Answer: Cellular oncogene formation: Carcinogenesis, tumorogenesis or oncogenesis are developed from normal cells into a lethal cancer due to the following mechanisms inside the cell. 1. Point mutation: This mutation induces alteration in cellular DNA sequence through synonymous nucleotide substitution result in normal gene becomes protooncogene finally become oncogene due to chromosomal DNA replication. For example normal Ras protein synthesizing gene become mutant Ras oncogene due to point mutation. 2. Gene amplification: This is the process of abnormal amplification of DNA in chromosomes and generates protooncogenes into oncogenes due to numerous replications of chromosomal DNA in succession. Example is presence of MYC gene family in lung and breast cancer cells due to amplied DNA homogeneously. 3. Chromosomal translocation: BCR-ABL leukemia is the due to chromosomal translocation and meticulous translocation of chromosmomal regions leading to coding of a fusion protein from an oncogene. Ex. Philadelphia chromosome 4. DNA rearrangement: Insertions, deletions, transposition & inversion of nitrogen bases of nucleotide sequences in DNA rearrangement generates cellular oncogenes. These rearrangements are due to exposure of cells to carcinogenic agent 5. Insertional mutagenesis: This type of oncogene development is mainly due to retrovirus as explained below For example: The genetic changes are expected to alter the activity of the gene product --> loss of heterozygosity ---> abnormal phenotype Mutations result in genetic drift, which in turn results in the loss of heterozygosity. This loss of one parental copy of nucleotide gene bases may lead to the lethal and dangerous consequences of the living being in the following of life. This loss or drift may result in the occurrence of cancer (breast cancer) hereditary retinoblastoma, because there may be nonexistence of the functional tumor suppressor gene in the lost region. One parental copy only can be noticed at that lost region there by hemizygosity. But however there is one more functional gene copy inside the genome copy thereby offspring can get resistance proteins synthesis against the mutation induced cancer. If both copies are bad or one copy is become badly due to mutation the remaining gene copy responsible for the tumor growth (the tumor suppressor gene example p53) can be denaturated by another point mutation, result in complete suppression of gene to protect the body. A lot of catastrophic events and consequences may occur with loss of heterozygosity (LOH). Genetic drift results in loss of heterozygosity which may reduce and limit longevity of asexual organisms in a population there by low population size. During intermittent cancer development, usually inactivation of the TSG induced due to the two somatic mutations acting on respective 2 alleles. In contrast, during the familial cancer development merely one somatic mutation is considerably enough to generate inactivation of TSG (p.

1. Answer:
Cellular oncogene formation: Carcinogenesis, tumorogenesis or oncogenesis are developed from
normal cells into a lethal cancer due to the following mechanisms inside the cell.
1. Point mutation: This mutation induces alteration in cellular DNA sequence through
synonymous nucleotide substitution result in normal gene becomes protooncogene finally
become oncogene due to chromosomal DNA replication. For example normal Ras protein
synthesizing gene become mutant Ras oncogene due to point mutation.
2. Gene amplification: This is the process of abnormal amplification of DNA in chromosomes
and generates protooncogenes into oncogenes due to numerous replications of chromosomal
DNA in succession. Example is presence of MYC gene family in lung and breast cancer cells
due to amplied DNA homogeneously.
3. Chromosomal translocation: BCR-ABL leukemia is the due to chromosomal translocation and
meticulous translocation of chromosmomal regions leading to coding of a fusion protein from an
oncogene. Ex. Philadelphia chromosome
4. DNA rearrangement: Insertions, deletions, transposition & inversion of nitrogen bases of
nucleotide sequences in DNA rearrangement generates cellular oncogenes. These rearrangements
are due to exposure of cells to carcinogenic agent
5. Insertional mutagenesis: This type of oncogene development is mainly due to retrovirus as
explained
below
For example:
The genetic changes are expected to alter the activity of the gene product --> loss of
heterozygosity ---> abnormal phenotype
Mutations result in genetic drift, which in turn results in the loss of heterozygosity. This loss of
one parental copy of nucleotide gene bases may lead to the lethal and dangerous consequences of
the living being in the following of life. This loss or drift may result in the occurrence of cancer
(breast cancer) hereditary retinoblastoma, because there may be nonexistence of the functional
tumor suppressor gene in the lost region. One parental copy only can be noticed at that lost
region there by hemizygosity.
But however there is one more functional gene copy inside the genome copy thereby offspring
can get resistance proteins synthesis against the mutation induced cancer.
If both copies are bad or one copy is become badly due to mutation the remaining gene copy
responsible for the tumor growth (the tumor suppressor gene example p53) can be denaturated by
another point mutation, result in complete suppression of gene to protect the body.

2. A lot of catastrophic events and consequences may occur with loss of heterozygosity (LOH).
Genetic drift results in loss of heterozygosity which may reduce and limit longevity of asexual
organisms in a population there by low population size.
During intermittent cancer development, usually inactivation of the TSG induced due to the two
somatic mutations acting on respective 2 alleles. In contrast, during the familial cancer
development merely one somatic mutation is considerably enough to generate inactivation of
TSG (p53) since the affected individual already possess one inherited defective allele. Imprinting
of the tumor suppressor gene raises the vulnerability to cancer due the silencing of only one
individual allele there complete elimination of the function of the tumor suppressor gene. Loss of
heterozygosity (LOH) vs. defective tumor suppressor genes (TSGs) is responsible for the lion’s
share of these diseases.
Solution
Answer:
Cellular oncogene formation: Carcinogenesis, tumorogenesis or oncogenesis are developed from
normal cells into a lethal cancer due to the following mechanisms inside the cell.
1. Point mutation: This mutation induces alteration in cellular DNA sequence through
synonymous nucleotide substitution result in normal gene becomes protooncogene finally
become oncogene due to chromosomal DNA replication. For example normal Ras protein
synthesizing gene become mutant Ras oncogene due to point mutation.
2. Gene amplification: This is the process of abnormal amplification of DNA in chromosomes
and generates protooncogenes into oncogenes due to numerous replications of chromosomal
DNA in succession. Example is presence of MYC gene family in lung and breast cancer cells
due to amplied DNA homogeneously.
3. Chromosomal translocation: BCR-ABL leukemia is the due to chromosomal translocation and
meticulous translocation of chromosmomal regions leading to coding of a fusion protein from an
oncogene. Ex. Philadelphia chromosome
4. DNA rearrangement: Insertions, deletions, transposition & inversion of nitrogen bases of
nucleotide sequences in DNA rearrangement generates cellular oncogenes. These rearrangements
are due to exposure of cells to carcinogenic agent
5. Insertional mutagenesis: This type of oncogene development is mainly due to retrovirus as
explained
below
For example:

3. The genetic changes are expected to alter the activity of the gene product --> loss of
heterozygosity ---> abnormal phenotype
Mutations result in genetic drift, which in turn results in the loss of heterozygosity. This loss of
one parental copy of nucleotide gene bases may lead to the lethal and dangerous consequences of
the living being in the following of life. This loss or drift may result in the occurrence of cancer
(breast cancer) hereditary retinoblastoma, because there may be nonexistence of the functional
tumor suppressor gene in the lost region. One parental copy only can be noticed at that lost
region there by hemizygosity.
But however there is one more functional gene copy inside the genome copy thereby offspring
can get resistance proteins synthesis against the mutation induced cancer.
If both copies are bad or one copy is become badly due to mutation the remaining gene copy
responsible for the tumor growth (the tumor suppressor gene example p53) can be denaturated by
another point mutation, result in complete suppression of gene to protect the body.
A lot of catastrophic events and consequences may occur with loss of heterozygosity (LOH).
Genetic drift results in loss of heterozygosity which may reduce and limit longevity of asexual
organisms in a population there by low population size.
During intermittent cancer development, usually inactivation of the TSG induced due to the two
somatic mutations acting on respective 2 alleles. In contrast, during the familial cancer
development merely one somatic mutation is considerably enough to generate inactivation of
TSG (p53) since the affected individual already possess one inherited defective allele. Imprinting
of the tumor suppressor gene raises the vulnerability to cancer due the silencing of only one
individual allele there complete elimination of the function of the tumor suppressor gene. Loss of
heterozygosity (LOH) vs. defective tumor suppressor genes (TSGs) is responsible for the lion’s
share of these diseases.