Cancer is not a new dub for the people breathing in the 21st
century. It is as recurrent as our day to day usual activities. Every
year about a million of new cases of cancer are diagnosed throughout the
world. Most people loose their lives because of cancer. Treatment are
available but there is still no 100% surety of recovery from cancer.
Cancer influences almost every organ of human body transfiguring it into
ruins in later stages.
Truly speaking cancer is not a single disease, but a heterogeneous group of disorders that are characterized by the presence of cells that loose control on normal cell division. Cancer cells divide rapidly and continuously resulting in formation of tumours that eventually strike healthy tissues. These tumourous cells travel across healthy cells creating tumours in them. The most frequent cancers include cancers of breast, lung, prostrate, blood, colon, rectum, pancreas, liver etc.
Formation of Tumour
Basically normal cells grow, divide, mature and die in response to a complex set of internal and external signals. A normal cell receives both stimulatory as well as inhibitory signals which are responsible for its growth, division and maturation. In case of a cancer cell, these signals get disrupted, so the cell divides abnormally at a higher rate. After losing normal control, the cancer cell loose its normal shape and forms a distinct mass what we call a 'tumour'. If the cells of a tumour remain localized it is termed a 'benign tumour' but if the cells invade other tissues, the tumour is termed as 'malignant tumour'. Cells that travel to other sites of the body, they form secondary tumours and have undergone 'metastasis'.
Cancer- The Genetic Aspect
Cancer is the culmination of abnormal cell growth so needs attention both publicly as well as scientifically. A number of theories have been put forward regarding cancer but now researchers realize that most if not all cancers arise from the defects in DNA> Previous views recommend the genetic origin of cancer. Many agents like ionizing radiations, chemicals that we come across result in episode of mutations that cause cancer. Some cancers are often syndicated with chromosomal abnormalities, about 90% of people with chronic myeloid leukemia bear a reciprocal trans location between chromosome 22 and chromosome 9> These observations accord clues for the genetic origin of cancer. In 1971 Alfred Knudson proposed a model for defining the genetic basis of cancer. His model id designated as 'Knudson multistep model of cancer', he was studying retinoblastoma- a cancer that develops in only one eye but occasionally appears in both> Knudson's proposal highlights that cancer is a multistep process requiring several mutations, if one or more mutations are inherited additional mutations are also obligatory to disclose a cancer and the cancer will run in families. His model has been confirmed today.
Cancer starts when a single cell is encountered with mutation and results in its abnormal growth. This cell divides and forms a clone of cells each carrying same mutation. An additional mutation that occurs in any of the clone cells may further enhance adroitness of these cells to burgeon and cells with both mutations become dominant. In this process, depicted as clonal evolution, the tumour cells gain more mutations that allow them to become increasingly aggressive in their proliferate aspects. The rate of clonal evolution depends upon the frequency of occurrence of new mutations. The genes that regulate DNA repair have also been found to get mutated in progressive cancer stages and inherited disorders of DNA repair are usually depicted by intensified incidences of cancer. Normally DNA repair mechanisms eliminate many of the mutations but cells with defective DNA repair systems are more likely to remain mutated including the genes that regulate cell division. Many cells are aneuploid and hence accelerate cancer progression.
Are Environmental Factors Also Responsible For Cancer?
Smoking is a good paradigm of environmental factor confronted with cancer strongly. Other environmental factors incorporate certain types of chemicals such as benzene (industrial solvent), benzo [a] pyrene (cigarette smoke), polychlorinated biphenyls (transformers and capacitors). Ultraviolet light, ionizing radiations, viruses are other carcinogens associated with cancer. Most environmental factors cause somatic mutations that quicken cell division.
Genes Contributing Cancer
The signals that regulate cell division fall under two categories: molecules that speed up cell division and others that inhibit it. Because cell division is perturbed by these two factors, cancer can arise from mutations in any of these two factors. Mutations in stimulatory genes are usually dominant and are termed 'oncogenes'. Oncogenes were first identified cancer causing genes discovered by Peyton Rous in 1909. Michael Bishop, Harold Varmus and their colleagues in 1975 discovered that genomes of all normal cells carry DNA sequences that are closely related to viral oncogenes. These cellular genes are termed as protoncogenes. THey are blameworthy for basic cellular functions of normal cells but when mutated they become oncogenes and produce cancer. Many oncogenes have been pinpointed by experiments in which selectted fragments of DNA are added to cells in a culture.
Tumour suppressor genes are more difficultly discerned than oncogenes as they inhibit cancer and are reccessive in action. One of the first tumour suppressor gene to be spotted out was that of retinoblastoma in 1985 by Raymond White and Webster Cavenne.
Alteration In Stucture And Number Of Chromosome Also Cause Cancer
Most tumours possess mutations. It is now clear that mutations in chromosomes appear to be both cause and be a result of cancer. At least three kinds of chromosome rearrangements- deletions, inversions and trans locations may be associated with cancer. Deletions may result in loss of one or more tumour suppressor genes. Inversions and trans locations may result in disruption of functions tumour suppressor genes and generation of fused proteins that may stimulate symptoms of cancer. Fusion proteins are generally formed in myelogenous leukemia, a form of leukemia affecting bone marrow cells. A third process by which cancer may arise due to chromosomal rearrangement is by the transfer of a potential cancer causing gene to a new location where it is activated by regulatory sequences, Burkitt lymphoma is common example.
Viruses Also Cause Cancer
About 95% of the women with cervical cancer are infected with human papiloma viruses (HPVs). Similarly, infection with the virus that causes hepatitis B increases the risk of liver cancer. Epstein-Barr virus causes mononucleosis embracing Burkitt's lymphoma. There are only few retroviruses that cause cancer in humans. Other human cancers are associated with DNA viruses which like retroviruses integrate into the host chromosome but disparate retroviruses donot reverse transcription.
Changes In DNA Methylation Are Often Associated With Cancer
In many cancerous cells the ornamentation of DNA methylation are found to be altered. In some cases, the DNA of cancer cells is over methylated (hypermethylated) or undermethylated (hypomethylated). Hypermethylation is seen to contribute to cancer by silencing the expression of tumour suppressor genes. However, hypomethylation also contributes to cancer requires further research. The role of DNA methylation is interesting because unlike other genetic changes DNA methylation is reversible. These types of reversible genetic alterations are called epigenetic processes.
The treatment of cancer is accessible at present inclusive of chemotherapy, bone marrow transplantation, radiotherapy etc. but the question to be 100% free from cancer still preponderates.
Truly speaking cancer is not a single disease, but a heterogeneous group of disorders that are characterized by the presence of cells that loose control on normal cell division. Cancer cells divide rapidly and continuously resulting in formation of tumours that eventually strike healthy tissues. These tumourous cells travel across healthy cells creating tumours in them. The most frequent cancers include cancers of breast, lung, prostrate, blood, colon, rectum, pancreas, liver etc.
Formation of Tumour
Basically normal cells grow, divide, mature and die in response to a complex set of internal and external signals. A normal cell receives both stimulatory as well as inhibitory signals which are responsible for its growth, division and maturation. In case of a cancer cell, these signals get disrupted, so the cell divides abnormally at a higher rate. After losing normal control, the cancer cell loose its normal shape and forms a distinct mass what we call a 'tumour'. If the cells of a tumour remain localized it is termed a 'benign tumour' but if the cells invade other tissues, the tumour is termed as 'malignant tumour'. Cells that travel to other sites of the body, they form secondary tumours and have undergone 'metastasis'.
Cancer- The Genetic Aspect
Cancer is the culmination of abnormal cell growth so needs attention both publicly as well as scientifically. A number of theories have been put forward regarding cancer but now researchers realize that most if not all cancers arise from the defects in DNA> Previous views recommend the genetic origin of cancer. Many agents like ionizing radiations, chemicals that we come across result in episode of mutations that cause cancer. Some cancers are often syndicated with chromosomal abnormalities, about 90% of people with chronic myeloid leukemia bear a reciprocal trans location between chromosome 22 and chromosome 9> These observations accord clues for the genetic origin of cancer. In 1971 Alfred Knudson proposed a model for defining the genetic basis of cancer. His model id designated as 'Knudson multistep model of cancer', he was studying retinoblastoma- a cancer that develops in only one eye but occasionally appears in both> Knudson's proposal highlights that cancer is a multistep process requiring several mutations, if one or more mutations are inherited additional mutations are also obligatory to disclose a cancer and the cancer will run in families. His model has been confirmed today.
Cancer starts when a single cell is encountered with mutation and results in its abnormal growth. This cell divides and forms a clone of cells each carrying same mutation. An additional mutation that occurs in any of the clone cells may further enhance adroitness of these cells to burgeon and cells with both mutations become dominant. In this process, depicted as clonal evolution, the tumour cells gain more mutations that allow them to become increasingly aggressive in their proliferate aspects. The rate of clonal evolution depends upon the frequency of occurrence of new mutations. The genes that regulate DNA repair have also been found to get mutated in progressive cancer stages and inherited disorders of DNA repair are usually depicted by intensified incidences of cancer. Normally DNA repair mechanisms eliminate many of the mutations but cells with defective DNA repair systems are more likely to remain mutated including the genes that regulate cell division. Many cells are aneuploid and hence accelerate cancer progression.
Are Environmental Factors Also Responsible For Cancer?
Smoking is a good paradigm of environmental factor confronted with cancer strongly. Other environmental factors incorporate certain types of chemicals such as benzene (industrial solvent), benzo [a] pyrene (cigarette smoke), polychlorinated biphenyls (transformers and capacitors). Ultraviolet light, ionizing radiations, viruses are other carcinogens associated with cancer. Most environmental factors cause somatic mutations that quicken cell division.
Genes Contributing Cancer
The signals that regulate cell division fall under two categories: molecules that speed up cell division and others that inhibit it. Because cell division is perturbed by these two factors, cancer can arise from mutations in any of these two factors. Mutations in stimulatory genes are usually dominant and are termed 'oncogenes'. Oncogenes were first identified cancer causing genes discovered by Peyton Rous in 1909. Michael Bishop, Harold Varmus and their colleagues in 1975 discovered that genomes of all normal cells carry DNA sequences that are closely related to viral oncogenes. These cellular genes are termed as protoncogenes. THey are blameworthy for basic cellular functions of normal cells but when mutated they become oncogenes and produce cancer. Many oncogenes have been pinpointed by experiments in which selectted fragments of DNA are added to cells in a culture.
Tumour suppressor genes are more difficultly discerned than oncogenes as they inhibit cancer and are reccessive in action. One of the first tumour suppressor gene to be spotted out was that of retinoblastoma in 1985 by Raymond White and Webster Cavenne.
Alteration In Stucture And Number Of Chromosome Also Cause Cancer
Most tumours possess mutations. It is now clear that mutations in chromosomes appear to be both cause and be a result of cancer. At least three kinds of chromosome rearrangements- deletions, inversions and trans locations may be associated with cancer. Deletions may result in loss of one or more tumour suppressor genes. Inversions and trans locations may result in disruption of functions tumour suppressor genes and generation of fused proteins that may stimulate symptoms of cancer. Fusion proteins are generally formed in myelogenous leukemia, a form of leukemia affecting bone marrow cells. A third process by which cancer may arise due to chromosomal rearrangement is by the transfer of a potential cancer causing gene to a new location where it is activated by regulatory sequences, Burkitt lymphoma is common example.
Viruses Also Cause Cancer
About 95% of the women with cervical cancer are infected with human papiloma viruses (HPVs). Similarly, infection with the virus that causes hepatitis B increases the risk of liver cancer. Epstein-Barr virus causes mononucleosis embracing Burkitt's lymphoma. There are only few retroviruses that cause cancer in humans. Other human cancers are associated with DNA viruses which like retroviruses integrate into the host chromosome but disparate retroviruses donot reverse transcription.
Changes In DNA Methylation Are Often Associated With Cancer
In many cancerous cells the ornamentation of DNA methylation are found to be altered. In some cases, the DNA of cancer cells is over methylated (hypermethylated) or undermethylated (hypomethylated). Hypermethylation is seen to contribute to cancer by silencing the expression of tumour suppressor genes. However, hypomethylation also contributes to cancer requires further research. The role of DNA methylation is interesting because unlike other genetic changes DNA methylation is reversible. These types of reversible genetic alterations are called epigenetic processes.
The treatment of cancer is accessible at present inclusive of chemotherapy, bone marrow transplantation, radiotherapy etc. but the question to be 100% free from cancer still preponderates.
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