and therapeutic innovations such as targeted therapies as a standard therapeutic approach or personalised cancer medicine apart from the revival of immunotherapy, requiring specialised training for medical oncology trainees. Thus, several new chapters on technical contents such as molecular pathology, translational research or molecular imaging and on conceptual attitudes towards human principles like genetic counselling or survivorship have been integrated in the GC. The GC edition 2016 consists of 12 sections with 17 subsections, 44 chapters and 35 subchapters, respectively. Besides renewal in its contents, the GC underwent a principal formal change taking into consideration modern didactic principles. It is presented in a template-based format that subcategorises the detailed outcome requirements into learning objectives, awareness, knowledge and skills. Consecutive steps will be those of harmonising and implementing teaching and assessment strategies

A randomized clinical trial with high dose of chloroquine for treatment of Plasmodium falciparum malaria in Brazil Ensaio clínico aleatório duplo cego com cloroquina em dose alta para tratamento da malária por Plasmodium falciparum no Brasil

This clinical trial compared parasitological efficacy, levels of in vivo resistance and side effects of oral chloroquine 25 mg/Kg and 50 mg/Kg in 3 days treatment in Plasmodium falciparum malaria with an extended followed-up of 30 days. The study enroled 58 patients in the 25 mg/Kg group and 66 in the 50 mg/Kg group. All eligible subjects were over 14 years of age and came from Amazon Basin and Central Brazil during the period of August 1989 to April 1991. The cure rate in the 50 mg/Kg group was 89.4% on day 7 and 71.2% on day 14 compared to 44.8% and 24.1% in the 25 mg/Kg group. 74.1% of the patients in the 25 mg/Kg group and 48.4% of the patients in the 50 mg/Kg group had detectable parasitaemia at the day 30. However, there was a decrease of the geometric mean parasite density in both groups specially in the 50 mg/Kg group. There was 24.1% of RIII and 13.8% of RH in the 25 mg/Kg group. Side effects were found to be minimum in both groups. The present data support that there was a high level resistance to chloroquine in both groups, and the high dose regimen only delayed the development of resistance and its administration should not be recommended as first choice in malaria P. falciparum therapy in Brazil.<br>Comparou-se a eficácia parasitológica, níveis de resistência "in vivo" e efeitos colaterais da cloroquina oral nas dosagens de 25 mg/kg e 50 mg/kg no tratamento da malária por Plasmodium falciparum com seguimento de 30 dias. O estudo foi conduzido de agosto de 1989 a abril de 1991 e incluiu 124 pacientes, selecionados aleatoriamente em blocos de 10 pacientes, do ambulatório da Fundação Nacional de Saúde-Goiânia, Brasil. Todos os pacientes eram procedentes da Bacia Amazônica e Brasil - Central, sendo 58 alocados no grupo de 25 mg/kg (C25) e 66 no grupo de 50 mg/kg (C50). Os efeitos colaterais foram mínimos em ambos os grupos. A taxa de cura no C50 foi 89,4% no dia 7 e 71,2% no dia 14 enquanto para o C25 as taxas foram de 44,8% e 24,1%, respectivamente. Setenta e quatro por cento dos pacientes do C25 e 48,4% no C50 apresentaram parasitemia detectável no dia 30. Entretanto, houve uma queda da média geométrica da densidade parasitária (MGDP) em ambos os grupos, especialmente no C50. Resistência tipo III e II foi detectada respectivamente em 24,1% e 13,8% dos pacientes no grupo C25. No grupo de 50 mg/kg não foi detectado nenhum caso de RII registrando-se apenas um caso de RIII. Um grande número de RI tardio foi detectado em ambos os grupos, o que poderia retardar o tempo de portador e contribuir para disseminação de cepas resistentes. Desta forma, o presente estudo conclui que cloroquina, em qualquer das doses testadas, não deve ser utilizada no tratamento da malária por P. falciparum, em nosso meio

Breast cancer hypothesis: a single cause for the majority of cases

STUDY OBJECTIVE—The main cause of breast cancer remains unknown. Numerous causal factors or predisposing conditions have been proposed, but account for only a small percentage of the total disease. The current search for multiple causes is unavailing. This report explores whether any single aetiological agent may be responsible for the majority of cases, and attempts to define its properties.
METHODS—Examination of all relevant epidemiological and biological evidence.
MAIN RESULTS—Genetic inheritance is not the main cause of breast cancer because most cases are sporadic, there is a low prevalence of family history, and genetically similar women have differing rates after migration. Environmental exposure, such as pollution by industrialisation, is not a major cause, as deduced from a spectrum of epidemiological data. The possibility of infection as cause is not persuasive as there is no direct biological evidence and no epidemiological support. Oestrogen status is closely related to breast cancer risk, but there are numerous inconsistencies and paradoxes. It is suggested that oestrogens are not the proximate agent but are promoters acting in concert with the causal agent. Dietary factors, and especially fat, are associated with the aetiology of breast cancer as shown by intervention and ecological correlation studies, but the evidence from case-control and cohort studies is inconsistent and contradictory.
CONCLUSIONS—The hypothesis that best fits the epidemiological data is that dietary fat is not itself the causal agent, but produces depletion of an essential factor that is normally protective against the development of breast cancer. Many of the observed inconsistencies in the epidemiology are explainable if deficiency of this agent is permissive for breast cancer to develop. Some properties of the putative agent are outlined, and research investigations proposed.


Keywords: breast cance