Cancer Scenario in India & RAS protein CA1 (Soumili Sanki).pdf
1. TITLE-CANCERSCENARIO IN INDIA
NAME- SOUMILI SANKI
ROLL NO- 30028021006
M.sc in Molecular Biology
INTRODUCTION-
Cancer is a disease when a normal cells have lost the control over their divisions, differentiation and apoptosis and they
become tumour cells . All genes have change their epigenetic changes and causes due to the activation of Oncogenes and
inactivation of Tumour suppressor gene. In World, 10 million people are diagnosed and more than 6 million die in a year. In India
, there will be about 800,000 new cancer cases in every year.
2. • PROBLEMS
IN WORLD
1.In every yrear ,10 million peopleare diagnosed and more than 6 million die in the year .
2.22.4 million peopleare living with cancer in 2000.
3.Most common cancers in World are-lungs cancer(12.3%),breast(10.4%) and cholesterol cancer(9.4%)..
IN INDIA
In India,the common cancer are-in male-esophagus,
stomach, lower respiratorytract.
In female-breast,cervix,oropharynx.
Thereason ofcancer in Indiathe use ofTobacco,91%oropharynx
cases in use of Tobacco.In female,61% cases are breast ,cervix
ovary cancer
.
3. • Reference :
These alldata is collected from google ,I used PUBMED ,QUORA,NCBI websites to collect al kind of data
and images .
• ACKNOWLEDGEMENT-
I am thankful to my mentor Dr. Suryyani Deb madam for her enormous support to complete
this presentation. Also thanks are due to all those unknown indivisuals whose pictures I have used
for making this presentation.
THANK
YOU
4. PPT
01.08.22
[ MAKAUT ]
Signal transduction & Oncology
Supervised by :- Dr. Jaya Bandyopadhyay.
RAS PROTEIN
“& REGULATION”
SOUMILI SANKI.
Roll no : 30028021006
Reg No : 213001828010006
M.Sc in Molecular Biology (SEM III)
6. INTRODUCTION
Ras protein is a small G protein which activation of downstream pathways ,plays an important role in cellular differentiation ,
proliferation and survival and apoptosis.
This is done by –
1. Gene Transcription
2. Cell differentiation
Ras protein conserved GTPase enzyme.
Variants- H Ras, K Ras, N Ras, M Ras.
It is made up of 6β sheets and 5αhelix.
Alternates between GDP bound(inactive) and GTP bound (active).
If Ras protein failure its function-
1.Early apoptosis will be occur.
2. Causes cancer.
3. Inappropriate differenciation means that cells expressed incorrect proteins.
7. STRUCTURE
1. The Ras genes, which are proto- oncogenes that are
mutated in human cancers, are encoded by three
expressed genes H, K and N Ras encoded 188-189
residue proteins.
2. Ras protein constitute a class of phosphate binding
loop proteins that work as molecular switches
between the GDP bound inactive and GTP bound
active.
8. RAS PROTEIN REGULATION
NORMAL Ras PROTEIN REGULATION –
1. Extra cellular signal influences the Ras protein.
2. Ras activated by phosphorylation of bound GDP that is transferred GDP to GTP.
3. Ras protein activated and started activation of the several gene
through the cascade and enters to the nucleus.
4. Signals regulates transcription of gene involved
in cell division controlled manner.
MUTANT Ras PROTEIN REGULATION-
1. Extra cellular signal.
2. Inactivates GTP ase activity. Ras is not
activated.
3. Uncontrolled cell division will be occur.
9.
10. DRUG THERAPIES
Study: exposed mouse fibroblast cells to H-Ras
1. Caused the cells to die.
2.Reduces over expression of proteins.
3. Reduces cell proliferation and division.
4. Reduces risks of tumour and cancer.
Drug : Farnesyl transferase inhibitor
1. Stops the function Ras post translational
Modification ,(farnesyl isoprenoid group).
2. This means that Ras protein can not attach to
the cell membrane.
3. Therefore can not transduce signals.
11. ACKNOWLEDGEMENT
I AM THANKFUL TO MY MENTOR DR. JAYA BANDYOPADHYAY MADAM FOR HER
ENORMOUS SUPPORT TO COMPLETE THIS PRESENTATION. ALSO THANKS ARE DUE TO
ALL THOSE UNKNOWN INDIVISUALS WHOSE PICTURES I HAVE USED FOR MAKING THIS
PRESENTATION.