Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15
years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we
present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it
is time to embrace the central role of epigenetics in cancer.
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15
years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we
present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it
is time to embrace the central role of epigenetics in cancer.
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
Dna methylation ppt
definition of Dna methylation ppt
discovery of Dna methylation ppt
types of Dna methylation ppt
history of Dna methylation ppt
process of Dna methylation ppt
mechanism of Dna methylation ppt
methylation in cancer
cytosine methylation
genomic imprinting
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy
Dna methylation ppt
definition of Dna methylation ppt
discovery of Dna methylation ppt
types of Dna methylation ppt
history of Dna methylation ppt
process of Dna methylation ppt
mechanism of Dna methylation ppt
methylation in cancer
cytosine methylation
genomic imprinting
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy
ABSTRACT- Lung cancer is the most common cause of cancer related mortality worldwide. The epidermal-growth-factor receptor (EGFR) cascades the signaling pathway that regulates tumor-cell proliferation, invasion, angiogenesis, metastasis, and apoptosis. Since EGFR is often over-expressed in NSCLC and the level of EGFR expression correlates with poor prognosis. EGFR inhibitors have been developed as a novel therapy for non-small-cell lung cancer (NSCLC). Gefitinib is the first molecular targeted agent approved for the treatment of advanced NSCLC. It is a highly effective EGFR TK inhibitor (TKI) selectively blocks the signal transduction pathways implicated in cancer growth. Key-words- Lung Cancer, EGFR, NSCLC, Tyrosine Kinase Inhibitor (TKI)
Functional p53 is required for rapid restoration of daunorubicin-induced lesi...Enrique Moreno Gonzalez
The tumour suppressor and transcription factor p53 is a major determinant of the therapeutic response to anthracyclines. In healthy tissue, p53 is also considered pivotal for side effects of anthracycline treatment such as lesions in haematopoietic tissues like the spleen. We used a Trp53null mouse to explore the significance of p53 in anthracycline (daunorubicin) induced lesions in the spleen.
This oral presentation made during ESMO 2016 highlight novel targets and drugs developed for patients with advanced neuroendocrine tumors. This includes targeted agents aiming probing cell signaling in tumor microenvironment and immune responses. Genetic alterations on major anti-oncogenes are reported in the perspective of pathway activations. Combinations using VEGFR, mTOR, Somatostatin receptors inhibitors with novel strategies and immunotherapy are also suggested. This presentation focuses mainly on gastrointestinal neuroendocrine tumors but may also be of interest for those involved in the care of patients with thoracic neuroendocrine tumors.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
Welcome to TechSoup New Member Orientation and Q&A (May 2024).pdfTechSoup
In this webinar you will learn how your organization can access TechSoup's wide variety of product discount and donation programs. From hardware to software, we'll give you a tour of the tools available to help your nonprofit with productivity, collaboration, financial management, donor tracking, security, and more.
How to Split Bills in the Odoo 17 POS ModuleCeline George
Bills have a main role in point of sale procedure. It will help to track sales, handling payments and giving receipts to customers. Bill splitting also has an important role in POS. For example, If some friends come together for dinner and if they want to divide the bill then it is possible by POS bill splitting. This slide will show how to split bills in odoo 17 POS.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
Model Attribute Check Company Auto PropertyCeline George
In Odoo, the multi-company feature allows you to manage multiple companies within a single Odoo database instance. Each company can have its own configurations while still sharing common resources such as products, customers, and suppliers.
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
Palestine last event orientationfvgnh .pptxRaedMohamed3
An EFL lesson about the current events in Palestine. It is intended to be for intermediate students who wish to increase their listening skills through a short lesson in power point.
Digital Tools and AI for Teaching Learning and Research
Role of p53 gene
1. Activity of p53 in Cancer
Progression and metastasis
By
Ashish Kumar
M.Tech 1st year
2. OUTLINE
• CANCER Introduction
• Structure of p53
• Function of p53
• Literature Review
• Conclusion
• References
• Summary
• Questionnaire
3. Objective
• To give knowledge of cancer along with brief
description of p53 gene
4. Current Scenario
• In 2012, an estimated 14.1 million new cases of cancer
occurred worldwide.
• Out of 10 deaths 4 from cancer
• There are 100 different forms of cancer.
• Most common types of cancer are lung, breast, bowel and
prostate which accounts for 4 death in 10 cancer patients
• Lung cancer is common in Men’s and Breast cancer in Female
5. Cancer
• Single type of cell proliferate continuously
becomes immortal further into a tumor.
• Two types of tumor
– Benign Tumor
– Malignant Tumor
7. p53 Gene
• "the guardian of the genome"
• TP53 gene is located on the short arm
of chromosome 17 (17p13.1)
• TP53 gene encodes at least 15 protein
isoforms [1]
• Actual molecular weight is 43.7 kda [2]
13. INACTIVATION OF NORMAL p53 AND
ACTIVATION OF MUTATED p53
N-Terminus
C-Terminus
Point Mutation Acquires GOF
14. RECRUITMENT MECHANISM TO THE PROMOTER
• To analyze GOF
• mtp53 can be recruited to promoters via interaction with
other transcriptional factors acc. to [4,5,6,7,8]
• Binding factors- E2F1, NF-Y, VDR, ETS1, ETS2, and
SP1 also binds with normal p53 acc. To [4,5,6,7,8,9]
• Mtp53 gene expression with help MRD1 promoter and
stated ETS-1 can interact with mtp53 not with normal
p53. ETS factor is require for transcriptional regulatory
activity of mtp53. [10]
• Other studies revealed ETS1 also require to
normal p53 gene for transcription regularities.
18. Reference
• 1 Surget S, Khoury MP, Bourdon JC (19 December 2013). "Uncovering the role of p53 splice variants in human
malignancy: a clinical perspective". OncoTargets and Therapy 7: 57–
68. doi:10.2147/OTT.S53876. PMID 24379683.
• 2 Ziemer MA, Mason A, Carlson DM (1982). "Cell-free translations of proline-rich protein mRNAs". J. Biol.
Chem. 257 (18): 11176–80. PMID 7107651.
• 3 http://www.ncbi.nlm.nih.gov/
• 4. Di Agostino S, Strano S, Emiliozzi V, Zerbini V, Mottolese M, Sacchi A, et al. Gain of function of mutant p53:
the mutant p53/NF-Y protein complex reveals an aberrant transcriptional mechanism of cell cycle regulation.
Cancer Cell (2006) 10(3):191–202. doi:10.1016/j.ccr.2006.08.013
• 5. Fontemaggi G, Dell’Orso S, Trisciuoglio D, Shay T, Melucci E, Fazi F, et al. The execution of the transcriptional
axis mutant p53, E2F1 and ID4 pro-motes tumor neo-angiogenesis. Nat Struct Mol Biol (2009) 16(10):1086–93.
doi:10.1038/nsmb.1669
• 6. Stambolsky P, Tabach Y, Fontemaggi G, Weisz L, Maor-Aloni R, Siegfried Z, et al. Modulation of the vitamin
D3 response by cancer-associated mutant p53. Cancer Cell (2010) 17(3):273–85. doi:10.1016/j.ccr.2009.11.025
• 7. Do PM, Varanasi L, Fan S, Li C, Kubacka I, Newman V, et al. Mutant p53 cooperates with ETS2 to promote
etoposide resistance. Genes Dev (2012) 26(8):830–45. doi:10.1101/gad.181685.111
• 8. Zhu J, Sammons MA, Donahue G, Dou Z, Vedadi M, Getlik M, et al. Gain- of-function p53 mutants co-opt
chromatin pathways to drive cancer growth. Nature (2015) 525(7568):206–11. doi:10.1038/nature15251
• 9. Borellini F, Glazer RI. Induction of Sp1-p53 DNA-binding heterocomplexes during granulocyte/macrophage
colony-stimulating factor-dependent proliferation in human erythroleukemia cell line TF-1. J Biol Chem (1993)
268(11):7923–8.
• 10.Sampath J, Sun D, Kidd VJ, Grenet J, Gandhi A, Shapiro LH, et al. Mutant p53 cooperates with ETS and
selectively up-regulates human MDR1 not MRP1. J Biol Chem (2001) 276(42):39359–67.
doi:10.1074/jbc.M103429200