Cancer is a multifactorial disease that has a direct connection to variations in our genomes. The accumulation of somatic mutations is the main cause for the development of cancer. Cancer genomes are characterized by heterogeneity seen across tumor types, within clinical entities and among individual cases and between individual cancers. Exposure to carcinogenic agents and conditions such as tobacco smoke, ultraviolet light, and even some drugs used for cancer treatment have an important direct role in driving oncogenetic events. The impact of some viral infections - such as from human papillomavirus (HPV) and hepatitis-associated viruses - on oncogenesis has been well recognized. Additionally, life style related risks such as alcohol consumption, malnutrition and lack of physical activity have been found to be associated with a number of malignant diseases. However, the connection of individual and population related risk factors to their molecular mechanisms still has to be elucidated for many malignancies, with the aim to develop specific risk assessment, diagnosis, and control strategies.
Driven by rapid advances in high-throughputs "-omics" technologies, the last decades have provided a fundamental increase in our understanding of the somatic mutations that aid malignant transformation and disease progression. A large number of studies have addressed the genomic profiling of solid tumors as well as functional studies of specific cancer related genes. Focus has always been on investigating germline variants that affect cancer susceptibility, predisposition and disease. However, only in recent years, has it become more feasible to investigate these variants due to a dramatic increase in genomic profiling data. Such variants can be highly population- and ancestry-specific and can provide a part of the explanation why certain cancers are more prevalent among individual populations. For example, prostate cancer has been reported with higher prevalence among the individuals of Afro-American ancestry, lung cancer is more common among admixed Latin Americans and oral cancer is more common among East Asians. However, while such observations may point to shared underlying genome-based variations in susceptibility for certain kinds of cancer, they may also be related to shared environmental or socio-economic factors with higher prevalence in selected populations.
In this special issue, we welcome studies that focus on the germline variants associated with the predisposition of various cancers and can be linked to cancer heterogeneity. The studies can focus on association-based analysis (GWAS/EWAS), genomic profiling, ancestry/population specific variation in cancer susceptibility and disease progression, and individual specific variation driving cancer heterogeneity.
Scope
• Multidimensional approaches to mutational profiling
• Genomic profiling of solid tumors
• Population/Ancestry specific variation in cancer susceptibility and disease progression
• Evaluation of population specific genomic in contrast to extrinsic effects in cancer susceptibility and prevalence
• Evolutionary dynamics and fitness landscape in cancer
• Individual specific genetic variation driving cancer heterogeneity
• Trans-ancestry variation in germ line variants, associated with various cancer types
We welcome the following article types: Original Research, Brief Research Report, Methods, Perspective, Review, Mini Review, and Systematic Review.
Cancer is a multifactorial disease that has a direct connection to variations in our genomes. The accumulation of somatic mutations is the main cause for the development of cancer. Cancer genomes are characterized by heterogeneity seen across tumor types, within clinical entities and among individual cases and between individual cancers. Exposure to carcinogenic agents and conditions such as tobacco smoke, ultraviolet light, and even some drugs used for cancer treatment have an important direct role in driving oncogenetic events. The impact of some viral infections - such as from human papillomavirus (HPV) and hepatitis-associated viruses - on oncogenesis has been well recognized. Additionally, life style related risks such as alcohol consumption, malnutrition and lack of physical activity have been found to be associated with a number of malignant diseases. However, the connection of individual and population related risk factors to their molecular mechanisms still has to be elucidated for many malignancies, with the aim to develop specific risk assessment, diagnosis, and control strategies.
Driven by rapid advances in high-throughputs "-omics" technologies, the last decades have provided a fundamental increase in our understanding of the somatic mutations that aid malignant transformation and disease progression. A large number of studies have addressed the genomic profiling of solid tumors as well as functional studies of specific cancer related genes. Focus has always been on investigating germline variants that affect cancer susceptibility, predisposition and disease. However, only in recent years, has it become more feasible to investigate these variants due to a dramatic increase in genomic profiling data. Such variants can be highly population- and ancestry-specific and can provide a part of the explanation why certain cancers are more prevalent among individual populations. For example, prostate cancer has been reported with higher prevalence among the individuals of Afro-American ancestry, lung cancer is more common among admixed Latin Americans and oral cancer is more common among East Asians. However, while such observations may point to shared underlying genome-based variations in susceptibility for certain kinds of cancer, they may also be related to shared environmental or socio-economic factors with higher prevalence in selected populations.
In this special issue, we welcome studies that focus on the germline variants associated with the predisposition of various cancers and can be linked to cancer heterogeneity. The studies can focus on association-based analysis (GWAS/EWAS), genomic profiling, ancestry/population specific variation in cancer susceptibility and disease progression, and individual specific variation driving cancer heterogeneity.
Scope
• Multidimensional approaches to mutational profiling
• Genomic profiling of solid tumors
• Population/Ancestry specific variation in cancer susceptibility and disease progression
• Evaluation of population specific genomic in contrast to extrinsic effects in cancer susceptibility and prevalence
• Evolutionary dynamics and fitness landscape in cancer
• Individual specific genetic variation driving cancer heterogeneity
• Trans-ancestry variation in germ line variants, associated with various cancer types
We welcome the following article types: Original Research, Brief Research Report, Methods, Perspective, Review, Mini Review, and Systematic Review.
