Molecular Genetics Of Lung Cancer Research Articles

Prognostic Factors and Markers in Non-Small Cell Lung Cancer: Recent Progress and Future Challenges.

Lung cancer is a highly aggressive neoplasm and, despite the development of recent therapies, tumor progression and recurrence following the initial response remains unsolved. Several questions remain unanswered about non-small cell lung cancer (NSCLC): (1) Which patients will actually benefit from therapy? (2) What are the predictive factors of response to MAbs and TKIs? (3) What are the best combination strategies with conventional treatments or new antineoplastic drugs? To answer these questions, an integrative literature review was carried out, searching articles in PUBMED, NCBI-PMC, Google Academic, and others. Here, we will examine the molecular genetics of lung cancer, emphasizing NSCLC, and delineate the primary categories of inhibitors based on their molecular targets, alongside the main treatment alternatives depending on the type of acquired resistance. We highlighted new therapies based on epigenetic information and a single-cell approach as a potential source of new biomarkers. The current and future of NSCLC management hinges upon genotyping correct prognostic markers, as well as on the evolution of precision medicine, which guarantees a tailored drug combination with precise targeting.

Molecular genetics of lung cancer

Lung cancer is one of the most common cancers with high mortality and is described as one of the leading causes of cancer-related deaths worldwide. Lung cancer is classified into two main histological groups: small cell lung cancer (SCLC) and non-SCLC (NSCLC). Using tobacco products is the most important risk factor for lung cancer development and appears to be responsible for 80%–90% of total lung cancers. It is thought that lung cancer is the end result of exposure to environmental risk factors in people with genetic susceptibility. Lung cancer cells contain many genetic alterations such as mutation, amplification, insertion, deletion, and translocation. The information obtained from research suggests that these genetic changes are also associated with characteristics such as smoking status, race, and gender. Significant progress has been made in the last 10–15 years to understand the molecular basis of lung cancer, and the discovery of oncogenic precursor mutations has created new pathways in the NSCLC classification and has also provided new therapeutic targets for anticancer therapy. With the introduction of targeted agents such as epidermal growth factor receptor and anaplastic lymphoma kinase in the treatment of adenocarcinomas in an effective manner, personalization of treatment strategies has become especially important for advanced lung cancer patients. The 2015 World Health Organization guideline for the classification of lung cancer recommends the preservation of pathologic specimens for molecular examinations and emphasizes the importance of molecular testing in the individualized treatment of advanced lung cancer patients.

Preface-molecular genetics of lung cancer.

The molecular genetic alterations underpinning lung cancer have been of great interest to researchers for many years. The discovery of small molecule inhibitors that target some of the key driver genetic alterations of lung cancer has fuelled this interest and catapulted genetic testing of tumours for somatic mutations into routine clinical practice. Successful and rapid translational lung cancer research has enabled patients of today to clinically benefit from these recent advances. It is therefore most fitting to dedicate a special issue on molecular genetics of lung cancer in Translational Lung Cancer Research (TLCR). In this issue, we bring together a range of original articles and reviews that summarise current clinical practice of molecular testing in lung cancer and preview exciting developments that may impact patient care in the future.

One size does not fit all

Advances in non-small-cell lung cancer over the past decade have resulted in new treatments with minimal toxic effects and dramatic clinical benefits. 2010 saw continued advancement in our understanding of the molecular genetics of lung cancer and of specific targeted inhibitors with remarkable clinical benefit in selected populations.

Molecular genetics of lung cancer in people who have never smoked

Lung cancer is a major cause of cancer-related mortality in the USA, and tobacco smoke is the major risk factor for this disease. However, many patients with lung cancer have never smoked (never smokers). Patients with lung cancer who have never smoked are more likely to have mutations in epidermal growth factor receptor (EGFR) tyrosine kinase and have better response to its inhibitors than do patients with tobacco-associated lung cancer. Furthermore, the prevalences of mutations in KRAS and P53 differ for patients with lung cancer who have never smoked and those with tobacco-associated lung cancer. Genetic mutations seem to be more common in patients with tobacco-associated lung cancer than in never smokers. Current evidence indicates that the two types of lung cancer are biologically distinct. Here, we review published studies of the molecular genetics of lung cancer in never smokers and identify the specific differences from tobacco-associated lung cancer.

Cytogenetics and molecular genetics of lung cancer.

The development and progression of lung cancer is a multistep process characterized by the accumulation of numerous genetic and epigenetic alterations, some of which occur early in the course of disease. In this review, we summarize cytogenetic imbalances and molecular genetic/epigenetic changes seen in human small-cell and non-small-cell lung cancer. Alterations of tumor suppressor genes and oncogenes leading to perturbations of key cell-regulatory and growth-control pathways are highlighted. The translational implications of molecular biomarkers for risk assessment, early detection, and monitoring of chemoprevention trials are discussed.

Molecular genetics of lung cancer.

Lung cancer results from multiple changes in the genome of susceptible pulmonary cells caused by exposure to carcinogens found in tobacco smoke, the environment, or the workplace. Recent studies suggest that histologically apparent lung cancer is due to the sequential accumulation of specific genetic and morphologic changes to the normal epithelial cells of the lung. Positive signallers, such as those mediated by the oncogene RAS, and negative signallers, such as those mediated by the tumor suppressor retinoblastoma protein (RB), contribute to unchecked cell growth and proliferation. Other key molecular derangements can also be considered hallmarks of cancer, including evasion of apoptosis and senescence, angiogenesis, tissue invasion, and metastases. Epigenetic inactivation of genes via DNA methylation provides another novel way of evading normal cellular control mechanisms. The new knowledge of the human genome coupled with global methods of detecting genetic abnormalities and profiling gene expression in tumor cells may enable us to understand the signaling pathways of lung cancer cells. These are molecular targets for new cancer therapeutics such as receptor tyrosine kinase inhibitors. This information could advance risk assessment, early detection, prognosis, and therapy for lung cancer.

Biology and Molecular Genetics of Lung Cancer

Biology and Molecular Genetics of Lung Cancer

Molecular genetics of lung cancer

Molecular genetics of lung cancer

Molecular genetics of lung cancer.

Molecular genetics of lung cancer.