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Apoptosis Essays

7 samples in this category

“Introduction to Apoptosis”

Apoptosis is a programmed death for the cell in other words it is a cell suicide therefore, it is totally different from necrosis where the cell dies as a result of injury. In the apoptosis process, the cell’s components are packed by immune cells.

Apoptosis is very important because it maintains the balance of the body by eliminating cells during development and removing the possibly cancerous cells and cells infected by viruses. In a lot of cases, it’s a bad thing for cells to die such as dying from injury. However, it’s beneficial to us that some cells of our bodies die, of course in a controlled way.

“Introduction to Apoptosis and cancer”

Cancer can be seen as the consequence of a progression of genetic changes during which a typical cell is changed into a malignant cell while the absence of apoptosis is one of the fundamental changes that cause this malignant transformation. In the early 1970s, Kerr et al illustrated the connection between apoptosis and the removal of potentially malignant cells, tumor succession, and hyperplasia. Hence, the elimination of apoptosis has an important role in carcinogenesis. There are numerous ways a malignant cell can decrease apoptosis. In general, the mechanisms that eliminate apoptosis can be divided into:

  1. Damage death receptor signaling.
  2. Disrupt the equilibrium of pro and anti-apoptotic proteins.
  3. Reduced caspase function.

Mechanisms that contribute to apoptosis evasion and carcinogenesis.

“Ways to eliminate apoptosis and cause carcinogenesis”

1) Damage death receptor signaling:

The ligands of the death receptors and the death receptors themselves are central participants in the apoptosis pathway. The death receptors have a death domain and there is a death signal that triggers it, then several molecules get attracted to the death domain which activates the signaling cascade. Many abnormalities in the death signaling process that can lead to the elimination of apoptosis have been identified. These abnormalities may occur to the receptors or to death signals. For example, a reduced expression of CD95 was proved to have an essential role in the resistant treatment of leukemia.

2) Disrupt the equilibrium of pro and anti-apoptotic proteins:

A change in some of the components of the apoptotic pathway may have an essential role in the creation of resistance to chemotherapy in several types of tumors. interference in the stability of anti-apoptotic and pro-apoptotic members of the Bcl-2 family affects in the apoptosis in the affected cells. This may be because of overexpression of anti-apoptotic proteins or reduction of pro-apoptotic proteins or a combination of both. Anti-apoptotic Bcl-2 over-expression was found in multiple human cancers, such as prostate cancer, melanoma, DLBCL, etc. Colorectal cancer has also been linked to Bcl-xL overexpression. Overexpression causes tumor cells to participate in the resistance of drugs and prevents them from having apoptosis. Antiapoptotic proteins Bcl-2 and Bcl-xL expression levels have been connected to cisplatin resistance and tumor recurrence in several types of cancer, including lung cancer (NSCLC), head and neck, breast, and ovarian.

3) Reduced caspase function:

Caspases are good candidates for putative tumor suppressors because they are needed for apoptosis. CASP8 has been reported to be silenced due to gene deletion or promoter methylation in several studies, especially in pediatric tumors. The expansion of the MYCN oncogene and high levels of the corresponding protein is often associated with the loss of caspase-8 expression. However, it is unclear if these two genetic changes functionally lead to tumor development. In the clinic, methylation-independent caspase-8 expression reduction has also been discovered. CASP8 mutations have also been found in several types of cancers like colorectal cancer and gastric cancer but in lower frequencies. In primary breast tumor samples taken from patients having breast surgery, researchers discovered that about 75% of the tumors and morphologically normal peritumoral tissue samples have no caspase-3 transcripts and protein expression. Two studies, on the other hand, show that caspase-3 is upregulated in clinical breast tumor samples.

“Apoptosis and cancer therapy”

Gaining control of or probably terminating the uncontrolled growth of cancer cells is one way to treat cancer. Using the cell’s own death mechanism is a very successful technique. Apoptosis-targeting is perhaps the most effective non-surgical procedure. Apoptosis avoidance is a characteristic of cancer and is nonspecific to the cause, so targeting it is appropriate for all forms of cancer.

Two of the common strategies for therapy are activating proapoptotic molecules and inhibiting antiapoptotic molecules. Patients with leukemia or lymphoma have the strongest connections between apoptosis and treatment sensitivity in human cancer. P53 mutations are linked to brief remissions and drug resistance after treatment in these cancers. Bcl-2 has been linked to drug resistance in patients in a few studies, and high Bcl-2 levels could be a strong prognostic predictor for breast cancer. Finally, in clonogenic assays, loss of Bcl- 2 and p53 slows therapy-induced apoptosis in some cases but does not improve long-term survival.

“Apoptosis as a link between cancer genetics and cancer therapy”

The studies described above show that apoptosis disruption promotes tumor initiation, progression, and treatment resistance. It’s remarkable that the same genetic changes that affect apoptosis during tumorigenesis also affect treatment sensitivity. For example, c-Myc promotes apoptosis in the presence of low levels of survival factors or oxygen, as well as after exposure to a variety of cytotoxic agents, on the other hand, loss of p53 and overexpression of Bcl-2 inhibit apoptosis caused by oncogenes, survival factor depletion, hypoxia, and cytotoxic drugs. As a result, anti-apoptotic mutations that arise during tumor progression will select for chemo-resistant cells at the same time.

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The Apoptosis And Regeneration Of The Animal Model Of Obstructive Atrophy Parotid Gland

To explore the regeneration and recovery of parotid gland after parotid duct ligation and recanalization in rat. Methods: Wistar rats’ parotid duct was ligated for 7 days (group A), 14 days (group B), 21 days (group C) and then released. HE staining、Immunohistochemical and Tunel fluorescence detection were used to observe apoptotic and regeneration changes of parotid specimens which were obtained at 60 and 90 days after releasing the duct. Results: Day0, acinar cells atrophy and decrease while ductal cell proliferation...
6 Pages 2618 Words

Apoptosis And Necrosis Through Differential Staining With Hoechst 33342 And Propidium Iodide

Apoptosis and necrosis Cellular death is a naturally occurring phenomenon. Cells often die due to a harmful environment or through a regulated process of death, with the former termed necrosis and the latter termed apoptosis. While apoptosis is regarded as cell death resulting from normal healthy processes, necrosis results from external factors or disease. (Fink and Cookson, 2005) When cells are exposed to toxins or extreme conditions, damage of the internal cellular environment occurs. Environments such as increased temperatures or...
2 Pages 971 Words

The Structural Characteristics Of Apoptosis

Introduction Apoptosis refers to normal and coordinated death of cells where cells degrade their cytoplasmic contents and DNA. [1] It takes place in multicellular organisms as a programmed response of defense against noxious agents. It can also take place during the regulation of cell populations within the tissues. This analysis will further the definition provided above and explore causes of apoptosis. It will describe the morphologic and biochemical changes that are associated with apoptosis to develop a good understanding of...
1 Page 561 Words

Difference Between Apoptosis Vs Necrosis

Many biological students often wonder about the difference between necrosis and apoptosis because the two occurrences share many similarities. Despite the striking semblance, they also have lots of dissimilarities. So, if you are one of those people who struggle to spot those disparities, you have absolutely nothing to worry about because this informative guide gives a detailed breakdown of the cell activities. However, in keeping with our usual tradition, we have to kick off this piece with their definitions. Later,...
1 Page 668 Words

The Biochemistry Of Apoptosis

Programmed Cell Death Apoptosis is defined as programmed cell death. Apoptosis recently is not considered as the only cell death pathway since various cell death pathways are discovered. More accurately programmed cell death is defined as cell death that is dependent on genetically encoded signals or activities within the dying cell. Therefore, the designation programmed refers to the fixed pathway followed by dying cells, regardless of the mechanism or of whether the characteristic features of apoptosis accompany the process. Acute...
6 Pages 2720 Words

The Definition And Meaning Of Apoptosis

Apoptosis goes early back into the 1970’s where kinetic studies of development of tumour growth stated that cell loss from cancerous tumours were high and rates that were observed show less than 5% predicted of tumour growth that of measurements of proliferation (Kerr et al., 1972; Wyllie et al., 1980) Vast impact on tumour growth could have been from the changes from the loss of cell factor. However, this was suggested that the cause of cell loss was due to...
1 Page 464 Words

Role Of Protein Kinase Enzymes In Apoptosis

Introduction Protein Kinase A kinase is an enzyme serves as catalyst which facilitates the transfer of phosphate groups from high-energy, phosphate-donating molecules to specific substrates. This process is known as phosphorylation, where the substrate gains a phosphate group (and become phosphorylated substrate) and the high-energy ATP molecule donates a phosphate group (and become as ADP). On the other hand, the de-phosphorylation process is when the phosphorylated substrate donates a phosphate group back to the ADP which become as ATP accordingly....
3 Pages 1455 Words

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