Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
These hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis.
These hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis.
Cellular Signaling Pathways have direct implications on our understanding of tumor cell behavior. A general overview is presented here followed by a brief discussion of some of the major pathways currently implicated in cancer progression : Ras/RAF/MAP kinase pathway and PI3K/AKT/mTOR pathway s
Cancer is mainly caused by the conversion of proto-oncogenes into oncogenes. The process is known as oncogenesis.
This slide will help to get an idea about oncogenesis and also the proto-oncogenes which get converted.
Types of immunotherapy
Oncology
cancer vaccines
adoptive T cell transfer
oncolytic viruses
monoclonal antibodies
cytokine
treatment of cancer with immunotherapy
Cellular Signaling Pathways have direct implications on our understanding of tumor cell behavior. A general overview is presented here followed by a brief discussion of some of the major pathways currently implicated in cancer progression : Ras/RAF/MAP kinase pathway and PI3K/AKT/mTOR pathway s
Cancer is mainly caused by the conversion of proto-oncogenes into oncogenes. The process is known as oncogenesis.
This slide will help to get an idea about oncogenesis and also the proto-oncogenes which get converted.
Types of immunotherapy
Oncology
cancer vaccines
adoptive T cell transfer
oncolytic viruses
monoclonal antibodies
cytokine
treatment of cancer with immunotherapy
A presentation descripes tumors,pathogensis,devlopment,antigenes and genes.
how host responds to them and how tumors evade immunity with latest lines of therapy and prevention.
facaulity of pharmacy.Damascus university.master of libaratory diagnossis. immunology.
Baraa ALomar and feras deban
Signal Pathways in Immune Cell Development.pptxDr.Kanury Rao
Signaling pathways have a fine relation with cancer-causing mutations. Signaling pathways monitor the tumorigenesis that deceive signaling networks. Dr. Kanury Rao has invented an early detection cancer tool especially for women.
Introduction to Cancer
Stem cells and cancer cells
major pathways that lead to formation of tumors.
Tumor Supressors
Colon cancer to prove Knudson hypothesis.
The modern treatments available to treat cancer.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Hallmarks of cancer
1. Hallmarks of cancer
Mohammed Fathy Bayomy, MSc, MD
Lecturer
Clinical Oncology & Nuclear Medicine
Faculty of Medicine
Zagazig University
2.
3. Self-Sufficiency in Growth Signals
Normal cells require mitogenic growth signals to proliferate. These
signals are transmitted by transmembrane receptors, which bind
ligands such as diffusible growth factors, extracellular matrix
components, & cell–cell adhesion/ interaction molecules
In cancer cells, dependency on growth signals is lost by alterations
in extracellular growth signals, transcellular transducers or the
intracellular circuits
4. Cancer cells may:
* Synthesize growth factors (autocrine stimulation), e.g.
platelet-derived growth factor (PDGF) & transforming growth
factor α (TGF-α)
* Overexpress receptors, e.g. epidermal growth factor receptor
(EGFR)
* Show ligand-independent receptor activation by structural
changes
* Express different extracellular receptors
* Contain intrinsically active intracellular pathways
5. Insensitivity to antigrowth signals
In normal tissues, multiple antiproliferative signals operate to
maintain tissue homeostasis. These signals include soluble growth
inhibitors and immobilized inhibitors embedded in extracellular
matrix & on surfaces of surrounding cells. Antiproliferative
signals are perceived by transmembrane cell surface receptors
coupled to intracellular signaling circuits
6. Antiproliferative signals cause:
* Transition of cell out of cell cycle to resting state (G0).
Antiproliferative signals are funneled through retinoblastoma
protein (pRb). In cancer, disruption of the pRb pathway
renders cells insensitive to antiproliferative signals.
* Cell differentiation is a complex mechanism. One of factors of
differentiation is MYC oncogene. Myc protein associates with
another factor, Max. Max also associates with group of Mad
transcription factors, & this complex induces differentiation. If
MYC overexpression is present, balance is impaired & Myc–
Max complexes impair differentiation
7. Evading apoptosis
Tumor growth is balance between cell proliferation & programmed
cell death (apoptosis). Apoptosis is complex process, with
disruption of cell membranes, extrusion of cytosol, degradation of
chromosomes, & fragmentation of nucleus
Apoptotic machinery consists of sensors & effectors:
* Sensors
- These monitor extra- & intracellular environment for damage
- They regulate effectors.
- They are influenced by survival (insulin-like growth factor I & II
(IGF-I, -II) & interleukin-3 (IL-3)), death factors (Fas ligand&
tumor necrosis factor α (TNF-α))
8. * Effectors: Most pro-apoptotic signals have influence on
mitochondria, which release cytochrome c
- Pro-apoptotic signal proteins: Bax, Bak, Bid, Bim, p53
- Anti-apoptotic signals: Bcl-2, Bcl-xL, Bcl-w.
These signals release number of intracellular proteases (caspases)
that execute death program through selective destruction of
subcellular structures, organelles, & genome
Resistance to apoptosis in cancer may be by loss of pro-apoptotic
regulator (e.g. mutation of TP53 tumor suppressor gene) or by
abrogation of death signal (e.g. upregulation of non-functional
decoy receptor for Fas)
9. Limitless replicative potential
Normal cells have limited replicative potential, &, after number of
divisions, they stop growing (senescence). Mechanism of
senescence is due to limited number of telomeres, restricting
number of divisions
Telomere maintenance is present in almost all cancer cells, by
upregulation of enzyme telomerase, which adds hexanucleotide
repeats to end of telomeric DNA
10. Sustained Angiogenesis
Vasculature supplies oxygen and nutrients, which are essential for
cell function and survival
Growth of new blood vessels (angiogenesis) is regulated by anti-
angiogenic & angiogenic factors (e.g. vascular endothelial growth
factor (VEGF) & fibroblast growth factor 1 & 2 (FGF-1 & -2))
Tumors are able to activate angiogenic switch by changing this
balance & recruit blood vessels
11. Tissue invasion & metastasis
Cancer cell invasion & metastasis are due to changes in physical
coupling of cells to their microenvironment & activation of
extracellular proteases
* Interference with microenvironment: several classes of
proteins are involved in interaction of cells with
microenvironment, including cell–cell adhesion molecules
(CAMs: e.g. immunoglobulins & cadherins) & integrins,
which link cells to extracellular matrix substrates
12. - E-cadherin is expressed on epithelial cells. Coupling between
cells by E-cadherin bridges results in transmission of
antigrowth & other signals. E-cadherin function is lost in cancer
cells
- Neural cell adhesion molecule (NCAM) is immunoglobulin
with highly adhesive isoform that is changed to a poorly
adhesive form in certain cancer types (e.g. Wilms’ tumor,
neuroblastoma, & small cell lung cancer) or has reduced overall
expression level (e.g. in pancreatic & colorectal cancer)
- Growing tumor cells express different integrins that interfere
with extracellular matrix, enabling cancer cells to evade control
by extracellular matrix compounds
13. * Extracellular proteases: in cancer, protease genes are
upregulated, protease inhibitor genes are downregulated, &
inactive zymogen forms of proteases are converted into active
enzymes