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Dual staining for p16 and Ki-67 demonstrated good reproducibility, confirming its robustness, which is a necessary prerequisite for its adoption as a triage test in cervical cancer screening programs that use human papillomavirus DNA as a primary test. Cancer Cytopathol 2017;125:212-220. © 2016 American Cancer Society.

Non‐small cell lung cancer (NSCLC) is the leading cause of cancer death and in most cases it is often diagnosed at an advanced stage. Many genetic and microenvironmental factors are able to modify the cell cycle inducing carcinogenesis and tumor growth. Among the metabolic and genetic factors that come into play in carcinogenesis and tumor cell differentiation and growth there are two different proteins that should be considered which are glucose transporters (GLUTs) and p16 INK4 The first are glucose transporters which are strongly involved in tumor metabolism, notably accelerating cancer cell metabolism both in aerobic and anaerobic conditions. There are different subtypes of GLUT family factors of which GLUT 1 is the most important and widely expressed. By contrast, p16 is mainly a tumor‐suppressor protein that acts on cyclin‐dependent kinase favoring cell cycle arrest in the G1 phase. Our search focused on the action of the aforementioned factors.

IntroductionChronic obstructive pulmonary disease (COPD) is the fourth cause of mortality and it’s frequently associated with breathing sleep disorders.ObjectiveThe aim of the study is to point out the benefit of smoking cessation over three months in terms of improvement of respiratory functional variables.MethodsA retrospective analysis was performed evaluating the impact of smoking cessation on 145 patients with COPD and nocturnal oxygen desaturation. For this purpose, for all patients, overnight pulse oxymetry detection on room air, arterial blood sampling, plethysmography and exhaled test for carbon monoxide were performed at baseline and 3 months after the beginning. Smoking cessation was achieved by varenicline plus individual counselling.ResultsAbout 51% of patients quit smoking which was established by exhaledcarbon monoxide (eCO) measure (cut‐off 5 ppm). Patients who quit smoking displayed notably better results compared with patients who did not. The eCO significantly decreased by 16 ppm versus 4 (P = 0.01), oxygen desaturation index (ODI) was reduced by 3 points versus 0.8 (P = 0.01) and forced expiratory in 1 second volume increased by 7% of predicted value versus 1% (P = 0.01). The walking test was improved by 102 m versus 25 in sustainers (P = 0.01). The CAT score was also improved by 10 versus 8 in sustainers (P = 0.01) and PaO2 increased by 5 mm Hg versus 0.5 (P = 0.04). The percentage of SaO2 < 90% was improved by 6.7 versus 2.1 (P = 0.04).The logistic regression analysis displayed the possible influence of CAT (P = 0.02) and modified medical research council dyspnea test (P = 0.05) on ODI value.ConclusionsSmoking cessation notably improves pulmonary functional parameters in quitters reporting nocturnal oxygen desaturation.

Tumor-initiating cells constitute a population within a tumor mass that shares properties with normal stem cells and is considered responsible for therapy failure in many cancers. We have previously demonstrated that knockdown of the nuclear envelope component Lamin A/C in human neuroblastoma cells inhibits retinoic acid-mediated differentiation and results in a more aggressive phenotype. In addition, Lamin A/C is often lost in advanced tumors and changes in the nuclear envelope composition occur during tumor progression. Based on our previous data and considering that Lamin A/C is expressed in differentiated tissues, we hypothesize that the lack of Lamin A/C could predispose cells toward a stem-like phenotype, thus influencing the development of tumor-initiating cells in neuroblastoma. This paper demonstrates that knockdown of Lamin A/C triggers the development of a tumor-initiating cell population with self-renewing features in human neuroblastoma cells. We also demonstrates that the development of TICs is due to an increased expression of MYCN gene and that in neuroblastoma exists an inverse relationship between LMNA and MYCN expression.

Background/Aim: Non-small cell lung cancer (NSCLC) is the leading cause of cancer death. Patients eligible for surgery have better overall survival rate than patients who are not eligible. We investigated the prognostic value of p16 in patients who underwent surgery for lung cancer, in association with other factors such as PD-L1 and Ki-67. Materials and Methods: Expression of p16 was evaluated along with the presence of Ki-67 and PD-L1 in 256 NSCLC patients treated only surgically. Results: Adenocarcinoma was the prevalent histotype (56%) followed by squamous cell (29%) and differentiation grade of 3 was the most common (60%). p16 was detected in 83 patients (30%): low positivity (<10% cells) was observed in 30 samples (11%) and high positivity (>10 % cells) in 53 patients (20%). Ki-67 was detected in 89 patients (34%) with mild positivity in 46 patients (10-25% cells), moderate positivity (26-75% cells) in 30 patients (11%), and high positivity (>75% cells) in 13 patients (5%). An influence of p16 expression (p<0.05) along with grading and staging on overall survival (OS) was found. The average OS was 36 months, but the OS increased up to 54 months when patients were stratified according to p16 expression levels. The stratification by staging showed a significant prognostic value for p16 at an early stage (p<0.014). Conclusion: p16 significantly influences prognosis, notably at an early stage, along with other variables such as grading and staging.

Our results suggest that c-Myc could be considered as a good target for the study of new approaches in anticancer astrocytoma treatment.