INTRODUCTION
HISTORY
GENES INVOLVED IN CANCER
ONCOGENES
TUMOUR SUPPRESSOR GENES
ONCOGENE
INTRODUCTION
TYPES
ACTIVATION OF PROTO ONCOGENES
FUNCTION
TUMOUR SUPPRESSOR GENES
INTRODUCTION
EXAMPLE
RB GENE
TP53 GENE
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.
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.
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
Epigenetics is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence. -Wikipedia
HGP was conceived in 1984 & officially begun in earnest in October 1990.
HGP is a large multicentric, international collaborative venture, the main aim of which is to determine the nucleotide sequence of the entire human nuclear genome.
In 1997, United States established the National Human Genome Research Institute (NHGRI).
The HGP was an international research groups from six countries- USA, UK, France, Germany, Japan and China, & several laboratories and a large no. of scientists and technicians from various disciplines.
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
Epigenetics is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence. -Wikipedia
HGP was conceived in 1984 & officially begun in earnest in October 1990.
HGP is a large multicentric, international collaborative venture, the main aim of which is to determine the nucleotide sequence of the entire human nuclear genome.
In 1997, United States established the National Human Genome Research Institute (NHGRI).
The HGP was an international research groups from six countries- USA, UK, France, Germany, Japan and China, & several laboratories and a large no. of scientists and technicians from various disciplines.
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
INTRODUCTION
HISTORY
MECHANISM OF PROTEIN SYNTHESIS
TRANSCRIPTION
TRANSLATION
TRANSCRIPTION
INITIATION
ELONGATION
TERMINATION
TRANSLATION
AMINOACYLATION OF tRNA
INITIATION OF POLYPEPTIDE CHAIN
ELONGATION
TERMINATION
CONCLUSION
REFERENCES
Introduction.
History.
Central dogma.
Mechanism of protein synthesis.
Transcription.
Process of transcription
translation
Step of translation
Activation of amino acid.
Transfer of amino acid to tRNA.
Initiation of polypeptide chain
Elongation of polypeptide chain
Translocation
Termination of polypeptide chain
processing of released polypeptide chain
Main difference between protein synthesis in prokaryotes and eukryotes
Conclusion
Reference
Introduction
History
Geographical distribution
Genome Structure
Anatomy and Life Cycle
Significance of Arabidopsis in Plant Genetics
Conclusion
References.
INTRODUCTION
ABOUT DROSOPHILA
PHYSICAL APPEARANCE
CELL BIOLOGY OF DROSOPHILA DEVELOPMENT
LIFE CYCLE
THE DROSOPHILA GENOME
UNUSAL FEATURES OF DROSOPHILA
SEX DETERMINATION
GENETIC MARKERS
DEVELOPMENT IN DROSOPHILA
CLEAVAGE
THE ORIGINS OF ANTERIOR-POSTERIOR POLORITY {GENES}
CHROMOSOME ABERRATIONS
CONCLUSIONS
REFERENCES
Introduction And Classification
Anatomy Of Flower
Life Cycle Of Arabidopsis
Early Flower Development
Embryogenesis-
A. Formation Of Microspores
B. Formation Of Megaspores
Embryonic Development Starts By Establishing A Root-shoot Axis And Then Halts Inside The Seed
Arabidopsis Genome Is Rich In Developmental Control Genes.
Control Of Carpel & Fruit Development
Arabidopsis Thaliana A Model Plant
Conclusion
References
Introduction
About Drosophila
Genome of Drosophila
Life cycle
Differentiation
Development of Drosophila
* Embryonic development
* Dorsal -ventral and
* Anterior posterior development
* Body segmentation
* Homeotic gene
Conclusion
Reference
Introduction
The big question
Evolution of gene regulation
Gene regulation in eukaryotes
Points of control
Packing/unpacking DNA
Transcription
mRNA processing
mRNA transport
Translation
Protein processing
Protein degradation
Difference between eukaryotic &
prokaryotic gene expression
Conclusions
References
INTRODUCTION
DEFINATION
GAMETES
STRUCTURE OF GAMETES
SPERM
OVUM
RECOGNITION OF EGG AND SPERM
CAPACITATION
ACROSOME REACTION
SPECIES-SPECIFIC RECOGNITION
GAMETE BINDING AND RECOGNITION
GAMETE FUSION
PREVENTION OF POLYSPERMY
ACTIVATION OF GAMETE METABOLISM
FUSION OF THE GENETIC MATERIAL
SIGNIFICANCE OF FERTILIZATION
CONCLUSIONS
REFERENCES
Cellular response to environmental signals in plantKAUSHAL SAHU
INTRODUCTION
CELL SIGNALING:-
I) Unicellular and multicellular organism cell signaling.
II) Classification of intercellular communication.
RESPONSE TO STUMULI:-
(a) Plants
(b) Animals
SIGNAL TRANSDUCTION PATHWAY LINK INTERNAL AND ENVIRONMENTAL SIGNAL:
(a) Reception
(b) Signal transduction
(c) Response
HORMONE
CHEMICAL SIGNALS IN PLANTS
CONCLUSION
REFERENCE
ntroduction
2. Definition
3. Steps Of Signal Transduction
A) Reception
B) Transduction
C) Induction
4. Important component used in Signal Transduction
A) Calcium ion as second messenger
B) Protein Kinase
Types of Signal Transduction
A) Extra cellular Signal Transduction
B) Intra cellular Signal Transduction
C) Inter cellular Signal Transduction
6. Mechanism of Signal Transduction
A) GPCR pathway
B) RTK pathway
7. Example of Signal Transduction
A) In plants
B) In animals
8. Conclusion
9. Reference…
Introduction
Definition
History
Basic element in signal transduction
Basic Pathway of signal transduction
Types of signal transduction
Second messenger
Pathway of signal transduction
Conclusion
References
Introduction
Tumours
Types of Tumours
Formation of Tumours
How cancer cell differ from normal cells
Classification of cancer
The causes of cancer
Viruses and Cancer
Cancer and Gene: A. Oncogene
B. Tumours suppressor gene
Detection and Diagnosis
Therapy of cancer
How can cancer are prevented
Conclusion
References
INTRODUCTION
Definition
history
DIFFERENT PHASE
G0 PHASE
INTERPHASE
M PHASE
CHECKPOINT
HOW DOES IT WORK
Inhibitors
Mechanism of action
Function
CONCLUSION
references
GENERAL IDEA OF SIGNAL TRANSDUCTION
DEFINATION
WHAT DOES THE TERM SIGNAL TRANSDUCTION MEANS
HISTORY
BASIC ELEMENTS IN SIGNAL TRANSDUCTION
TYPES OF SIGNAL TRANSDUCTION
SIGNALLING MOLECULE
RECEPTOR MOLECULE
MODES OF CELL CELL SIGNALING
SECOND MESSENGER
SIGNAL TRANSDUCTION PATHWAY
SOME SIGNALING PATHWAYS
SIGNIFICANCE
CONCLUSION
REFERENCE
CELL CYCLE
CELL CYCLE CHECK POINT
PHASES IN CELL CYCLE CHECK POINT
ROLE OF CYLINE AND CDKS
MUTURATIONAL PROMOTING FACTOR
FUNCTION OF MPR
CONCLUSION
REFRENCE
ion channel and carrier protein By KK Sahu SirKAUSHAL SAHU
INTRODUCTION - DEFINITION OF ION CANALS- HISTORY AND DIVERSITY OF ION CANALS- CARRIER PROTEIN-DEFINITION - CLASSES OF CARRIER PROTEIN - MECHANISM OF ION CANALS AND CARRIER PROTEIN - MEMBRANE TRANSPORT- BIOLOGICAL ROLE OF ION CANALS AND CARRIER PROTEIN - CONCLUSION - REFERENCE
Molecular event during Cell cycle By KK Sahu SirKAUSHAL SAHU
WHAT IS CELL?
WHAT IS CELL DIVISION OR CELL CYCLE?
WHY DO CELL DIVIDE?
HISTORY
CELL CYCLE
INTERPHASE
M-PHASE
MOLECULAR EVENT DURING CELL CYCLE AND CELL REGULATION
TYPES OF CELL DIVISION
IMPORTANCE OF CELL DIVISION
ABNORMALTIES OF CELL CYCLE
REFRENCES
WHAT IS CELL?
WHAT IS CELL DIVISION OR CELL CYCLE?
WHY DO CELL DIVIDE?
HISTORY
CELL CYCLE
INTERPHASE
M-PHASE
MOLECULAR EVENT DURING CELL CYCLE AND CELL REGULATION
TYPES OF CELL DIVISION
IMPORTANCE OF CELL DIVISION
ABNORMALTIES OF CELL CYCLE
REFRENCES
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
The increased availability of biomedical data, particularly in the public domain, offers the opportunity to better understand human health and to develop effective therapeutics for a wide range of unmet medical needs. However, data scientists remain stymied by the fact that data remain hard to find and to productively reuse because data and their metadata i) are wholly inaccessible, ii) are in non-standard or incompatible representations, iii) do not conform to community standards, and iv) have unclear or highly restricted terms and conditions that preclude legitimate reuse. These limitations require a rethink on data can be made machine and AI-ready - the key motivation behind the FAIR Guiding Principles. Concurrently, while recent efforts have explored the use of deep learning to fuse disparate data into predictive models for a wide range of biomedical applications, these models often fail even when the correct answer is already known, and fail to explain individual predictions in terms that data scientists can appreciate. These limitations suggest that new methods to produce practical artificial intelligence are still needed.
In this talk, I will discuss our work in (1) building an integrative knowledge infrastructure to prepare FAIR and "AI-ready" data and services along with (2) neurosymbolic AI methods to improve the quality of predictions and to generate plausible explanations. Attention is given to standards, platforms, and methods to wrangle knowledge into simple, but effective semantic and latent representations, and to make these available into standards-compliant and discoverable interfaces that can be used in model building, validation, and explanation. Our work, and those of others in the field, creates a baseline for building trustworthy and easy to deploy AI models in biomedicine.
Bio
Dr. Michel Dumontier is the Distinguished Professor of Data Science at Maastricht University, founder and executive director of the Institute of Data Science, and co-founder of the FAIR (Findable, Accessible, Interoperable and Reusable) data principles. His research explores socio-technological approaches for responsible discovery science, which includes collaborative multi-modal knowledge graphs, privacy-preserving distributed data mining, and AI methods for drug discovery and personalized medicine. His work is supported through the Dutch National Research Agenda, the Netherlands Organisation for Scientific Research, Horizon Europe, the European Open Science Cloud, the US National Institutes of Health, and a Marie-Curie Innovative Training Network. He is the editor-in-chief for the journal Data Science and is internationally recognized for his contributions in bioinformatics, biomedical informatics, and semantic technologies including ontologies and linked data.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
1. CANCER GENETICS
By
KAUSHAL KUMAR SAHU
Assistant Professor (Ad Hoc)
Department of Biotechnology
Govt. Digvijay Autonomous P. G. College
Raj-Nandgaon ( C. G. )
4. INTRODUCTION
CANCER
• Cancer is a group of disease that
involve uncontrolled division of
cells.
• It is due to failure of the
mechanism that usually control the
growth and proliferation of cells.
5. • Cancer arises from a single cell which has
undergone mutation.
• TUMOUR is a cluster of cells resulting
from rapid cell growth
• Cancer genetics deals with the study of
genes involve in causing cancer.
• Most or all cause of cancer are genetic
damage.
6. HISTORY
• 1890- HANSEMANN -abnormal
behaviour of chromosome in cancer
cell.
• 1911- PEYTON ROUS -a virus can
cause cancer when injected into a
suitable host animal
• 1976- Dr.J.MICHAEL BISHOP and
HAROLD E. VARMUS oncogenes
were defective proto-oncogenes.
8. 1) ONCOGENES
• The word ONCO comes from a Greek word
onkos –bulk or mass
• Any gene that encodes a protein able to
transform cells in culture or to induce
cancer in animal.
• Oncogene encode protein that promote the
loss of growth control and conversion of a
cell to a malignant state.
9. TYPES
Cellular or c-oncogene -present in host
cell and carry out all the necessary
function of the host cell.
• Viral or v-oncogene- derived by capturing
a proto-oncogene from a host genome.
14. 1.Oncogenes That Encode Growth
Factors
• Cancer-causing simian sarcoma virus
contained an oncogene (sis) derived from
the cellular gene for platelet-derived
growth factor (PDGF), a protein present in
human blood.
• Cultured cells that are transformed with
this virus secrete large amounts of PDGF
into the medium, which causes the cells to
proliferate in an uncontrolled fashion.
15. 2. Oncogenes That Encode Growth Factors
Receptors(GFR)
• Malignant cells contain a much larger
number of the receptors which makes the cells
sensitive to much lower concentrations of the
growth factor.
•Proto-oncogene encode GFR can also activated
by mutation that cause the receptor monomer
to undergo dimerization in the absence of
exogenous ligand, which leads to their protein
kinase activity.
17. 4.Oncogenes That Encode Nuclear
Transcription Factors
•Cells that are not actively
growing and dividing tend to
withdraw from the cell cycle and
enter to G0,stage.
Myc is one of the first proteins to
appear when a cell in this quiescent stage
has been stimulated by
growth factors to renters the cell cycle
and divide.
19. 2) TUMOUR SUPPRESSOR GENES
(TSG)
TSG inhibit cell proliferation by
arresting progression through the cell
cycle.
Protein encoded by TSG act as
negative regulation of cell proliferation.
Their elimination promotes
uncontrolled cell growth
25. 2) TP53 GENE
• TP53 is a TSG that when absent is
responsible for a rare disorder called
Li-Fraumeni syndrome.
• Inherit one normal and one abnormal
(or deleted) allele of the TP53
tumour-suppressor gene.
Function of p53
p53 is a transcription factor that
activates the expression of genes
involved in cell cycle regulation and
apoptosis.
27. •The Role of p53:
•p53 is a transcription factor that activates
the expression of either-
•p21 gene, whose product cause cell arrest
or,
Bax gene, whose product cause apoptosis .
•genetic damage, as occurs if the cell is
subjected to ultraviolet light or chemical
carcinogens, the concentration of p53 rises
rapidly.
•p53 degradation is facilitated by a protein
called MDM2.
30. S.
No.
BOOKS AUTHOR
1. Cell and molecular
biology
Gerald karp
2. Molecular cell biology Lodish
3. Molecular biology of
cancer
F. Macdonald and
C.H.J. Ford
4. Internet www.kbiotech.com
5. Internet www.genetics.edu.au
References