Genetics of Cancer

Genetics of Cancer

Cancer Cancer is one of the most common and severe problems of clinical medicine. Cancer is not a single disease but rather a name applied to a great variety of malignant tumors that are formed by the same basic process of uncontrolled growth. Cell proliferation results in a mass that invades neighboring tissues and may metastasize to more distant sites. Some cancers , however, such as blood cancers, do not form tumors. Many aspects of cell function are controlled by a balance of positive and negative signals received from inside and outside the cell. In normal tissues , there is a balance between cell proliferation and cell death. In tumor , this balance is lost . Cancer has both genetic and environmental causes.

Cancer is one of the most common and severe problems of clinical medicine. Cancer is not a single disease but rather a name applied to a great variety of malignant tumors that are formed by the same basic process of uncontrolled growth. Cell proliferation results in a mass that invades neighboring tissues and may metastasize to more distant sites. Some cancers , however, such as blood cancers, do not form tumors.

Many aspects of cell function are controlled by a balance of positive and negative signals received from inside and outside the cell. In normal tissues , there is a balance between cell proliferation and cell death. In tumor , this balance is lost .

Cancer has both genetic and environmental causes.

Cell Cycle

Environmental & Genetic Factors There are cancers in which environmental factors are of primary importance and hereditary seems to play no part in causation. e.g . Industrial cancer which result from prolonged exposure to carcinogenic chemicals as cancer of the skin in tar workers , cancer of the bladder in aniline dye workers,….. In certain cancers, such as breast and bowel cancer, genetic factors play an important , but not exclusive role in the etiology.

There are cancers in which environmental factors are of primary importance and hereditary seems to play no part in causation. e.g . Industrial cancer which result from prolonged exposure to carcinogenic chemicals as cancer of the skin in tar workers , cancer of the bladder in aniline dye workers,…..

In certain cancers, such as breast and bowel cancer, genetic factors play an important , but not exclusive role in the etiology.

Nearly all cancers are caused by abnormalities in the genetic material of the transformed cell. In order for a normal cell to transform into a cancer cell , genes which regulate cell growth and differentiation must be altered . When normal regulation is altered, uncontrolled growth is initiated and a malignant tumor develop. Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. New aspects of the genetics of cancer pathogenesis, such as DNA methylation and microRNAs are increasingly recognized. The Genetic Nature of Cancer

Nearly all cancers are caused by abnormalities in the genetic material of the transformed cell.

In order for a normal cell to transform into a cancer cell , genes which regulate cell growth and differentiation must be altered . When normal regulation is altered, uncontrolled growth is initiated and a malignant tumor develop.

Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide.

New aspects of the genetics of cancer pathogenesis, such as DNA methylation and microRNAs are increasingly recognized.

These abnormalities may be due to Carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents (Viruses are involved in cancers) . Randomly acquired through errors in DNA replication or Inherited and thus present in all cells from birth . The heritability of cancers are usually affected by complex interactions between carcinogens and the host's genome.

These abnormalities may be due to

Carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents (Viruses are involved in cancers) .

Randomly acquired through errors in DNA replication or

Inherited and thus present in all cells from birth . The heritability of cancers are usually affected by complex interactions between carcinogens and the host's genome.

There are two basic kinds of genetic mutations Germline mutations are responsible for 5% to 10% of cancer cases . This is also called familial ( occurring in families ) cancer . Sporadic cancer or somatic mutation . Most cancers are caused by a series of mutations that develop during a person's lifetime called acquired mutations . Acquired mutations are caused by tobacco, over - exposure to UV radiation, and other toxins and chemicals . These mutations are not in every cell of the body and are not passed from parent to child .

Germline mutations are responsible for 5% to 10% of cancer cases . This is also called familial ( occurring in families ) cancer .

Sporadic cancer or somatic mutation . Most cancers are caused by a series of mutations that develop during a person's lifetime called acquired mutations . Acquired mutations are caused by tobacco, over - exposure to UV radiation, and other toxins and chemicals . These mutations are not in every cell of the body and are not passed from parent to child .

Genes That play a Role in Cancer Oncogenes Tumor suppressor genes DNA repair genes. These are genes that fix any mistakes made when DNA is replicated (copied). Mistakes that aren't fixed become mutations, which may eventually lead to cancer, especially if the mutation occurs in a tumor suppressor gene or oncogene.

Oncogenes

Tumor suppressor genes

DNA repair genes. These are genes that fix any mistakes made when DNA is replicated (copied). Mistakes that aren't fixed become mutations, which may eventually lead to cancer, especially if the mutation occurs in a tumor suppressor gene or oncogene.

Distribution of Oncogenes, Cancer Genes and Tumor Suppressor Genes in the Human Genome The two types have opposite effects in carcinogenesis. Oncogenes facilitate malignant transformation, whereas tumor suppressor genes , block tumor development by regulating genes involved in cell growth.

http :// upload . wikimedia . org / wikipedia / en / 7/73 / Cancer_requires_multiple_mutations_from_NIH . png Cancer develops when several genes in a cell become mutated in a way that overrides the checks and balances of the cell . However, many cancers cannot be tied to a specific gene, and some genes may interact in unpredictable ways with other genes or factors in the environment to cause cancer.

Oncogenes Oncogenes are known by three letter abbreviation which reflect their origin or the type of tumor with which they are associated. Cancer - promoting oncogenes : If oncogene is altered or overexpressed, either as a result of a mutation in the gene itself or by altered external control, the cell in which the change occurred can undergo uncontrolled growth, eventually malignant. Most oncogenes are mutated forms of normal genes, called proto-oncogenes.

Oncogenes are known by three letter abbreviation which reflect their origin or the type of tumor with which they are associated.

Cancer - promoting oncogenes : If oncogene is altered or overexpressed, either as a result of a mutation in the gene itself or by altered external control, the cell in which the change occurred can undergo uncontrolled growth, eventually malignant. Most oncogenes are mutated forms of normal genes, called proto-oncogenes.

Proto-oncogene proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. Those proto-oncogene which have been to mutate in any individual are called cellular oncogenes and are designated by the prefix c to distinguish them from viral oncogenes v-onc . Those protooncogenes that have not been found to mutate are called normal oncogene and are designated n . Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through its protein product.

proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. Those proto-oncogene which have been to mutate in any individual are called cellular oncogenes and are designated by the prefix c to distinguish them from viral oncogenes v-onc . Those protooncogenes that have not been found to mutate are called normal oncogene and are designated n .

Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through its protein product.

Types of Oncogene Oncogene can be classified according to their cellular location and function of their encoded oncoproteins in the signal transduction pathway: Growth factors Growth factor receptors GTP binding proteins Post receptor tyrosine kinase Cytoplasmic oncogenes Nuclear oncogenes Apoptotic oncogenes

Oncogene can be classified according to their cellular location and function of their encoded oncoproteins in the signal transduction pathway:

Growth factors

Growth factor receptors

GTP binding proteins

Post receptor tyrosine kinase

Cytoplasmic oncogenes

Nuclear oncogenes

Apoptotic oncogenes

Mutation within a proto - oncogene can cause a change in the protein structure, causing an increase in protein enzyme activity & a loss of regulation. An increase in protein concentration , caused by an increase of protein expression through misregulation, an increase of protein stability, prolonging its existence and thus its activity in the cell and a gene duplication one type of chromosome abnormality, resulting in an increased amount of protein in the cell. Chromosomal translocation An increased gene expression in the wrong cell type or at wrong times The expression of a constitutively active hybrid protein . This type of aberration in a dividing stem cell in the bone marrow leads to adult leukemia . Activation of Proto-oncogene

Mutation within a proto - oncogene can cause a change in the protein structure, causing an increase in protein enzyme activity & a loss of regulation.

An increase in protein concentration , caused by an increase of protein expression through misregulation, an increase of protein stability, prolonging its existence and thus its activity in the cell and a gene duplication one type of chromosome abnormality, resulting in an increased amount of protein in the cell.

Chromosomal translocation

An increased gene expression in the wrong cell type or at wrong times

The expression of a constitutively active hybrid protein . This type of aberration in a dividing stem cell in the bone marrow leads to adult leukemia .

The activities of activated proto-oncogenes are one of the key mechanisms involved in the malignant transformation of cells and the development of malignant cells that have escaped the constraints of normal regulated cell growth and differentiation. Activated oncogenes are involved in different phases of the initiation, progression, and/or metastasis of tumor cells. Most oncogenes transform cells by taking over the roles of growth factors, hormone receptors, G-proteins, intracellular effector systems, and transcription factors and expressing these functions in an uncontrolled manner.

The activities of activated proto-oncogenes are one of the key mechanisms involved in the malignant transformation of cells and the development of malignant cells that have escaped the constraints of normal regulated cell growth and differentiation.

Activated oncogenes are involved in different phases of the initiation, progression, and/or metastasis of tumor cells. Most oncogenes transform cells by taking over the roles of growth factors, hormone receptors, G-proteins, intracellular effector systems, and transcription factors and expressing these functions in an uncontrolled manner.

Characteristics of cellular proto - oncogenes These are typical cellular genes with typical control sequences . As with most eukaryotic genes, most have introns ( while retroviral oncogenes - v - oncs - do not ( . They show normal Mendelian inheritance because they are normal genes, essential to the functions of the cell . As with all genes in the eukaryotic genome, they are always at same place in genome. There are no LTR sequences ( v - oncs always are in an LTR context). Cellular oncogenes are expressed by the cell at some period in the life of the cell, often when the cell is growing, replicating and differentiating normally . They are usually proteins that are involved in growth control . Cellular oncogenes are highly conserved.

These are typical cellular genes with typical control sequences . As with most eukaryotic genes, most have introns ( while retroviral oncogenes - v - oncs - do not ( .

They show normal Mendelian inheritance because they are normal genes, essential to the functions of the cell .

As with all genes in the eukaryotic genome, they are always at same place in genome.

There are no LTR sequences ( v - oncs always are in an LTR context).

Cellular oncogenes are expressed by the cell at some period in the life of the cell, often when the cell is growing, replicating and differentiating normally . They are usually proteins that are involved in growth control .

Cellular oncogenes are highly conserved.

Function of Oncogenes ? Products of oncogenes that are nuclear proteins : e . g . myc , myb .These are involved in control of gene expression or the control of DNA replication . Products of oncogenes that are cytoplasmic or membrane - associated proteins : e . g . abl, src, ras . This type does not exhibit altered expression but seems to convert from proto - oncogene to oncogene by mutation .

Products of oncogenes that are nuclear proteins : e . g . myc , myb .These are involved in control of gene expression or the control of DNA replication .

Products of oncogenes that are cytoplasmic or membrane - associated proteins : e . g . abl, src, ras . This type does not exhibit altered expression but seems to convert from proto - oncogene to oncogene by mutation .

Viruses and Cancer Many viruses infect humans but only a few viruses are known to promote human cancer . These include both DNA viruses and retroviruses, a type of RNA virus. Viruses associated with cancer include human papillomavirus ( genital carcinomas ) , hepatitis B ( liver carcinoma ) , Epstein - Barr virus ( Burkitt's lymphoma and nasopharyngeal carcinoma ) , human T - cell leukemia virus ( T - cell lymphoma ) ; and, probably, a herpes virus called KSHV ( Kaposi's sarcoma and some B cell lymphomas ).

Many viruses infect humans but only a few viruses are known to promote human cancer . These include both DNA viruses and retroviruses, a type of RNA virus.

Viruses associated with cancer include human papillomavirus ( genital carcinomas ) , hepatitis B ( liver carcinoma ) , Epstein - Barr virus ( Burkitt's lymphoma and nasopharyngeal carcinoma ) , human T - cell leukemia virus ( T - cell lymphoma ) ; and, probably, a herpes virus called KSHV ( Kaposi's sarcoma and some B cell lymphomas ).

DNA Tumor Viruses Viruses can also contribute to cancer by inserting their DNA into a chromosome in a host cell . Insertion of the virus DNA directly into a proto - oncogene may mutate the gene into an oncogene, resulting in a tumor cell . Insertion of the virus DNA near a gene in the chromosome that regulates cell growth and division can increase transcription of that gene, also resulting in a tumor cell . Human papillomavirus makes proteins that bind to two tumor suppressors, p53 protein and RB protein, transforming these cells into tumor cells .

Viruses can also contribute to cancer by inserting their DNA into a chromosome in a host cell .

Insertion of the virus DNA directly into a proto - oncogene may mutate the gene into an oncogene, resulting in a tumor cell .

Insertion of the virus DNA near a gene in the chromosome that regulates cell growth and division can increase transcription of that gene, also resulting in a tumor cell .

Human papillomavirus makes proteins that bind to two tumor suppressors, p53 protein and RB protein, transforming these cells into tumor cells .

Retroviral Oncogenes Oncogenes were detected initially as retroviral genes directly responsible for the immortalisation of eukaryotic cells and malignant transformation both in vitro and in vivo. Many of the viral oncogenes (general abbr. v-onc) have homologous cellular counterparts (general abbr. c-onc) known as proto-oncogenes. The study of retroviral oncogene functions has provided insights into the role of cellular proto-oncogenes .

Oncogenes were detected initially as retroviral genes directly responsible for the immortalisation of eukaryotic cells and malignant transformation both in vitro and in vivo. Many of the viral oncogenes (general abbr. v-onc) have homologous cellular counterparts (general abbr. c-onc) known as proto-oncogenes.

The study of retroviral oncogene functions has provided insights into the role of cellular proto-oncogenes .

The ability of retroviruses to promote cancer is associated with the presence of oncogenes in these viruses . These oncogenes are very similar to proto - oncogenes in animals . Retroviruses have acquired the proto - oncogene from infected animal cells . An example of this is the normal cellular c - SIS proto - oncogene, which makes a cell growth factor . The viral form of this gene is an oncogene called v - SIS . Cells infected with the virus that has v - SIS overproduce the growth factor, leading to high levels of cell growth and possible tumor cells . RNA Tumor Viruses

Most oncogenes are dominant mutations ; a single copy of this gene is sufficient for expression of the growth trait . This is also a " gain of function " mutation because the cells with the mutant form of the protein have gained a new function not present in cells with the normal gene . Similarly, one copy of an oncogene is sufficient to cause alterations in cell growth . The presence of an oncogene in a germ line cell ( egg or sperm ) results in an inherited predisposition for tumors in the offspring . However, a single oncogene is not usually sufficient to cause cancer, so inheritance of an oncogene does not necessarily result in cancer .

Most oncogenes are dominant mutations ; a single copy of this gene is sufficient for expression of the growth trait . This is also a " gain of function " mutation because the cells with the mutant form of the protein have gained a new function not present in cells with the normal gene . Similarly, one copy of an oncogene is sufficient to cause alterations in cell growth . The presence of an oncogene in a germ line cell ( egg or sperm ) results in an inherited predisposition for tumors in the offspring . However, a single oncogene is not usually sufficient to cause cancer, so inheritance of an oncogene does not necessarily result in cancer .

Tumor Suppressor Genes Tumor suppressor gene or anti oncogene: In contrast to oncogene, tumor suppressor genes are normal genes implicated in the control of cell cycle, repair DNA mistakes, and tell cells when to die (apoptosis or programmed cell death). When tumor suppressor genes don’t work properly, cells can grow out of control, which can lead to cancer.

Tumor suppressor gene or anti oncogene: In contrast to oncogene, tumor suppressor genes are normal genes implicated in the control of cell cycle, repair DNA mistakes, and tell cells when to die (apoptosis or programmed cell death). When tumor suppressor genes don’t work properly, cells can grow out of control, which can lead to cancer.

Types of Tumor Suppressor Genes Genes that control cell division : Some tumor suppressor genes help control cell growth and reproduction . The ( RB1 ( retinoblastoma gene is an example of such a gene . Abnormalities of the RB1 gene can lead to a type of eye cancer ( retinoblastoma ) in infants, as well as to other cancers . Genes that repair DNA : The genes responsible for HNPCC ( hereditary nonpolyposis colon cancer ) are examples of DNA repair gene defects . When these genes do not repair the errors in DNA, HNPCC can result . HNPCC accounts for up to 5% of all colon cancers and some endometrial cancers. Cell " suicide " genes : If there is too much damage to a cell’s DNA to be fixed by the DNA repair genes, the p53 tumor suppressor gene is responsible for destroying the cell by a process sometimes described as " cell suicide .".

Genes that control cell division : Some tumor suppressor genes help control cell growth and reproduction . The ( RB1 ( retinoblastoma gene is an example of such a gene . Abnormalities of the RB1 gene can lead to a type of eye cancer ( retinoblastoma ) in infants, as well as to other cancers .

Genes that repair DNA : The genes responsible for HNPCC ( hereditary nonpolyposis colon cancer ) are examples of DNA repair gene defects . When these genes do not repair the errors in DNA, HNPCC can result . HNPCC accounts for up to 5% of all colon cancers and some endometrial cancers.

Cell " suicide " genes : If there is too much damage to a cell’s DNA to be fixed by the DNA repair genes, the p53 tumor suppressor gene is responsible for destroying the cell by a process sometimes described as " cell suicide .".

Retinoblastoma is a juvenile eye cancer that is caused by a mutation in the Rb gene located on chromosome 13 of humans . This gene suppresses the development of cancer as its dominant phenotype . Therefore both alleles must be mutant for the disease to develop .

Retinoblastoma is a juvenile eye cancer that is caused by a mutation in the Rb gene located on chromosome 13 of humans . This gene suppresses the development of cancer as its dominant phenotype . Therefore both alleles must be mutant for the disease to develop .

p53 , located human chromosome 17, is another gene with tumor suppressor activities . This protein contains 393 amino acids and a single amino acid substitution can lead to loss of function of the gene . Mutations at amino acids 175, 248, and 273 can lead to loss of function and changes at 273 ( 13% ) are the most common . These all act as recessive mutations . About 50% of human cancers can be associated with a p53 mutation including cancers of the bladder, breast, cervix, colon, lung, liver, prostate, and skin . p53 related cancers are also more aggressive and have a higher degree of fatalities .

p53 , located human chromosome 17, is another gene with tumor suppressor activities . This protein contains 393 amino acids and a single amino acid substitution can lead to loss of function of the gene . Mutations at amino acids 175, 248, and 273 can lead to loss of function and changes at 273 ( 13% ) are the most common . These all act as recessive mutations . About 50% of human cancers can be associated with a p53 mutation including cancers of the bladder, breast, cervix, colon, lung, liver, prostate, and skin . p53 related cancers are also more aggressive and have a higher degree of fatalities .

Inherited Abnormalities of Tumor Suppressor Genes have been found in several cancers that tend to run in families . In addition to mutations in p53, RB1, and the genes involved in HNPCC, several other mutations in tumor suppressor genes can be inherited . A defective APC gene causes familial polyposis , a condition in which people develop hundreds or thousands of colon polyps, some of which may eventually acquire several sporadic mutations and turn into colon cancer . Abnormalities of the BRCA genes account for 5% to 10% of breast cancers . Non - inherited mutations of tumor suppressor genes : Mutations of tumor suppressor genes have been found in many cancers . For example, abnormalities of the p53 gene have been found in over 50% of human cancers . Acquired mutations ( those which happen during a person’s life ) of the p53 gene appear to be involved in a wide range of cancers, including lung, colorectal, and breast cancer, as well as many others . The p53 gene is believed to be among the most frequently mutated genes in human cancer . However, acquired changes in many other tumor suppressor genes also contribute to the development of sporadic ( not inherited ) cancers .

Inherited Abnormalities of Tumor Suppressor Genes have been found in several cancers that tend to run in families . In addition to mutations in p53, RB1, and the genes involved in HNPCC, several other mutations in tumor suppressor genes can be inherited . A defective APC gene causes familial polyposis , a condition in which people develop hundreds or thousands of colon polyps, some of which may eventually acquire several sporadic mutations and turn into colon cancer . Abnormalities of the BRCA genes account for 5% to 10% of breast cancers .

Non - inherited mutations of tumor suppressor genes : Mutations of tumor suppressor genes have been found in many cancers . For example, abnormalities of the p53 gene have been found in over 50% of human cancers . Acquired mutations ( those which happen during a person’s life ) of the p53 gene appear to be involved in a wide range of cancers, including lung, colorectal, and breast cancer, as well as many others . The p53 gene is believed to be among the most frequently mutated genes in human cancer . However, acquired changes in many other tumor suppressor genes also contribute to the development of sporadic ( not inherited ) cancers .

Heterogeneity of p53 inactivation in human cancer . p53 mutations can be found in 50% of human cancers, but their penetrance is highly heterogeneous, as reflected by the diverse remaining transactivation activity that ranges from O to 100%. Various DNA viruses, such as SV40, HPV or adenoviruses, encode proteins that target p53 protein . In inflammatory breast cancer and neuroblastoma, p53 is predominantly found in the cytoplasm. mdm2 accumulation is found in numerous cancers, such as sarcoma or breast carcinomas. PTEN, a p53 regulated gene, is mutated in various types of cancer including glioblastoma . Although no mutation of AKT has been found in human cancer, constitutive activation of its kinase activity has been observed via deregulation of the upstream pathway . Mutations in various pathways upstream of p53 ( ATM, p19ARF or Hcdk2 gene ) can be observed in various types of cancer .

Heterogeneity of p53 inactivation in human cancer .

p53 mutations can be found in 50% of human cancers, but their penetrance is highly heterogeneous, as reflected by the diverse remaining transactivation activity that ranges from O to 100%.

Various DNA viruses, such as SV40, HPV or adenoviruses, encode proteins that target p53 protein .

In inflammatory breast cancer and neuroblastoma, p53 is predominantly found in the cytoplasm.

mdm2 accumulation is found in numerous cancers, such as sarcoma or breast carcinomas.

PTEN, a p53 regulated gene, is mutated in various types of cancer including glioblastoma .

Although no mutation of AKT has been found in human cancer, constitutive activation of its kinase activity has been observed via deregulation of the upstream pathway .

Mutations in various pathways upstream of p53 ( ATM, p19ARF or Hcdk2 gene ) can be observed in various types of cancer .

The heritability of cancers are usually affected by complex interactions between carcinogens and the host's genome. Most forms of cancer are " sporadic " , and have no basis in heredity . There are, however, a number of recognized syndromes of cancer with a hereditary component, often a defective tumor suppressor allele . Famous examples are : Certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast cancer and ovarian cancer Tumors of various endocrine organs in multiple endocrine neoplasia MEN types 1, 2a, 2b. Li - Fraumeni syndrome various tumors such as osteosarcoma , breast cancer , soft tissue sarcoma, brain tumors due to mutations of p53 Turcot syndrome brain tumors and colonic polyposis . Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon carcinoma Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome ) can include familial cases of colon cancer uterine cancer , gastric cancer and ovarian cancer without a preponderance of colon polyps Retinoblastoma when occurring in young children, is due to a hereditary mutation in the retinoblastoma gene . Down syndrome patients, who have an extra chromosome 21are known to develop malignancies such as l eukemia and testicular cancer , though the reasons for this difference are not well understood.

The heritability of cancers are usually affected by complex interactions between carcinogens and the host's genome.

Most forms of cancer are " sporadic " , and have no basis in heredity . There are, however, a number of recognized syndromes of cancer with a hereditary component, often a defective tumor suppressor allele . Famous examples are :

Certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast cancer and ovarian cancer

Tumors of various endocrine organs in multiple endocrine neoplasia MEN types 1, 2a, 2b.

Li - Fraumeni syndrome various tumors such as osteosarcoma , breast cancer , soft tissue sarcoma, brain tumors due to mutations of p53

Turcot syndrome brain tumors and colonic polyposis .

Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon carcinoma

Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome ) can include familial cases of colon cancer uterine cancer , gastric cancer and ovarian cancer without a preponderance of colon polyps

Retinoblastoma when occurring in young children, is due to a hereditary mutation in the retinoblastoma gene .

Down syndrome patients, who have an extra chromosome 21are known to develop malignancies such as l eukemia and testicular cancer , though the reasons for this difference are not well understood.

Inherited susceptibility for the common cancers The level of risk for persons with a family history of one of the common cancers such as bowel or breast cancer depends on a number of factors. These include the number of person at risk to the affected individuals and the age at which the affected family members develop cancers,… Persons at risk of an inherited cancer susceptibility can be screened for associated features of a familial cancer predisposing syndrome or for particular cancer.

The level of risk for persons with a family history of one of the common cancers such as bowel or breast cancer depends on a number of factors. These include the number of person at risk to the affected individuals and the age at which the affected family members develop cancers,…

Persons at risk of an inherited cancer susceptibility can be screened for associated features of a familial cancer predisposing syndrome or for particular cancer.

Conclusion Cancer is a genetic disorder in which the normal control of cell growth is lost. The basic mechanism in all cancer is mutation , either in the germ line or much more frequently, in somatic cells. Cancer is multi-factorial diseases, much remains to be learned about the genetic processes of carcinogenesis and about he environmental factors that alter DNA and thus lead to malignancy.

Cancer is a genetic disorder in which the normal control of cell growth is lost. The basic mechanism in all cancer is mutation , either in the germ line or much more frequently, in somatic cells. Cancer is multi-factorial diseases, much remains to be learned about the genetic processes of carcinogenesis and about he environmental factors that alter DNA and thus lead to malignancy.

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