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By using the theory of fixed point index and spectral theory of linear operators, we study the existence of positive solutions for Riemann-Liouville fractional differential equations at resonance. Our approach will provide some new ideas for the study of this kind of problem.

Background: Many survivors of a first primary cancer (FPCs) are at risk of developing a second primary cancer (SPC), with effects on patient prognosis. Primary cancers have different frequencies of specific SPC development and the development of SPCs may be closely related to the FPC. The aim of this study was to explore possible correlations between SPCs and FPCs. Methods: Relevant literature on SPCs was retrospectively searched and screened from four databases, namely, PubMed, EMBASE, Web of Science, and PMC. Data on the number of patients with SPC in 28 different organ sites were also collected from The Surveillance, Epidemiology, and End Results (SEER) 8 Registry and NHANES database. Results: A total of 9 617 643 patients with an FPC and 677 430 patients with an SPC were included in the meta-analysis. Patients with a first primary gynaecological cancer and thyroid cancer frequently developed a second primary breast cancer and colorectal cancer. Moreover, those with a first primary head and neck cancer, anal cancer and oesophageal cancer developed a second primary lung cancer more frequently. A second primary lung cancer and prostate cancer was also common among patients with first primary bladder cancer and penile cancer. Patients with second primary bladder cancer accounted for 56% of first primary ureteral cancer patients with SPCs. Conclusions: This study recommends close clinical follow-up, monitoring and appropriate interventions in patients with relevant FPCs for better screening and early diagnosis of SPCs. Our study is the first to use a meta-cohort of 726 019 patients with SPCs, incorporating up to 28 human organs as FPC sites to perform a systematic and pan-cancerous study of the possible correlation between SPCs and FPCs. We found multiple epidemiological clusters of organs of FPCs: FPCs of the uterus, ovary, thyroid, fallopian tube, vulva and vagina are more likely to develop into SPCs of the breast and colorectum; second primary lung cancer is more frequently developed in patients with FPCs of the head and neck, anus and oesophagus; FPCs of the bladder and penis are more likely to develop into second primary prostate cancer and lung cancer; and among patients who had an FPC in the ureter and developed an SPC, the rate of second primary bladder cancer was as high as 56%. We recommend close clinical follow-up, monitoring and appropriate interventions in patients with relevant FPCs for better screening and early diagnosis of SPCs to prolong patient survival. [ABSTRACT FROM AUTHOR]

To assure faithful chromosome segregation, cells make use of the spindle assembly checkpoint, which can be activated in aneuploid cancer cells. In this study, the efficacies of inhibiting polo-like kinase 1 (PLK1) on the radiosensitization of non-small-cell lung cancer (NSCLC) cells were studied. Clonogenic survival assay was performed to identify the effects of the PLK1 inhibitor on radiosensitivity within NSCLC cells. Mitotic catastrophe assessment was used to measure the cell death and histone H2AX protein ([gamma]H2AX) foci were utilized to assess the DNA double-strand breaks (DSB). The transcriptome was analyzed via unbiased profiling of microarray expression. The results showed that the postradiation mitotic catastrophe induction and the DSB repair were induced by PLK1 inhibitor BI-6727, leading to an increase in the radiosensitivity of NSCLC cells. BI-6727 in combination with radiation significantly induced the delayed tumor growth. PLK1-silenced NSCLC cells showed an altered mRNA and protein expression related to DNA damaging, replication, and repairing, including the DNA-dependent protein kinase (DNAPK) and topoisomerase II alpha (TOPO2A). Furthermore, inhibition of PLK1 blocked 2 important DNA repair pathways. To summarize, our study showed PLK1 kinase as an option in the therapy of NSCLC. Key words: polo-like kinase 1, non-small-cell lung cancer, DNA double-strand break, spindle assembly checkpoint. Afin d'assurer la fidelite de la segregation des chromosomes, les cellules utilisent le point de controle de l'assemblage du fuseau qui peut etre active chez les cellules cancereuses aneuploides. Dans cette etude, l'efficacite de l'inhibition de la kinase PLK1 (<< polo-like kinase 1 >>) dans la radiosensibilisation des cellules de cancer bronchopulmonaire non a petites cellules (CBNPC) a ete examinee. Un test clonogenique de survie a ete realise pour identifier les effets de l'inhibiteur de la PLK1 sur la radiosensibilite des cellules de CBNPC. L'evaluation de la catastrophe mitotique a ete utilisee pour mesurer la mort cellulaire et les foyers d'histone H2AX ([gamma]H2AX) ont ete utilises pour evaluer les cassures double brin (CDB) d'ADN. Le transcriptome a ete analyse au moyen de l'etablissement d'un profil non biaise d'expression sur microreseau. Les resultats ont montre que l'induction de la catastrophe mitotique post-radiation et la reparation des CDB etaient induites par l'inhibiteur de la PLK1, le BI-6727, provoquant un accroissement de la radiosensibilite des cellules de CBNPC. La combinaison du BI-6727 et de la radiation induisait un retard de la croissance tumorale de maniere significative. Le silencage de la PLK1 dans les cellules de CBNPC provoquait une modification du profil d'expression de transcrits lies au dommage, a la replication et a la reparation de l'ADN, dont ceux de la DNAPK (<< DNA-dependent protein kinase >>) et de la TOPO2A (topoisomerase II alpha). De plus, l'inhibition de la PLK1 bloquait deux voies de reparation d'ADN importantes. En resume, les travaux des auteurs ont montre que la kinase PLK1 constitue une option therapeutique dans le CBNPC. [Traduit par la Redaction] Mots-cles : << polo-like kinase 1 >>, cancer bronchopulmonaire non a petites cellules, cassure double brin d'ADN, point de controle de l'assemblage du fuseau., Introduction Aneuploidy serves as a sign of cancer cells where chromosomes are inappropriately partitioned between the daughter cells due to aberrant mitosis. During every division of cell, the mitotic spindle [...]