A tumor marker is a substance found in your blood, urine, or body tissue. The term "tumor markers" may refer to proteins that are made by both healthy
....
An oncovirus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, often called oncornaviruses to denote their RNA virus origin. It now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with "tumor virus" or "cancer virus".
A tumor marker is a substance found in your blood, urine, or body tissue. The term "tumor markers" may refer to proteins that are made by both healthy
....
An oncovirus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, often called oncornaviruses to denote their RNA virus origin. It now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with "tumor virus" or "cancer virus".
Cancer (Concept of oncogenes and tumor suppressor genes with special referenc...RubinSahu5
Cancer (Concept of oncogenes and tumor suppressor genes with special referencetop53, Retinoblastoma and Ras and APC)
Cancer is a non-infectious disease. It starts at the molecular level of the cell and, ultimately affects the cellular behavior.
It can be defined as uncontrolled proliferation of cells without any differentiation.
Cancer is a genetic disease because it can be traced to alterations within specific genes.
Most cancer cells experience a breakdown in all of these regulatory influences that protect the body from chaos and self‐destruction.
Cancer cells proliferate uncontrollably, producing Malignant tumors that invade surrounding healthy tissue.
Malignant tumors tend to metastasize, that is, to spawn renegade cells that break away from the parent mass, enter the lymphatic or vascular circulation, and spread to distant sites in the body where they establish lethal secondary tumors that are no longer amenable to surgical removal.
All types of cancer can result from uncontrolled Cell Growth And Division of any of the different kinds of cells in the body.
The uncontrolled cell growth produces a mass of cells which are called tumors or neoplasm tumors may be Benign or Malignant.
Oncogenes encode proteins that promote the loss of growth control and the conversion of a cell to a malignant state and Cell Proliferation.
Oncogenes may lead to genetic instability, prevent a cell from becoming a victim of apoptosis, or promote metastasis.
Tumor‐suppressor genes act as a cell’s brakes; they encode proteins that restrain cell growth and prevent cells from becoming malignant.
The first tumor suppressor gene to be studied and eventually cloned is associated with a rare childhood cancer of the retina of the eye, called Retinoblastoma.
The gene responsible for this disorder is named RB .
RAS refers to a family of genes that encode proteins involved in cell signaling pathways regulating cell growth and differentiation.
APC stands for Adenomatous Polyposis Coli.
It's a tumor suppressor gene that plays a critical role in regulating cell proliferation and maintaining the integrity of the epithelial lining of the colon and rectum.
Mutations in the APC gene are associated with familial adenomatous polyposis (FAP), an inherited condition characterized by the development of numerous polyps in the colon and rectum, leading to a significantly increased risk of colorectal cancer.
The cells of patients with this condition were found to contain a deletion of a small portion of chromosome 5, which was subsequently identified as the site of a tumor‐suppressor gene called Adenomatous Polyposis Coli, or APC .
APC is known to suppress the Wnt pathway, which activates the transcription of genes, that promote cell proliferation.
Loss of APC function could therefore lead directly to abnormal chromosome segregation and aneuploidy.
Oncology - For nursing students - tumors classification, cancer, differences between benign and malignant neoplasm,spread of cancer, pathophysiology with cancer cells, carcinogenesis, etiology, cancer screening, cancer prevention, management of cancer, radiation therapy, chemotherapy, bone marrow transplantation, oncologic emergencies
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.
Cancer (Concept of oncogenes and tumor suppressor genes with special referenc...RubinSahu5
Cancer (Concept of oncogenes and tumor suppressor genes with special referencetop53, Retinoblastoma and Ras and APC)
Cancer is a non-infectious disease. It starts at the molecular level of the cell and, ultimately affects the cellular behavior.
It can be defined as uncontrolled proliferation of cells without any differentiation.
Cancer is a genetic disease because it can be traced to alterations within specific genes.
Most cancer cells experience a breakdown in all of these regulatory influences that protect the body from chaos and self‐destruction.
Cancer cells proliferate uncontrollably, producing Malignant tumors that invade surrounding healthy tissue.
Malignant tumors tend to metastasize, that is, to spawn renegade cells that break away from the parent mass, enter the lymphatic or vascular circulation, and spread to distant sites in the body where they establish lethal secondary tumors that are no longer amenable to surgical removal.
All types of cancer can result from uncontrolled Cell Growth And Division of any of the different kinds of cells in the body.
The uncontrolled cell growth produces a mass of cells which are called tumors or neoplasm tumors may be Benign or Malignant.
Oncogenes encode proteins that promote the loss of growth control and the conversion of a cell to a malignant state and Cell Proliferation.
Oncogenes may lead to genetic instability, prevent a cell from becoming a victim of apoptosis, or promote metastasis.
Tumor‐suppressor genes act as a cell’s brakes; they encode proteins that restrain cell growth and prevent cells from becoming malignant.
The first tumor suppressor gene to be studied and eventually cloned is associated with a rare childhood cancer of the retina of the eye, called Retinoblastoma.
The gene responsible for this disorder is named RB .
RAS refers to a family of genes that encode proteins involved in cell signaling pathways regulating cell growth and differentiation.
APC stands for Adenomatous Polyposis Coli.
It's a tumor suppressor gene that plays a critical role in regulating cell proliferation and maintaining the integrity of the epithelial lining of the colon and rectum.
Mutations in the APC gene are associated with familial adenomatous polyposis (FAP), an inherited condition characterized by the development of numerous polyps in the colon and rectum, leading to a significantly increased risk of colorectal cancer.
The cells of patients with this condition were found to contain a deletion of a small portion of chromosome 5, which was subsequently identified as the site of a tumor‐suppressor gene called Adenomatous Polyposis Coli, or APC .
APC is known to suppress the Wnt pathway, which activates the transcription of genes, that promote cell proliferation.
Loss of APC function could therefore lead directly to abnormal chromosome segregation and aneuploidy.
Oncology - For nursing students - tumors classification, cancer, differences between benign and malignant neoplasm,spread of cancer, pathophysiology with cancer cells, carcinogenesis, etiology, cancer screening, cancer prevention, management of cancer, radiation therapy, chemotherapy, bone marrow transplantation, oncologic emergencies
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.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
Acetabularia Information For Class 9 .docxvaibhavrinwa19
Acetabularia acetabulum is a single-celled green alga that in its vegetative state is morphologically differentiated into a basal rhizoid and an axially elongated stalk, which bears whorls of branching hairs. The single diploid nucleus resides in the rhizoid.
Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
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.
Chapter 3 - Islamic Banking Products and Services.pptx
CANCER Basic Oncology and viral agents.pdf
1. Cancer
-In young animal, cell multiplication exceeds cell death, so animal
increase in size
-In adults, the process of cell birth and death are balanced
-Sometimes, Control system for cell multiplication break down, and
a cell begins to grow and divide in an unregulated fashion
Descendant cells inherit this property proliferate without
responding to regulation, forming a mass called a tumor
A cancer is mainly caused by mutation in somatic cells, number
of mutation may vary from 3-20
2. ONCOGENES
◼ Normal cells contains highly related but not
identical copies of retroviral transforming
genes
◼ Proto oncogenes are found in all animals,
exert normal cellular function
◼ Components of regulatory pathways to control
cell proliferation, division and differentiation.
◼ Incorrect expression of any component might
result in uncontrolled growth of cells.
3. Oncology and Oncogenic Viruses
Terminologies
◼ Oncogenes: encode proteins that associated with oncgenesis
◼ Transformation: stable and heritble change in the genes for
growth control
◼ Contact inhibition: Stop growing upon contact with
neighboring cell
◼ Immortalization: Cell divides for indefinite period
◼ Benign tumor: Composed of cells with abnormal growth but
non-invasive
◼ Malignant tumor: Composed of cells with abnormal growth
that invade to other organs
◼ Metastasis: Invasion of cancer to other part of the body
◼ Neoplasm: formation of new cells
◼ Hyper plastic: abnormal cell growth
4. Cancers Originate in Proliferating
Cells
◼ Cancers must occur in dividing cells so that mutations
are passed on many progeny cells
◼ Mutations in non-dividing cells do not induce cancer
◼ Stem cell present in different organs and tissues
divide continuously and generate more stem cells
◼ Oncogenic mutations in theses stem cells DNA can
accumulate and eventually transforming them into
cancer cells
◼ Cells that have acquired mutations have abnormal
proliferation capacity but can not undergo normal
process of differentiation
5. Benign vs. Malignant Tumors
Benign Malignant
Grow slowly Grow rapidly
Well-defined capsule Not encapsulated
Not invasive Invasive
Well differentiated Poorly differentiated
Low mitotic index High mitotic index
Do not metastasize Can spread distantly
(metastasis)
6. Classification & Nomenclature
◼ Benign
◼ Named according to the tissue from which
they arise, and includes the suffix - “oma”
◼ Lipoma
◼ Glioma
◼ Leiomyoma
◼ Chondroma
7. Classification & Nomenclature
• Malignant tumors
Named according to the tissues from which they
arise
Epithelial tissue – carcinoma
Ductal or glandular epithelium – adenocarcinoma
Example: mammary adenocarcinoma
Connective tissue – sarcoma
Example: rhabdomyosarcoma
Lymphatic – lymphomas
Blood forming cells – leukemia
8. Classification & Nomenclature
◼ Carcinoma in situ (CIS)
◼ Preinvasive epithelial malignant tumors of glandular or
Squamous cell origin that have not broken through the
basement membrane or invaded the surround stroma
◼ Cervix, skin, oral cavity, esophagus and bronchus
(epithelium)
◼ Stomach, endometrium, breast, large bowel (glandular)
9. Cancer cells accumulate mutations
• Most cancer cells have increased
number of mutations then the
normal cells
• As the cancer progresses, the
number of mutation increases
• Inactivation of mutator genes
decreases the repair damage of
DNA, and increase the rate of
mutation
• The occurrence of different
mutations creates an opportunity
to select population of cells with
particular properties
10. Cancer arise from a
single clone
• The occurrence of different mutations
creates an opportunity to select the
cells with particular properties
• In the case of cancer, a mutation that
increases the growth potential of a cell
will give it a selective advantage
• A cell that divides more often, will
generate more descendants
• At each stage during the progression
of a cancer, the cell population is
selected for those cells that can grow
more aggressively
11. Tumor cells are immortalized
and transformed
Three types of changes that occur when a
cell becomes tumorigenic
-Immortalization
-Transformation
-Metastasis
When cells are placed in culture,
-grow for division
-enter a senescent stage
-go through the crisis
-survival of crisis are capable of
dividing indefinitely
12. Properties of a transformed cell
Most prominent changes are
◼ Alteration in growth pattern- increased
growth rate, anchorage independence
◼ Alteration in cell surface
◼ Alteration in intracellular component
and biochemical processes- increase
protease and protease activators
◼ Tumorigenecity- forms tumor upon
injection in animals
13. Tumor Cells have altered Morphology
Cells cultured from tumors show
changes in some or all of these
properties. They are said to be
transformed
• A transformed cell grows in a much
less restricted manner
• It has reduced serum-dependence,
• It does not need to attach to a solid
surface
• The cells pile up into a focus instead of
growing as a surface monolayer.
• The cells may form tumors when
injected into appropriate test animals.
14. Seven types of protein control
cell growth
◼ Cancers can result from expression of
mutant from proteins like:
Growth factors (I)
Growth factor receptors (II)
Signal transduction Proteins (III)
Transcription factors (IV)
Pro- or anti- apoptotic proteins (V)
Cell cycle control proteins (VI)
DNA repair proteins (VII)
15. . Growth factor (I)
Growth factor
receptor (II)
Intracellular
transducer (III)
Intracellular effector
region (PTK)
Second messenger
(phosphorylated proteins)
Transcription factors (IV)
DNA
Transcription
DNA repair
Proteins (VII)
RNA
Cell cycle control
proteins (VI)
mRNA Proteins
Anti-apoptosis
proteins (V)
Intracellular
receptors (II)
Virus encoded
activators of
growth –factor
receptors (Ia)
16. Mechanisms of oncogenic
activation
◼ Mechanisms of activation of proto
oncogene and converting to a cancer
gene vary
- over expression
- constituently active
- express in wrong time
- express in wrong place
Interaction of proto-oncogene product
with other proteins altered
17. Mechanisms of activations
◼ Transduction by retroviruses
◼ Insertional mutagenesis
◼ Translocation
◼ Gene amplification
◼ mutation
18. Transduction
◼ Cellular proto oncogenes may
transduced into retroviral genome
◼ Transduced gene replicated and
transmitted like viral genes
◼ Upon infection the transduced gene
expressed abundantly under viral signal
19. Insertion
◼ Insertion of a retroviral promoter
adjacent to cellular oncogene
◼ First occurred in avian leucosis virus
Host
gene
5’LTR 3’ LTR
C- myc
20. Translocation
◼ Translocation of a proto-oncogene near a
strong regulatory sequence
◼ Translocation may affect the expression of
proto-oncogene or gene product
Translocation in Burkitt’s lymphoma
H pro.
H-gene
C-myc pro.
C-myc gene
H pro.
C-myc gene
C-myc pro.
H-gene
Chromosome 14 8 Chromosome 14 8
21. Gene Amplification
◼ Increase in copy number of a potential
gene resulting in excess production of
the encoded protein
◼ Amplification of oncogene HER-2/neu
occur in breast cancer
◼ Gene amplification mostly occur at the
late stage of tumor progression
22. Mutation
◼ Point mutation or deletion might change
the function of a protein,
◼ Substrate specificity,
◼ cell binding property,
◼ Binding specificity of a transcription
factors etc.
◼ Altered protein may lead to oncogenic
activation, eg. C-ras gene
23. Oncogenic Viruses
◼ DNA Viruses
- Human papilomaviruses (HPV)
- Epstein Barr Virus (EBV)
- Hepatitis B Virus (HBV)
◼ RNA Viruses
-Retroviruses
-Hepatitis C Virus
◼ RNA tumor viruses introduce a transforming gene into the cell
(??HCV)
◼ DNA tumor viruses induce or alter the expression of a pre existing
cellular gene/s (proto-oncogene)
24. Transformation by DNA and RNA Viruses
◼ DNA tumor Viruses do not carry any
transduced oncogene but, most of
the RNA tumor viruses do
◼ DNA tumor Viruses do not produce
tumor in their natural host cells, but
replicate there.
◼ RNA tumor viruses cause cancer in
their natural host
◼ Both kind of tumor viruses integrate
their genome into host DNA; at
least a few copies of gene
25. Transformation ……… Viruses (cont)
• Permissive cells are productively
infected. The virus proceeds
through a lytic cycle that is
divided into the usual early and
late stages. The cycle ends with
release of progeny viruses and
(ultimately) cell death.
• Nonpermissive cells cannot be
productively infected, and viral
replication is abortive. Some of the
infected cells are transformed; in
this case, the phenotype of the
individual cell changes and the
culture is perpetuated in an
unrestrained manner.
26. Transformation ……… Viruses (cont)
• The oncogenes of DNA transforming viruses
carry out early viral functions.
• The oncogene becomes integrated into the
host cell genome and is expressed
constitutively.
• The oncogenes of polyomaviruses are T
antigens, which are expressed by alternative
splicing from a single locus.
• Adenoviruses express several E1A and E1B
proteins from two genes.
27. Retroviruses activate or incorporate
cellular genes
◼ Retroviruses can transfer
genetic information both
horizontally and vertically.
◼ Horizontal transfer is
accomplished by the normal
process of viral infection, in
which increasing numbers of
cells become infected in the
same host.
◼ Vertical transfer results
whenever a virus becomes
integrated in the germ line of
an organism as an endogenous
provirus; like a lysogenic
Bacteriophage.
28. • Nondefective viruses follow the usual retroviral life cycle.
They provide infectious agents that have a long latent period,
and often are associated with the induction of leukemias.
Two classic models are FeLV (feline leukemia virus) and
MMTV (mouse mammary tumor virus).
• Tumorigenicity does not rely upon an individual viral
oncogene, but upon the ability of the virus to activate a
cellular proto-oncogene (s).
⚫ Acute transforming viruses have gained new genetic
information in the form of an oncogene. This gene is not
present in the ancestral (nontransforming virus); it originated
as a cellular gene that was captured by the virus by means of
a transduction event during an infective cycle. These viruses
usually induce tumor formation in vivo rather rapidly, and
they can transform cultured cells in vitro. Reflecting the fact
that each acute transforming virus has specificity toward a
particular type of target cell, these viruses are divided into
classes.
• Acute transforming retroviruses have oncogenes that are
derived from cellular genes.
29. ◼ When a retrovirus captures a cellular gene by
exchanging part of its own sequence for a
cellular sequence, some of the original retro -
viral sequences are replaced by a cellular
sequence, creates a transducing virus that has
two important properties,
-Usually these viruses are replication-defective, cannot
replicate by itself, but they can propagate with a
wild-type "helper" virus
-During an infection, their expression may alter the
phenotype of the infected cell