Assignment # 01
Submitted by: MARIA ARIF
Submitted to: MAM_ SARA
Department: BS_CHEMISTRY
Semester: (2nd)
College name: ASPIRE COLLEGE WAZIRABAD
Subject:
A patient diagnosed with cancer. As we know in Cancerous cells there is uncontrolled division
of cells . Identify the reason behind the abnormal growth of cell by identifying the faulty steps
in cell cycle ?
Answer
All cells undergoes series of changings in which cells divide to their daughter cells . But this
mechanism or cell cycle occurs in a regulatory manner. Cells can regulate their mechanism , if any
error occur , these mutated cells can undergo apoptosis i-e cell death by which abnormal cells can be
removed .
But once this regulatory manner altered, it can lead to serious life threating conditions , one of them
is tumor formation.
Cancer cells may make their own growth factors, have growth factor pathways that are stuck in the
"on" position, or, in the context of the body, even trick neighboring cells into producing growth
factors to sustain them.
Cancer cells also ignore signals that should cause them to stop dividing. For instance, when normal
cells grown in a dish are crowded by neighbors on all sides, they will no longer divide. Cancer cells,
in contrast, keep dividing and pile on top of each other in lumpy layers.
S-Phase of Cell Cycle
One of the main checkpoint of cell cycle surveillance is proper DNA replication which occur in s-
phase of cell cycle .
Even a small percentage of error may pass to daughter cells. If mutatio occur in DNA neuclotide of
coding portion of gene , it will lead to malformation of specific protein that play important role in Cell
reproduction .
These faulty genes will pass to replicated gene and this faulty instruction leads to abnormal protein
production that does not work functions as it should .
Oncogenes
Positive cell cycle regulators may be overactive in cancer. For instance, a growth factor receptor may
send signals even when growth factors are not there, or a cyclin may be expressed at abnormally high
levels. The overactive (cancer-promoting) forms of these genes are called oncogenes, while the
normal, not-yet-mutated forms are called proto-oncogenes. This naming system reflects that a normal
proto-oncogene can turn into an oncogene if it mutates in a way that increases its activity.
Mutations that turn proto-oncogenes into oncogenes can take different forms. Some change the amino
acid sequence of the protein, altering its shape and trapping it in an “always on” state. Others
involve amplification, in which a cell gains extra copies of a gene and thus starts making too much
protein. In still other cases, an error in DNA repair may attach a proto-oncogene to part of a different
gene, producing a “combo” protein with unregulated activity.
Many of the proteins that transmit growth factor signals are encoded by proto-oncogenes. Normally,
these proteins drive cell cycle progression only when growth factors are available. If one of the
proteins becomes overactive due to mutation, however, it may transmit signals even when no growth
factor is around. In the diagram above, the growth factor receptor, the Ras protein, and the signaling
enzyme Raf are all encoded by proto-oncogenes .
Overactive forms of these proteins are often found in cancer cells. For instance, oncogenic Ras
mutations are found in about 90% of pancreatic cancers. Ras is a G protein, meaning that it switches
back and forth between an inactive form (bound to the small molecule GDP) and an active form
(bound to the similar molecule GTP). Cancer-causing mutations often change Ras’s structure so that it
can no longer switch to its inactive form, or can do so only very slowly, leaving the protein stuck in
the “on” state.
Summary
Each successive cell division will give rise to daughter cells with even more accumulated damage .
Due to these mutations , all checkpoints become non-functional and rapid uncontroll production of
cells can occur .
These rapid cells produced are overlapped and form cancerous lesions or other types of cancera such
as leukemia .
