The notion that PTHrp triggers EMT in prostate cancer and promotes skeletal invasion and suggests that inhibiting the action of PTHrp might decreases its metastatic effects. a novel study has screen library of compounds and identified major compounds that are capable of inhibiting PTHrp in lung cancer cells. These compounds are cyclic thiourea compounds and bis-cyclic
Darker specimens will absorb more light and more bright patterns will absorb less light. The detector measures the amount of light that is transmitted through the sample. The various electronic components convert this measurement in% transmittance reading, which is a percentage of source light, which has made its way through the sample.
Oncogenes are the mutant form of proto-oncogenes. An example of a transformation of a proto-oncogene to an oncogene is the p53 gene, which encodes a nuclear protein that acts as a transcription factor. The p53 gene is usually a tumor suppressor gene that controls passage of the cell from one phase of mitosis to another. The mutations in p53 gene are estimated to be associated with over half of all cancers.
Cancer is characterized by several distinct features including uncontrolled cell division, resistance to growth inhibitors, evasion of apoptosis, invasion of distant tissues, ability to induce angiogenesis and immortality (Hanahan and Wei...
The Human Papilloma Virus has two sub-types, one of which has very little or no oncogenic potential (HPV 6, 11, 42, 43, 44). The term oncogenic describes a gene that causes normal cells to change into cancerous tumor cell...
The article begins by stating that the tumor suppressor p53 has great importance in the prevention of cancer growth and expansion. Although cancer is the most spoken about topic and p53’s significance against it, p53 also has a hand in ischemia, neurodegeneration, and ageing. While this tumor suppressor seems to be very busy it also regulates the repair of DNA and death of the cell, just to name a few. The activity of p53 can be seen when binding to the DNA at target sequences for transcription. It was pointed out that the doings of p53 are not designated to the nucleus such as other transcription factors as determined over time. Further mentioned in the introduction is a statement that lists this as the most studied mechanism while also related to the material covered in class is apoptosis. P53 inducts apoptosis in the by intrinsic mitochondria-mediated pathway, also transcriptionally through pro-apoptotic parts of the pathway, and in a transcription–independent way which has been recently been looked further into. As if the roles above were not plentiful enough cytoplasmic p53 is also thought to influence autophagy, movement of vesicles, signal transduction, cell metabolism and possibly stem cell expansion, but all are truly determined. Towards the end of the introductory section the authors state that there are still many mechanisms of cytoplasmic p53’s activation leading to apoptosis that are uncertain as well as some p53 missense mutants that lead to oncogenesis. The authors express that the article mainly will speak about the proper or improper activities performed by p53 on the mechanism in the cytoplasm while also looking for areas where beneficial treatments may be used.
The tumor suppressor gene p53 plays an extremely important role in the cell cycle and for maintaining a tumor-free system overall. So it is not surprising that p53 mutations are found to be connected to many different types of cancer (Johnson, 2013). Such p53 mutations give rise to mutant p53 proteins, which have lost its normal function of suppressing tumor formation and have ga...
Decreased ID4 expression in prostate adenocarcinoma as compared to adjacent normal prostate (Fig. 1A) was observed in The Cancer Genome Atlas (TCGA) (22) prostate cancer adenocarcinoma (PRAD) gene expression (IlluminaHiseq) database. ID4 expression was also down-regulated in 51.8% of cases (mRNA expression, all complete tumors, Z-score threshold +2.0) in the MSKCC Prostate Adenocarcinoma (23) dataset (cBio cancer genomics portal (24,25)), with a significant reduction in disease free survival as compared to cases expressing ID4 (p=0.02) (Fig. 1B). These results are consistent with decreased ID4 expression reported in our earlier studies in PCa (9,12).
The mechanisms by which cancer occurs are incompletely understood. The cancer is thought to develop from cells with changed the typical mechanisms for manage of proliferation and growth. Recent proofs strengthen the notion of carcinogenesis as a genetically regulated multistage process (Mediana et al., 2008).
Almeida, L. O., Abrahao, A. C., Rosselli-Murai, L. K., Giudice, F. S., Zagni, C., Leopoldino, A. M., et al. (2014). NFκB mediates cisplatin resistance through histone modifications in head and neck squamous cell carcinoma (HNSCC). FEBS Open Bio, 4, 96-104. Retrieved March 7, 2014, from http://dx.doi.org/10.1016/j.fob.2013.12.00
Similarly, cancerous lymph node associations cause promoter hypermethylations, which overexpress Twist1.2 Through that overexpression, the WR domain (N-terminus of Twist1) binds to the transcription factor complex responsible for post translational modifications, called RELA (NF-kB subunit).2 Then, an activated RELA promotes the epithelial-to-mesenchymal transition (EMT) in a downstream pathway.1 Considering EMT regulates cancer cell metastasis, overexpression results in upregulation of EMT effectors N-cadherin and vimentin, with the downregulation of EMT effector E-cadherin (Fig 2).7 Consequently, the alteration in regulation patterns of the EMT effectors induces cellular intrusion and metastasis (Fig. 2).