Cancer Genes

Chromosome 13 represents around 4 percent of the total cellular DNA with 115 million base pairs. It is home to various tumor suppressors and oncogenes, such as ADP ribosylation factors like GTPase-11 (ARL11), Retinoblastoma-1 (RB1), Ras-related protein Rap-2a (RAP2A), etc. Most of the somatic mutations in this chromosome lead to cancer development. Further, deletion in this chromosome has been reported to support the cancer of leukemias, lymphomas, etc. In this chapter, we have tried to list cancer-causing genes and their possible oncogenesis in cancer development.

Cancer genetics has focused on several mutational events within a tumor cell for many years. Recently, the study on cancer genetics has been widened by concentrating on the importance of intercellular communication and epigenetic events causing tumor progression and development. The translocation of genetic material betwixt chromosome 14 and other chromosomes may engender the formation of various types of tumors. Recent studies emphasize that these chief translocations between two chromosomes may disrupt the genes crucial for controlling cell growth and cell division. The translocations involving chromosome-14 and other chromosomes have been found in tumors including acute myeloid Leukemia, acute lymphoblastic leukemia, acute bilineal leukemia, follicular lymphoma, small cell lung cancer, non-Hodgkin’s lymphoma, Burkitt lymphoma and multiple myeloma. The tumor suppressor genes, such as ARID4A, ARID4B, BCL11B, BMP4, CCNB1IP1, CEBPE, DICER1, DLK1, ESR2, FOXN3, HIF1A, MAX, MEG3, NDRG2 and TTF-1/NKX2-1 under chromosome 14, play a hypercritical role by enhancing cellular differentiation, migration, proliferation, metastasis, invasion, cellular growth, and development in several tumors, including breast cancer, pancreatic tumor, osteosarcoma, lung cancer, endocrine tumor, T-ALL, cystic nephroma, Hodgkin lymphoma, pleuropulmonary blastomas, Sertoli Leydig ovarian tumors and rhabdomyosarcoma. Chapter 14 meticulously discusses the importance of each predominant gene under chromosome 14 in mediating tumorigenesis. In cancer genetics, these cardinal genes play a crucial role by acting as an oncogene or a tumor suppressor in several cancers. Thus, targeting these tumor-causing genes would provide a breakthrough in cancer biology and oncology when concerned with future perspectives.

The genomic alteration at chromosome 15 has been widely recognized as the utmost significant and prevalent alteration in several cancers, including non-small-cell lung cancer, breast cancer, ovarian cancer, prostate cancer, gastrointestinal cancer, acute lymphoblastic leukemia, colorectal carcinoma, hepatocellular carcinoma, myeloma, pituitary adenomas, etc. Emerging reports suggest that the abnormalities of prime genes in chromosome 15 have drastic effects on tumor development and progression, and can be candidate biomarkers of disease prognosis, disease progression, and response to treatment. The translocations involving chromosome 15 and other chromosomes have been found in tumors, including mucoepidermoid carcinomas, mixed-lineage leukemia, colorectal cancer, pancreatic cancer, sarcoma, lung adenocarcinoma, melanoma, brain cancer, cholangiocarcinoma, spitz tumor, congenital mesoblastic nephroma, papillary thyroid cancer, pontine glioma tumors, and acute promyelocytic leukemia. The tumor suppressor genes such as C15orf65, CSK, CRABP1, DAPK2, FES, GREM1, KNSTRN, NEDD4-1, NTRK3, PML, SPRED1, TPM1, and TCF12 under chromosome 15 play a crucial role by enhancing cellular growth, proliferation, migration, invasion, metastasis, cellular differentiation, and development in various cancer, including colorectal cancer, acute promyelocytic leukemia, myeloid leukemia, breast cancer, thyroid carcinoma, glioblastoma, intrahepatic cholangiocarcinoma, chondrosarcoma, cartilaginous cancer, Squamous cell carcinoma, non- small-cell lung carcinomas, mucosal melanoma, and oral squamous cell carcinoma. Chapter 15 discusses the significance of each important gene under chromosome 15 in mediating oncogenesis. The elevated or attenuated expression levels of these cardinal genes can either act as an oncogene or a tumor suppressor. Thus, shedding light on these genes would be a game changer in the field of cancer genetics and theragnostic.

Cancer is a heterogeneous disorder with invasive and metastatic potential. It is a deadly disorder affecting 1 in 6 people worldwide. Hence, it is important to eliminate the disease. Genetic alterations remain an underlying cause of cancer, and several gene mutations were involved in causing different types of cancer. Recently, researchers have been investigating the role of genetic mutations in causing cancer. For this reason, the genes associated with chromosome 16 were investigated for their role in causing cancer. This study revealed 70 genes associated with cancer. Of which, the cadherin genes (CDH11, CDH13, and CDH1), AXIN-1, ANKRD11, BANP, CYLD, CBFA2T3, IR8, MVP, MT1F, NQO1 and PYCARD was the tumor suppressor, and the gene MSLN is the potential oncogene. CBFB and MYH11 are well-known fusion genes associated with this chromosome. Loss of heterogeneity was noted in the q arm of this chromosome. The chromosome translocations, t (16;16) (16) (p13q22), t (16;21) (21) (p11;q22), t (12;16) (q13; p13; p11), t(16;21) (p11;q22) and t(7;16) (q33; p11) led to the development of acute myeloid leukemia, leukemia, and sarcoma. Several other genes associated with chromosome 16 responsible for cancer initiation and proliferation are summarized in this chapter. A novel insight into the genetic biomarkers and therapeutic targets has been provided to develop potential therapeutic strategies against cancer. 

Cancer is a disease in which the body's cells divide disorderly and are likely to spread to other organs. It has always been one of the world's top causes of death. A growing population, low mortality rate, and lifestyle changes lead to an increase in the number of cancer cases. It can be caused by genetic or environmental factors or a combination of both. The risk of cancer increases with age as the body loses its ability to eliminate the damaged cells. Cancer-causing genes can be inherited or acquired due to exposure to carcinogens. Cancers are inherited when a mutation occurs in the germ cells. The carcinogens can alter the DNA of a normal gene (a proto-oncogene) converting it into a cancerous oncogene. Genes that slow cell division, fix DNA errors, or undergo programmed cell death (apoptosis) are tumor suppressor genes. Tumor suppressor genes that don't function properly can cause cells to develop out of control, leading to cancer. Cancer expresses itself differently in each individual, making it challenging to identify and treat. Studying the types of genetic mutations, as well as the genes, proteins, and signaling pathways involved in cancer formation will help better understand the underlying cause of cancer. Identifying which genes are expressed in various cancer types will enable scientists to develop novel techniques for curing the disease. This chapter will explain how different cancer types are linked to specific genes and their locations on chromosome 17. 

Cancer is an abnormal or unusual growth of cells in the body with invasive and migrating potential. It leads to loss of function, weakens the immune system, and is the second leading cause of death worldwide. This makes it important to eliminate the disease. Genetic predisposition imposes a high relative risk for several kinds of cancer. Inherited genetic mutations are responsible for causing 5 to 10 percent of all cancers. Scientists have investigated mutations in specific genes with more than 50 hereditary cancer syndromes. For this, chromosome 18 was explored for its genes associated with cancer and this study unveiled 30 genes involved in causing cancer. Of these, the genes DCC, EPB41L3, MBD1 PHLPP1, and RBBP8 were the potential tumor suppressors. This chromosome consists of the target genes of the transforming growth factor-beta (TGF-β) signaling pathway. The SMAD family genes (SMAD4, SMAD7, and SMAD2) are encoded by this chromosome, of which SMAD4 acts as a tumor suppressor. SERPINB5 and TCF-4 were the potential oncogenes. The enzyme coded by TYMS was a potential therapeutic target for chemotherapy. Several fusion genes of this chromosome (SS18-SSX2B, SS18-SSX2, and SS18-SSX4) have been identified to cause cancer. Therefore, this chapter provides a summary of the genes in chromosome 18 that are involved in the initiation and proliferation of cancer and provides an insight into the potential biomarkers and therapeutic targets for clinical application to develop a cancer-free world.

Gene is considered discrete coding units that contain the information for individual proteins. These lot of genes were combined and named DNA which is tightly coiled many times over the histone protein to form Chromosomes. Humans have got 23pairs of chromosomes, including the sex chromosome. The current study is about the major genes and their functions that are present in chromosome 19. There are approximately 1500 genes present in this chromosome, and changes in chromosome 19 are identified in many cancers. Dislocation of the chromosome, a mutation in genes that are present in a chromosome (rearrangements, deletions, or duplications) of DNA in the chromosome, epigenetic modification, and lifestyle changes are some of the chromosomal abnormalities that are responsible for cancer-causing. These changes will trigger the growth of normal cells and induce cancer cell proliferation, migration, invasion, angiogenesis, and metastasis. The signaling pathways like PI3K/AKT, JAK/STAT, NF-κB, and TGF-β are responsible for the various cellular functions with the result of autocrine, juxtacrine, intracrine, paracrine, or endocrine. When the dysregulation of these signaling pathways leads to cancer progression and metastasis. Prostate cancer, breast cancer, gastric cancer, pancreatic cancer, colon cancer, gastric cancer, lung cancer, leukemia, and cervical cancer are the major cancers that are caused because of mutation that occurs in chromosome 19.

Over the years, many scientists and doctors have been treating the deadly disease of cancer but are not able to find a permanent treatment for this disease. Also, sometimes it becomes very difficult to understand the mechanisms and causes of cancer as it is a very complex disease that involves many biological processes. Due to the redundancy in our biological system, cancer progression becomes very easy, thus making it difficult to cure. To find the root cause of this disease, we should know what genetic alterations are undergoing, which is causing cancer to progress, and know who is participating in these alterations, like proteins, signaling pathways, or genes. Cancer is caused due to various reasons; it can be due to genetics but mostly due to carcinogens, causing mutations in the genes, thereby making them an oncogene. The Proto-oncogenes are those genes that usually assist the growth of tumor cells. The alteration, mutation, or increased copy number of a particular gene may turn into a proto-oncogene which could end up completely activated or turned on. Many Tumor-causing alterations or mutations related to oncogenes are usually acquired and not inherited. These tumor-causing mutations often actuate oncogenes via chromosomal rearrangement, or alterations in the chromosome, which sequestrates one gene after another, thereby permitting the first gene to prompt the alternative. Search which genes are involved in different cancer types would help scientists proceed with new methods for finding a cure for this disease. This article will depict which genes and their location on which chromosomes, specifically on chromosome 20, are related to different types of cancer.

The significance of human chromosome 21 is that the trisomy of human chromosome 21 causes Down syndrome in children. There are about 235 protein-coding genes on chromosome 21. Mutations like translocation in human chromosome 21 cause different conditions such as partial monosomy 21, core binding factor acute myeloid leukemia, ring chromosome 21, and other types of cancers such as acute lymphoblastic leukemia. Mutation in the DSCAM gene causes mental retardation and facial deformities in down syndrome. The human chromosome 21 also comprises the APP gene, where the expression of the gene causes Alzheimer's disease. The genes that are involved in causing Down syndrome and Alzheimer's diseases are also involved in cancer. This chapter discusses 63 genes of human chromosome 21 that are involved in different types of cancer.

When the collection of human Chromosome 22 was first suggested in 1999, it became the most extended, non-stop stretch of DNA ever decoded and assembled. Chromosome 22 became the first of the 23 human chromosomes to decode due to its minimal length and affiliation with numerous diseases. Chromosome 22 involves several genes that contribute to cancer genetics in one way or the other. The contribution of chromosome 22 in abnormalities is evident through somatic translocations, germline and somatic, and in certain cases, overexpression of genes. One famous example is the Philadelphia translocation, particularly in chronic myeloid leukemia cells. Various gene contributions about types of cancer such as Acute Myeloid Leukemia, colorectal, lung, breast cancer and many more have been reported in studies related to chromosome 22. This chapter takes a run-through of important targeted studies of a gene that facilitates itself as a part of cancer genetics.

X Chromosome is the sex chromosome that is found in many organisms. Both males and females, including mammalians, have X Chromosomes. Females have XX sets of chromosomes, and males have XY sets of chromosomes. X Chromosome aids in identifying the sex of the organism. The Human X chromosome contains approximately 1500 genes. These genes may undergo some genetic alterations and eventually lead to complex diseases. Genetic mutations in some of the genes of the X chromosome are associated with cancer. Some specific mutations are observed in human cancer cells. This chapter specifically relayed on X chromosomal genes that are associated with different types of cancer and gave information on the location of the gene in the X chromosome. Moreover, the function of the specific gene and information regarding how many types of cancers were associated with a particular gene, has also been provided.

Sex chromosome constitution vary genetically in both genders, such as XY in male and XX in female. Even though the chromosomes X and Y advanced from the autosomal pair of the same ancestor, male-specific genes were harbored by the Y chromosome. This Y chromosome plays a crucial role in germ cell differentiation, sex determination in males, and numerous tissue masculinization. Translocations or deletions of SRY, the sex-determining gene of the Y chromosome, enable sex development disorders with dysgenic gonads. Gonadal improvement failure outturns not only in infertility but also in the highest possibilities of GCT (Germ Cell Tumour), like various kinds of testicular GCT and gonad blastoma. Studies have shown that selected somatic cancers are closely related to both losses of Y chromosome genes, ectopic expression, or Y chromosome. These observations remark that genes of the Y chromosome are associated with male diseases and health more than attic turns out not only in infertility but also in the highest possibilities of GCT (Germ Cell Tumour) like various kindspated. Even though only a compact amount of protein-coding genes are seen in Y chromosomes male-specific region, the effects of those Y chromosomal genes on human disease are still predominantly unknown. In this part, we can find the participation of selected genes of the Y chromosome in cancer growth in men.