The Cellular Basis of Cancer

This article explores the cellular basis of cancer, including the different types of cancers, the cell cycle, and the difference between cancer cells and normal cells. It discusses how cancerous cells grow and spread, the role of oncogenes and tumor suppressor genes, and the characteristics that distinguish cancer cells from healthy cells.

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The Cellular Basis of Cancer
Student’s Name
Institutional Affiliation

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The Cellular Basis of Cancer
Introduction
Cancer is a collective term for diseases caused by uncontrolled cell growth. The
persistent growth of body cells causes tumors, which are the abnormal tissues on various organs.
However, tumors do not characterize other types of cancers, such as leukaemia. There are
different types of cancers, named according to the places or tissue of origin (Roopashree et al.,
2015). Carcinomas begin in the cells lining organs, for example, the liver and skin. Sarcoma
refers to the cancers that begin in the connective tissues. Cartilages, muscles, and blood form the
connective tissues that provide support to organs and the skeleton framework. More also,
leukaemia starts in the bone marrow often resulting in the production of abnormal blood cells
also known as leukemia cells (Roopashree et al., 2015). The cells of the immune system grow
uncontrollably, which characterizes the lymphoma and myeloid. Besides, the central nervous
system (CNS) cancers begin in the brain or spinal cord. Notably, cancer tumors can be benign or
malignant. Benign tumors are not cancerous while the malignant ones are cancerous, and life-
threatening when treatment is delayed. Molecular alteration of cells and DNA often triggers most
cancers, which affects the normal cell cycle. Consequently, cancerous cells are distinct from
healthy cells in different capacities, for instance, in their ability to proliferate and colonize new
sites.
Cells in Cancerous Tissues
Cancerous cells grow abnormally. Cell division regulates the growth, repair, and
degradation of body cells. In this process, parent cells divide forming daughter cells that favor
the growth of new tissues or replacement of the old or damaged cells. For healthy body cells, the
parent cells stop to divide when there is no need for the daughter cells in growth or repair

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processes. However, the abnormal or cancerous cells continue to multiply, and metastasize.
According to Mueller, Hassel, & Grealy (2015), the cancerous cells can spread locally or
regionally into the tissues and organs around or far from the site of disease. At advanced stages,
it often metastases to distant body organs. The tumor cells detach from their original locations;
they travel through the blood stream or lymphatic; elude the immune system; and colonize new
locations. Such forms of cancers are known as metastatic cancers. For instance, prostate cancer
can metastasize into the lymph nodes or bones. In this situation, this cancer is referred to as
metastatic prostate cancer (Mueller, Hassel, & Grealy, 2015). There are histological features that
distinguish tumor cells from healthy cells. Cancer cells have altered shapes, textures, and
composition. The nuclei are large with dents. They may have dispersed or aggregated chromatin.
By contrast, all normal cells are round and regular in shape.
The Cell Cycle and Cancer
The cell cycle involves a sequence of mechanisms, which allow the replication of DNA,
the detachment of the cytoplasm and organelles to yield daughter cells. The process is also
known as mitosis. It involves mechanisms that correct the erroneous DNA fragments to prevent
mutations. The cells may also undergo apoptosis; a controlled death process that arises due to the
action of biochemical processes. In this process, the cells shrink; the nuclei and chromosomes
fragment; and the DNA decay. However, the normal cell cycle could malfunction due to genetic
mutations. The mutations that alter the functionality of cells include deletions, substitutions, and
insertions. Cancerous cells rely on the malfunctioned cell cycle for replication processes, which
results in uncontrolled cell proliferation. They thrive in conditions where healthy cells cannot.
The normal cell cycle completes in four stages: the gap one (G1), synthesis (S), gap two
(G2), and mitosis or M stages (Barnum & O’Connell, 2014). Cellular contents grow in G1 phase,

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and as it approaches the end, G1/S checkpoint controls the start or end of DNA replication. The
checkpoint examines the presence of erroneous DNA to confirm that the cells have the necessary
tools for a successive mitosis (Barnum & O’Connell, 2014). At this point, the cells with an intact
genetic component proceed to the S stage while those that fail repair mechanisms die through
apoptosis. In the S stage, the chromosomes duplicate producing more copies of DNA. The vital
checkpoint at the end of this G2 stage where the cells checks for any error before division in the
M stage (Vassilev & DePamphilis, 2017). The checkpoint uses cyclin dependent kinases to
signal the “molecular switches” to stop or allow the process to proceed to mitosis. In
combination with other regulatory proteins, the cyclin dependent kinase, control cell division by
initiating the death of impaired cells (Karimian, Ahmadi & Yousefi, 2016). In normal body cells,
these regulatory proteins act by suppressing abnormal growth, and inducing apoptosis. However,
genetic mutations that often occur during mammalian development or due to age interfere with
the functionality of the regulatory proteins present at the checkpoints (Vassilev & DePamphilis,
2017). As a result, the impaired “molecular switches” may turn on permanently causing an
uncontrollable division of cells that often triggers oncogenesis; the process where normal cells
transform into cancerous cells.
The normal DNA duplication processes rely on DNA polymerases for the precise pairing
of DNA strands during DNA synthesis; however, these enzymes make erroneous mistakes of one
per 100,000 nucleotides in a sequence. DNA is subject to damage, and according to Roos,
Thomas & Kaina (2016), it is estimated that the human genome has about 60,000 errors
following the replication process since humans have 6.16 × 109 base pairs. Under normal
conditions, these errors are repaired at the checkpoints in the cell cycle, and cancers do not
develop. Nonetheless, since cell division occurs in every few days throughout a person’s life, the

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number of stem cells that will replicate leads to a higher frequency of mutations present in
cancerous cells. As noted in all cancers, the number of chromosomal abnormalities is
exceedingly higher than in the healthy cells. According to Grady & Markowitz (2014), an
examination on 58 colon tumors showed that there were, 11,000 genomic alterations in the tumor
cells, which suggests that genomic alterations favors the occurrence of tumors.
Uncontrolled Cell Division
Remarkably, the mutations on the oncogenes and tumor suppressor genes are beneficial
to cancerous cells. Both genes are vital in controlling the cell division process by activation or
deactivation mechanisms (Vander Heiden & DeBerardinis, 2017). Healthy cells have the proto-
oncogenes that code for proteins necessary for cell differentiation; however, they turn into
oncogenes when mutated or overexpressed. Oncogenes transform healthy cells into cancerous
cells, which results into the various forms of cancers (Blake & Der, 2017). The oncogenes hinder
the successive completion of a cell cycle due to the activation of the positive regulator. For
instance, the aberrations that allow the activation of cyclin-dependent kinases in the absence of
cyclin will cause the cells to bypass the vital checkpoints before all the errors are corrected
(Santo, Siu & Raje, 2015). The resultant cells will undergo mitosis to produce daughter cells
with an equal number of chromosomes as the parent, and the subsequent generations of cells will
accrue voluminous mutations that often leads to cancer. Evidently, oncogenes supersede the cell
cycle points, which accelerates the cell cycle process producing more virulent cancer cells. More
also, any mutation on the ras gene, a proto-oncogene, tasked with encoding for signal
transduction proteins would result into rasD, an oncogene that will cause uncontrolled growth
signaling (Hobbs, Der & Rossman, 2016). Congenital modifications of proto-oncogenes that lead
to the activation of the oncogenes causes most cancers. However, most cancer-causing

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aberrations than involve the oncogene are non-inheritable, instead they are acquired. These
aberrations activate the oncogenes by re-arranging the chromosomes, which alters the sequence
of genes placing one gene next to a different that are then activated.
Tumor suppressor genes are also known as anti-oncogenes since they are the negative
controllers of the oncogenes. They are present in healthy body cells, and in their proper function,
they regulate cell growth, proliferation, and apoptosis hence suppressing tumor development
(Abreu & Howard, 2015). Several mutations that lead to the loss of function of tumor-suppressor
genes are deletions, insertions, and missense mutations. Insertions and deletions change the
number of DNA bases by adding or removing a nucleotide respectively (Riadi et al., 2017). On
the other hand, missense mutations alter an amino acid by substituting it using a protein in a
DNA base pair. Tumors grow when the anti-oncogenes are mutated. At the cellular level, the
anti-oncogenes are recessive, and so, they require the inactivation of two copies in the genes.
Notably, the aberrations in these genes can be acquired due to aging or inherited when a parent
passes a copy of the mutation is to their offspring. Thus, the offspring will require a second copy
of genes to activate the ones encoded in the germline hence initiating the tumor formation
process. For instance, TP53 genes code for P53 proteins found at the G1 checkpoint and
modifications in these genes are known to cause most cancers (Joyce & Kai, 2019). Under
normal circumstances, the P53’s role is monitoring the DNA, triggering repair mechanisms, and
if unsuccessful, initiates apoptosis. Cells with malfunctioned P53 cannot detect or repair faulty
DNA, as well as trigger programmed-cell death (Joyce & Kai, 2019). As a result, the cell cycle
will involve the production of cancerous cells.

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The Difference Between Cancer Cells and Normal Cells
The cells in cancerous tissues differ with the healthy cells in their growth control,
morphology, interaction with other cells, and gene expression. Cancer cells grow and replicate
uncontrollably even when enough cells are present. As a result, lumps develop due to the
accumulation of cells, which grows over time as the disease progresses (National Cancer
Institute, 2015). Tumors contain millions of copies the different forms of cancer tissues.
However, some cancers such the blood cancers do not form tumors, instead the numerous
presence of abnormal cells in the circulatory system characterize it.
Cancer cells disregard the chemical signs produced by various cells. Numerous cells have
nuclei that contain the genetic component, DNA. Again, these cells are in constant
communication with other cells within the body, and often use chemical signals to communicate
(National Cancer Institute, 2015). Such signals attach to the receptors found on the surface of
these cells, which initiates the flow of signals into the nuclei. As a result, the nucleus can control
the genes expressed. However, in cancerous tissues, the nucleus may receive numerous or no
signal at all (Mueller, Hassel, & Grealy, 2015). Also, these cells may lack or have excess
receptors that will convey wrong information to the nuclei. Thus, vital genes are either activated
or suppressed wrongly.
Cells in cancerous tissues spread and do not stick together. Normal healthy cells have
adhesins that maintain the integrity of cells in addition to relaying signals. On the other hand,
cancer cells detach from each other; spread through the lymphatic or blood circulatory system
into distal organs; and colonize the new sites forming metastases (National Cancer Institute,
2015). Metastases are the secondary cancers that develop in tissue far from primary sites
(Massague & Obenauf, 2016). Notably, metastases are named with reference to the primary site

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of infection; for instance, breast cancer that spreads into the bones is known as breast cancer with
bone metastases.
Cancerous cells are unspecialized. Contrary to the normal cells, cancerous cells do not
differentiate and specialize. They do not develop into specific cell types (National Cancer
Institute, 2015). Instead, they grow uncontrollably without being able to specialize. Immature
cells lack functionality as seen in the cancer cells. The somatic cells, in healthy cells, are diploid
and are present in all tissues. Such cells specialize to perform specific functions, for example,
leukocytes function to protect the body from infections.
Cancer cells do not repair and self-repair. The cells in cancerous tissues do not die as
expected as they continue to grow uncontrollably (National Cancer Institute, 2015). Any errors
that occur during the replication of the DNA cannot be corrected since the cancer cells ignore
signals. On the contrary, the normal cells self-repair and undergo apoptosis. DNA polymerase
rectifies replication mistakes, and where it fails, it triggers the programmed death of a cell. As a
result, no erroneous cells or genes are produced following a complete cell cycle.
Conclusion
Cancer is the collective term for diseases that arise from uncontrolled cell division due to
the breakdown of mechanism that control the four stages of the cell cycle. The change in DNA
sequence of genes that code for the regulatory proteins alters the standard cell cycles causing its
malfunction. Faulty signals results in proteins that produces errors during a cell’s growth,
division, and replication. Any errors that occur during the cell cycle pass to daughter cells, and
subsequent cell divisions produce daughter cells with accrued genetic errors or damage.
Eventually, the regulatory checkpoint malfunction. Genetic alterations of the proto-oncogenes
and tumor suppressor genes activate and suppress the cell division process respectively;

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therefore, producing more cancer cells. These cells vary from the healthy cells in aspects of self-
repair, apoptosis, specialization, signaling mechanisms, and their integrity.

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