The Cellular Basis of Cancer

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The Cellular Basis of Cancer
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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