Research in causation of cancer is an important part of cancer research in general and is an essential prerequisite for cancer prevention. The effective primary prevention is not visible without evidence based knowledge in the causation of cancer in humans.

There is sufficient evidence that certain life style and environment factors cause cancer in humans. These factors include: smoking and other types of tobacco consumption, overweight and obesity, lack of physical activity, diet rich in processed meat and poor in vegetables and fruits, certain types of viral and bacterial infection, ultraviolet radiation, ionizing radiation, ambient air pollution, carcinogens at workplace, exogenous hormones.

Cancer mortality is decreasing in majority of developed countries, including Russia. This mortality trend is mostly due to decrease in incidence and death rates of lung and other smoking related cancers and is caused by decline in smoking prevalence and change in tar content of cigarette smoke.

In Russia trend in mortality from all cancers is as well determined by decrease in incidence and mortality from gastric cancer, which is due to decline in prevalence of Helicobacter pylori infection and improvement of diet, increase in consumption of fruits and vegetables. Thus the decline in cancer mortality is mostly the result of primary prevention which is the most effective avenue of cancer control. 

Contrary to the generally accepted opinion about stable DNA as the carrier of hereditary information, in a normal (not just cancer) cell, this molecule is subject to the continuous changes as a result of copying errors (in the course of replication), defects of chromosome segregation (in mitosis) and direct chemical attacks (by reactive oxygen species). Genetic diversification of cells starts during embryonic development and lasts during whole life, generating a phenomenon of the somatic mosaicism. New data on genetic variety of somatic cells lead to a different, than earlier, perception of cancer etiology, pathogenesis and prevention.

Scaffold proteins coordinate the assembling of multicomponent protein complexes and participate in transduction of cellular signals via multiple signaling pathways therefore acting as important regulators of cell properties. IQ Motif Containing GTPase Activating Proteins (IQGAPs) are promising targets for studying the role of scaffold proteins in intracellular signaling regulation and development of cancer and other diseases. IQGAP family includes 3 proteins (IQGAP1, IQGAP2 and IQGAP3) that differ considerably by their expression patterns and functions. Distinct genomic aberrations and expression changes in various tumors were reported for all three IQGAP family members. The present paper thoroughly reviews the structure of IQGAP proteins, their involvement in regulation of cell characteristics and interactions with components of intracellular signaling pathways. Special attention is given to the up-to-date data on deregulation of IQGAP genes functions in different tumor types, analysis of their possible role in tumor progression and their associations with clinicopathological tumor characteristics.

Bronchopulmonary neuroendocrine tumors (NET) comprise one of the most common categories within the heterogeneous group of human neuroendocrine neoplasms. Tumors of this type often occur in practical pathology diagnosis; however, their classification and histological grading are not the same as for the gastrointestinal and pancreatic NET. Terminology of lung NET is still based on using the term «carcinoid». In the recent World Health Organization classification of lung tumors published in 2015, all NETs of this localization for the first time were presented in one single chapter. According to the current classification scheme the group of neuroendocrine proliferation processes consists of carcinoid tumors (including typical carcinoid and atypical carcinoid), large-cell neuroendocrine carcinoma and small cell lung carcinoma, along with diffuse idiopathic pulmonary neuroendocrine cell hyperplasia as a pre-invasive lesion with a potential toward the development of carcinoids. Each tumor category has characteristic morphological and immunohistochemical features, which are the key diagnostic criteria of these tumors. Histology parameters for grading have remained unchanged in new edition. However, uncertainties remain in relation to the role of Ki-67 in tumor grading in resection specimens and small samples. This review outlines the main key questions in the field of classification and pathology diagnosis of lung NET, the answers to which are still inconclusive. Thus additional research is required to improve our understanding on NET of this localization.