Adherence of North-African Pulmonologists to the 2017-Global Initiative for Chronic Obstructive Lung Disease (GOLD) Pharmacological Treatment Guidelines (PTGs) of Stable Chronic Obstructive Pulmonary Disease (COPD).

BACKGROUND: No previous study has investigated the adherence rate of North-African pulmonologists to the 2017-GOLD PTGs. AIMS: To investigate the adherence rate of Tunisian pulmonologists to the 2017-GOLD PTGs and to identify the barriers to their adherence. METHODS: This was a cohort study involving clinically stable COPD patients who presented to a pulmonology outpatient consultation. The patients were classified as having been appropriately and inappropriately (over- or undertreatment) treated for the GOLD group. Logistic regression was performed to determine the adherence barriers to the 2017-GOLD PTGs. RESULTS: A total of 296 patients were included (88.1% males, mean age: 68 ± 10 years; GOLD A (7.1%), B (36.1%), C (4.1%), and D (52.7%)). The pulmonologists' adherence rate to the 2017-GOLD PTGs was 29.7%. There was a significant statistical difference between the adherence rates among the four GOLD groups (A: 19.0%, B: 20.6%, C: 8.3%, and D: 39.1%; p = 0.001). Differences were statistically significant between the GOLD group D and groups B (p = 0.001). Differences were statistically significant between the GOLD group D and groups B (p = 0.001). Differences were statistically significant between the GOLD group D and groups B (. CONCLUSION: The adherence rate of Tunisian pulmonologists to the 2017-GOLD PTGs is low. It seems that the patients' age, socioeconomic level, national health insurance coverage, and GOLD groups influenced their adherence.

Evasion of Cell Senescence Leads to Medulloblastoma Progression.

How brain tumors progress from precancerous lesions to advanced cancers is not well understood. Using Ptch1(+/-) mice to study medulloblastoma progression, we found that Ptch1 loss of heterozygosity (LOH) is an early event that is associated with high levels of cell senescence in preneoplasia. In contrast, advanced tumors have evaded senescence. Remarkably, we discovered that the majority of advanced medulloblastomas display either spontaneous, somatic p53 mutations or Cdkn2a locus inactivation. Consistent with senescence evasion, these p53 mutations are always subsequent to Ptch1 LOH. Introduction of a p53 mutation prevents senescence, accelerates tumor formation, and increases medulloblastoma incidence. Altogether, our results show that evasion of senescence associated with Ptch1 LOH allows progression to advanced tumors.