Unfortunately several cancers are not predictable with simple tests rather required much intensive diagnosis. The whole genome sequence in determining the entire DNA in normal cells as well as in tumor cells provide the facility to compare and pin point the mutations occurring in the oncogenes or tumor suppressor genes responsible for causing the cancer seems to be a better approach. But such approaches are highly expensive and require expertise. Though, the whole genome sequencing is carried out pin pointing of specific driver mutations responsible for cancer phenotype would be a question. Some critical mutations can be identified in some cancer genome sequences while others are hard to find among the thousands of possibilities. The mutations like missense, nonsense frameshift, rearrangements may alter the coding sequences of any gene must be checked. The regulatory mutations that increase the transcription of oncogenes or decrease that of tumor suppressor genes are potentially important but are very difficult to find in a whole genome sequence. The catalogs of regulatory elements in human genomes provide list of certain potential sequences to be targeted. But the catalogs are rudimentary or incomplete. Therefore, the whole genome sequencing is not a panacea that will lead to immediate cures of all cancers. Recent studies have shown that the whole genome sequences of cells derived from different regions of same tumor have suggested an important reason for cancer reference. Certain cancers are heterogenous and cells within the tumor have different genomes. Certain mutations in oncogens or tumor suppressor genes are common to all cells in the tumor but some are not. These findings make a sense that accumulation of mutations in clone of cells cause cancer. Therefore, designing drug targeting specific cells protecting adult stem cells cannot be accomplished. Thus, effective cancer treatments would be directed against the common mutations but is difficult to identify the specific mutations without sequencing of genomes of many cells throughout the tumor. Cancer landscape is a large scale cancer genome sequencing project (cancer genome atlas) funded by National Institute of Health (NIH). In this project the whole genomes or exomex of several hundreds of cancer are being characterized. The recurrent patterns of mutations are subdivided cancers in to groups with probable clinical relevance. For example, 4 groups of breast cancers have been identified. Almost 178 lung squamous cell carcinoma’s genomes have been characterized and matched with DNA of normal cells from same patients. Mutations in certain tumor suppressor genes like p53 and certain oncogenes have shown relatively high frequencies among these cancers. The mutations of certain cancers resemble cancers in some other organs. For example, pattern of mutation in breast cancer resembles many ovarian cancers more than other types of breast cancers. These findings may help in designing the drugs .

1. Unfortunately several cancers are not predictable with simple tests rather required much
intensive diagnosis. The whole genome sequence in determining the entire DNA in normal cells
as well as in tumor cells provide the facility to compare and pin point the mutations occurring in
the oncogenes or tumor suppressor genes responsible for causing the cancer seems to be a better
approach. But such approaches are highly expensive and require expertise.
Though, the whole genome sequencing is carried out pin pointing of specific driver mutations
responsible for cancer phenotype would be a question. Some critical mutations can be identified
in some cancer genome sequences while others are hard to find among the thousands of
possibilities. The mutations like missense, nonsense frameshift, rearrangements may alter the
coding sequences of any gene must be checked. The regulatory mutations that increase the
transcription of oncogenes or decrease that of tumor suppressor genes are potentially important
but are very difficult to find in a whole genome sequence.
The catalogs of regulatory elements in human genomes provide list of certain potential
sequences to be targeted. But the catalogs are rudimentary or incomplete. Therefore, the whole
genome sequencing is not a panacea that will lead to immediate cures of all cancers. Recent
studies have shown that the whole genome sequences of cells derived from different regions of
same tumor have suggested an important reason for cancer reference. Certain cancers are
heterogenous and cells within the tumor have different genomes. Certain mutations in oncogens
or tumor suppressor genes are common to all cells in the tumor but some are not.
These findings make a sense that accumulation of mutations in clone of cells cause cancer.
Therefore, designing drug targeting specific cells protecting adult stem cells cannot be
accomplished. Thus, effective cancer treatments would be directed against the common
mutations but is difficult to identify the specific mutations without sequencing of genomes of
many cells throughout the tumor. Cancer landscape is a large scale cancer genome sequencing
project (cancer genome atlas) funded by National Institute of Health (NIH). In this project the
whole genomes or exomex of several hundreds of cancer are being characterized. The recurrent
patterns of mutations are subdivided cancers in to groups with probable clinical relevance.
For example, 4 groups of breast cancers have been identified. Almost 178 lung squamous cell
carcinoma’s genomes have been characterized and matched with DNA of normal cells from
same patients. Mutations in certain tumor suppressor genes like p53 and certain oncogenes have
shown relatively high frequencies among these cancers. The mutations of certain cancers
resemble cancers in some other organs. For example, pattern of mutation in breast cancer
resembles many ovarian cancers more than other types of breast cancers. These findings may
help in designing the drugs to treat one type of cancer might be effective for a cancer of different
organ. The finite number of mutations in oncogenes and tumor suppressor genes are the targets

2. for chemotherapies and would be hopeful to elicit new kind of treatments and drugs in this area
in near future.
Immune therapy is used to eliminate the stem cells in treatment of cancer cells in some types of
cancers. For example, in breast tumors the Her2 growth factor receptor is over expressed on the
cell surface. The location of the part of the Her2 protein outside the cell has become a potential
and useful site to target such cancers. A monoclonal antibody called Herceptin® that binds
tightly to the extracellular portion of the Her2 protein has been developed. The binding of
Herceptin to Her2 causes two effects. First Her2 receptors bind to Herceptin cannot trigger the
signaling cascade normally initiated by Her2’s interaction with the corresponding growth factor.
This results in non proliferation of Herceptin treated Her2 positive cells. Secondly the binding of
Herceptin to Her2 receptors stimulates specialized immune cells called killer T cells to target the
cancer cells and eventually destroy them. Herceptin was found to be a successful drug for Her2
positive breast cancers with considerable effectiveness. Herceptin was found to reduce the likely
hood of cancer reoccurrence by 25 – 50% after surgery or standard chemotherapy. The drug is
not efficient in some cases because of the acquisition new mutations that make them resistant to
Herceptin.
Solution
Unfortunately several cancers are not predictable with simple tests rather required much
intensive diagnosis. The whole genome sequence in determining the entire DNA in normal cells
as well as in tumor cells provide the facility to compare and pin point the mutations occurring in
the oncogenes or tumor suppressor genes responsible for causing the cancer seems to be a better
approach. But such approaches are highly expensive and require expertise.
Though, the whole genome sequencing is carried out pin pointing of specific driver mutations
responsible for cancer phenotype would be a question. Some critical mutations can be identified
in some cancer genome sequences while others are hard to find among the thousands of
possibilities. The mutations like missense, nonsense frameshift, rearrangements may alter the
coding sequences of any gene must be checked. The regulatory mutations that increase the
transcription of oncogenes or decrease that of tumor suppressor genes are potentially important
but are very difficult to find in a whole genome sequence.
The catalogs of regulatory elements in human genomes provide list of certain potential
sequences to be targeted. But the catalogs are rudimentary or incomplete. Therefore, the whole
genome sequencing is not a panacea that will lead to immediate cures of all cancers. Recent
studies have shown that the whole genome sequences of cells derived from different regions of
same tumor have suggested an important reason for cancer reference. Certain cancers are

3. heterogenous and cells within the tumor have different genomes. Certain mutations in oncogens
or tumor suppressor genes are common to all cells in the tumor but some are not.
These findings make a sense that accumulation of mutations in clone of cells cause cancer.
Therefore, designing drug targeting specific cells protecting adult stem cells cannot be
accomplished. Thus, effective cancer treatments would be directed against the common
mutations but is difficult to identify the specific mutations without sequencing of genomes of
many cells throughout the tumor. Cancer landscape is a large scale cancer genome sequencing
project (cancer genome atlas) funded by National Institute of Health (NIH). In this project the
whole genomes or exomex of several hundreds of cancer are being characterized. The recurrent
patterns of mutations are subdivided cancers in to groups with probable clinical relevance.
For example, 4 groups of breast cancers have been identified. Almost 178 lung squamous cell
carcinoma’s genomes have been characterized and matched with DNA of normal cells from
same patients. Mutations in certain tumor suppressor genes like p53 and certain oncogenes have
shown relatively high frequencies among these cancers. The mutations of certain cancers
resemble cancers in some other organs. For example, pattern of mutation in breast cancer
resembles many ovarian cancers more than other types of breast cancers. These findings may
help in designing the drugs to treat one type of cancer might be effective for a cancer of different
organ. The finite number of mutations in oncogenes and tumor suppressor genes are the targets
for chemotherapies and would be hopeful to elicit new kind of treatments and drugs in this area
in near future.
Immune therapy is used to eliminate the stem cells in treatment of cancer cells in some types of
cancers. For example, in breast tumors the Her2 growth factor receptor is over expressed on the
cell surface. The location of the part of the Her2 protein outside the cell has become a potential
and useful site to target such cancers. A monoclonal antibody called Herceptin® that binds
tightly to the extracellular portion of the Her2 protein has been developed. The binding of
Herceptin to Her2 causes two effects. First Her2 receptors bind to Herceptin cannot trigger the
signaling cascade normally initiated by Her2’s interaction with the corresponding growth factor.
This results in non proliferation of Herceptin treated Her2 positive cells. Secondly the binding of
Herceptin to Her2 receptors stimulates specialized immune cells called killer T cells to target the
cancer cells and eventually destroy them. Herceptin was found to be a successful drug for Her2
positive breast cancers with considerable effectiveness. Herceptin was found to reduce the likely
hood of cancer reoccurrence by 25 – 50% after surgery or standard chemotherapy. The drug is
not efficient in some cases because of the acquisition new mutations that make them resistant to
Herceptin.