Special Issue "Lung Cancer"

Guest Editor
Prof. Dr. Gerolama Condorelli
Department of Cellular and Molecular Biology and Pathology, Istituto di Endocrinologia e Oncologia Sperimentale ‘‘G. Salvatore’’-Consiglio Nazionale delle Ricerche, Faculty of Biotechnological Science, ‘‘Federico II’’ University of Naples, I-80121 Naples, Italy
Website: https://www.docenti.unina.it/cercaDocente.do?cognome=condorelli&submit1=avvia+ricerca
E-Mail:
Interests: apoptosis; cell death; TRAIL; microRNA; cell motility; chemotherapy resistance

Dear Colleagues,

Lung cancer is the leading cause of cancer death in both men and women worldwide. It is becoming apparent, through candidate gene and genome-wide approaches, that clinically evident lung cancers accumulate numerous clonal genetic and epigenetic alterations during a multistep process. These alterations include tumor suppressor gene inactivation and activation of growth or survival promoting oncogenes.

Despite advances in early detection and standard treatment, lung cancer is often diagnosed at an advanced stage and have poor prognoses. The development of innovative, targeted therapies may represent an alternative for the treatment of these cancers.

One of the most important factors that affect survival rate is resistance to therapeutic drugs. Thus development of effective therapeutic approaches is necessary for the management of these common cancers. MiRNAs are attractive drug targets since they regulate expression of many cellular proteins and are differentially
MicroRNAs are small noncoding RNAs that show expression loss or gain in most cancers, and there is growing evidence that they play substantial roles in the pathogenesis and prognosis of human malignancies.

The central focus of the special issue on “Lung Cancer” is identification of molecular pathways involved in lung tumorigenesis and therapeutic resistance. The main topics will include, but are not limited to, the role of cell death (e.g., apoptosis and necrosis) and cell survival pathways (e.g., autophagy) in tumorigenesis and chemotherapy resistance; role microRNAs and their targets in lung prognosis, diagnosis and response to therapy.
Thank you for your collaboration.

Prof. Dr. Gerolama Condorelli
Guest Editor

Submission

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• lung cancer
• MicroRNAs
• apoptosis
• autophagy
• caspases
• cell death
• cell survival
• death receptors
• oncogenes
• tumor suppressor genes

Type of Paper: Article
Title: Assessment of DNA Repair Mechanisms to Determine NSCLC Susceptibility to Alkylating Agents
Author: Ivette F. Emery
Affiliation: Maine Center for Cancer Medicine (MCCM), Clinical Trials Unit - MMC Cancer Institute (MMCCI), 100 Campus Drive, Suite 102, Scarborough, Maine 04074-9308, USA; E-Mail: emeryi@mmc.org
Abstract: Background: The status of DNA repair systems impacts the sensitivity of tumors to chemotherapeutics. The anti-neoplastic activity of temozolomide, an alkylating agent, is affected by the enzyme O⁶-Methylguanine-DNA methyltransferase (MGMT), and by the mismatch repair system (MMR). Lack of MGMT makes a tumor susceptible to temozolomide provided that MMR is functional. A non-functional MMR renders the tumor resistant to alkylating agents. We assayed MGMT and MMR in order to estimate the proportion of patients affected by NSCLC who may derive benefit from temozolomide, an agent not currently used in lung cancer. Method: MGMT and MMR were assayed by promoter methylation testing and by microsatellite instability testing, respectively, on 96 paraffin-embedded NSCLC samples. Methylation testing, which detects gene silencing, was conducted at OncoMethylome by methylation-specific PCR of the MGMT promoter. MSI testing, which detects a non-functional MMR, was conducted at LabCorp by multiplex PCR of six microsatellite regions. Results: Ninety three samples yielded interpretable results. Eighty of those (83%) had no defects detected in either MGMT or MMR. Nine samples (10%) had methylation of the MGMT promoter and four samples (4%) had microsatellite instability. The defects were not overlapping. Conclusions: Our results indicate that approximately 10% of NSCLC may be susceptible to alkylating agents, and that in the remaining population, only 4% will be resistant to these agents. Our understanding of the molecular characteristics of NSCLC suggests that alkylating agents, such as temozolomide, alone or in combination with MGMT inhibitors, may be viable option to treat selected NSCLC patients.