Response to Questions

Response to Questions
Question 1

There is growing evidence that many oncogenic drivers coordinately modulate multiple
hallmarks of cancer. Oncogenic drivers are mutations that lead to the uncontrolled growth of
cells, which can eventually form a tumor (Rogounovitch et al., 2021). These mutations can occur
in genes that control cell growth or repair damaged DNA. P53 is an oncogenic driver that acts as
a tumor suppressor, and mutations in its gene are responsible for nearly half of all human
malignancies. The p53 protein is responsible for stopping the cell cycle, repairing DNA, and
initiating apoptosis by binding to DNA and regulating the transcription of the genes involved in
these processes (Khadka et al., 2022). These tumor suppressor capabilities can be lost when p53
undergoes mutations, contributing to cancer's growth and progression. p53 mutations can
promote cell proliferation, evasion of apoptosis, angiogenesis, as well as metastasis, which are
all hallmarks of cancer. p53 mutations can also contribute to the development of cancer.
Uncontrolled cell proliferation can result from p53 mutations, leading to the deregulation
of genes associated with cell cycle regulation. This can result in cell proliferation. In apoptosis
resistance, p53 mutations could also lead to the deregulation of apoptosis-associated genes,
which can result in cancer cells that are immune to cell death (Khadka et al., 2022). This is called
apoptosis evasion. Angiogenesis of the gene expression involved in angiogenesis, or the
development of new blood vessels, can occur when p53 undergoes mutations. Providing the
tumor with oxygen and nutrients can encourage tumor growth and spread throughout the body.
Cancer cells can cause metastasis to other organs due to p53 mutations, which can upregulate the
expression of genes involved in cell motility and invasiveness. This results in cancer cells that
can metastasize.

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Question 2

Cancer is a disease caused by the abnormal growth of cells. There are many different
types of cancer, each with its own set of causes. However, one common feature of many types of
cancer is the presence of mutations in the DNA. These mutations can be caused by various
things, including defects in the DNA repair mechanisms. One crucial DNA repair mechanism is
mismatch repair (MMR), which helps correct errors during DNA replication (Deshpande et al.,
2020). If the MMR pathway is defective, errors in DNA replication can go unrepaired. Over
time, these errors can accumulate, leading to microsatellite instability (MSI). MSI is a condition
with a higher than an average number of short repeats of DNA sequence (microsatellites). MSI is
associated with several cancer types, including colorectal, endometrial, and gastric cancer. MSI
can cause cancer by several mechanisms. First, the presence of MSI can lead to the accumulation
of additional mutations in the DNA. These mutations can confer a growth advantage to the cells,
allowing them to increase and form a tumor. The microsatellites can also act as mutagenic sites,
causing additional mutations. Finally, MSI can cause changes in the expression of specific genes,
which can also contribute to cancer development.
The MMR pathway is a critical component of the immune system, and defects in this
pathway can lead to cancer. However, the MMR pathway can also be a target for cancer
treatment. Cancer cells often have defects in the MMR pathway, making them more sensitive to
certain anticancer drugs (Deshpande et al., 2020). A defective MMR pathway does offer some
therapeutic opportunities for treating cancer patients. One such opportunity is immunotherapy,
which can help activate the immune system and fight cancer cells. Additionally, targeted therapy
against the proteins involved in the MMR pathway may effectively treat cancer patients with a
defective MMR pathway. The MMR pathway can deliver anticancer drugs directly to cancer

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cells because the MMR pathway is often overexpressed in cancer cells, and this overexpression
can be used to target cancer cells with high levels of drug delivery.

Question 3

The epithelial-mesenchymal transition (EMT) is a process that allows epithelial cells to
acquire a mesenchymal phenotype. This process is associated with losing cell-cell adhesion,
increased motility, and acquiring a more invasive phenotype (Gloushankova et al., 2018). The
EMT program can induce various stimuli, including growth factor signaling, cytokines, and
extracellular matrix proteins. The EMT program is thought to play a role in tumorigenesis and
metastasi


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