The Theory Of Oncogenes

Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells.

2012) Lipid, protein... ... middle of paper ... ... complex mechanisms of each type of cancer, there may be different in details and may have to find out more. It would be useful to adopt the comprehensibly approach from the melanoma modality studies to ASS-negative type of cancer which has the high prevalence cancer in Thailand, HCC and cholangiocarcinoma (CCA). Beyond the complicated mechanisms of cancer cells, ADI treatment is interestingly combining with another chemotherapy in order to improve the treatment outcomes which aim to destroy the cancer synergistically. This is an interesting point to be made since cancer has changed itself to avoid the effects of the drug over time. Thereby forcing a change of cancer to apoptosis and reduce the resistance that might be occurred later on.

Impaired cell death is a characteristic of cancer cells, determining their resistance to apoptotic signals, (Adams and Cory 2007, Hartman and Czyz 2013) which is one of the six essential alterations in cell biological capabilities acquired during the multistep development of human tumours (Hanahan and Weinberg 2011, Hartman and Czyz 2013) and remains critical in effective cancer treatment strategies (Adams and Cory 2007). Two major apoptotic paths have been defined; death receptor (extrinsic) and mitochondrial (intrinsic) pathway and they are usually switched on in a stimulus-dependent manner (Steel, Doherty et al. 2004, Adams and Cory 2007, Hartman and Czyz 2013).Such that extra-cellular death inducing signals via Fas receptors and various intra cellular signals result in activation of caspases (Du, Fang et al. 2000) (caspase 8 and 9) respectively. Intrinsic apoptotic pathway is widely implicated as a barrier to cancer pathogenesis than extrinsic apoptosis pathway (Hanahan and Weinberg 2011).

The role of E17k AKT mutation in breast cancers Background: Tumorigenesis involves the alternation of cell signaling, resulting in unrestrained cell proliferations and cell survivals. The interruption of PI3K/AKT signaling pathway has previously shown to play a significant role leading to cancer development. This pathway is stimulated when growth factor encodes the receptor tyrosine kinase, which phosphorylates the phosphoinositide 3-kinase (PI3K) consisting of p85 and p110 subunits (Figure 1). The phosphorylation of PI3K would further phosphorylate phosphatidylinositol 4,5 diphosphates (Ptdins(4,5)P2) at the Carbon 3 position of the lipid to allow the production of phosphatidylinositol 3,4,5 triphosphates (Ptdin(3,4,5)P3). This lipid is plasma membrane bound and targets proteins with pleckstrin-homology (PH) domains, such as AKT, PDK1, mTORC2 complex and Rho GEFs.

“Treatment-induced Damage to the Tumor Microenvironment Promotes Prostate Cancer Therapy Resistance Through WNT16B." Nature Medicine. 18(9), 1–23.PDF

According to Jordan, Guzman, and Noble, “stem cells have three distinctive properties: self renewal, the capability to develop into multiple lineages, and the potential to proliferate extensively” (1253). The characteristic of ... ... middle of paper ... ... are sometimes a temporary means to an end , “cancers that appear to be successfully eliminated immediately following treatment may recur at a later time and often do so at a new site” (Goldthwaite, 93). Research and development are focusing on being able to target the cancer stem cell directly, and avoid damaging healthy tissues. Goldthwaite also shows us that, “If the CSC hypothesis proves to be correct, then a strategy designed to target CSCs selectively could potentially stop the “seeds” of the tumor before they have a chance to germinate and spread” (93). Eliminating the cancer stem cells that are responsible for tumor growth could potentially cure a patient.

Cancer cells within the tumor will then use the newly formed blood vessels as a port to metastasize to other localities. Including the drugs for colon cancer, a growing number of anticancer agents have been shown to inhibit hypoxia inducible factor (HIF) gene activity. For many of these, the mechanism of action has been established and involves a reduction in HIF-1 mRNA or protein levels by suppressing the HIF gene expression (Semenza, 2007). Hypoxia is the principal trigger to stimulate VEGF gene transcription and subsequently to angiogenesis. VEGF is responsible triggering the various steps in the angiogenesis cascade such as proliferation, migration and cell survival.

(Lindstrom, 2010) The increase in acetylated NPM1 is noted in cancer. (Lindstrom, 2010) Finding ways to de-acetylate NPM1 is cancer cells is a possible therapeutic strategy. (Lindstrom, 2010) During mitosis NPM1 binds GCN5 inhibits its acetylation of free and mono-nucelated histones. (Lindstrom, 2010) NPM1 also acts as a corepressor or coactivator of several transcription factors. (Lindstrom, 2010)

• Use of adjuvant therapy for example having p-glycoprotein inhibitors. • Use of growth factors and protein kinase C inhibitors. • Gene knockout using antisense molecules. This could be effective in blocking drug resistance. Putting Cancer Drug Resistance to good use: • Unwanted toxicity on the bone marrow is one of the major problems of chemotherapy.

These growth factors regulate progression to emit intracellular signals, allowing cells to progress through the cell cycle as well as cell growth. Cancerous cells use several methods to acquire the capability to sustain proliferative signaling including the production of growth factor ligand, resulting in autocrine proliferative stimulation. Another method used by cancerous cells is sending signals to stimulate normal cells within the supporting tumor-associated stroma to supply the cancer cells with the necessary growth factors. Cancer cells also showed higher levels of receptor p... ... middle of paper ... ...ks of cancer depicted in this article together dictate the malignant phenotype of cancer. These hallmarks of cancer are fundamental for cancer research, showing the remarkable similarity in the pathologic traits that are ultimate in tumor formation and progression.