SlideShare ist ein Scribd-Unternehmen logo
1 von 26
Rupen Chakma (17/BBT/11)
Bipasha Roy (17/BBT/24)
CONTENTS
 INTRODUCTION
 PROPERTIES
 CLASSIFICATION
 THEORIES
 REASONS FOR MUTATION
 HOW MUTATIONS CAUSE TUMOR
 REPAIR AND ANTI CANCER MECHSNISM
 RUNAWAY MECHANISM AND DIAGNOSIS
 CONCLUSION
 REFERENCE
What is a tumor ?
In spite of several check points in a cell cycle to
check any modifications in DNA before its
transfer to next generation, certain mutations
takes place in DNA leading to loss of certain
characters and control over its multiplication
rate.
The consequences of these modification result
in pathological over growth of modified tissues
generally referred as TUMOR or Neoplasia
(meaning new formation) or “cancer”.
There are two types of Tumors : Benign
tumors and Malignant Tumors.
BENIGN TUMORS :
• Benign tumors are generally not harmful due to their well-
defined growth with smooth boundaries.
• Simply grow in diameter and restricted to one place but can be
harmful if the tumor compresses the surrounding tissue against a
hard surface in the body.
• Usually grows at a relatively slow pace and may stop growing for a
time when it reaches a certain size.
• A complete cure can usually be achieved by removing the
abnormally grown tissue mass.
MALIGNANT TUMORS :
• The Malignant tumors are dreadful because their growth is not
restricted to one place.
• Their metastasis nature helps their spread from one place to other
locations in the body via lymph or blood.
•Unlike benign malignant tumors are properly referred to as
“Cancers”.
 The origin of the word cancer is credited to the Greek physician
Hippocrates (460-370 B.C.). In Greek cancer refers to a crab. It is
most likely applied to the disease to mind the shape of a crab,
because of finger – like projections spreading from a cancer tissue
mass resembles the structure of crab more over the spread of cancer
Altered biological properties of cancer cells
1) Acquistion of self-sufficiency in growth signals.
2) Loss of sensitivity to anti-growth signals.
3) Loss of apoptosis, in order to allow growth despite genetic
errors and external anti-growth signals.
4) Loss of senescence, leading to limitless replicative
potential (Immortality).
5) Acquistion of sustained “angiogenesis” (Growth of new
blood vessels from pre-existing vessels).
6) Acquistion of ability to invade neighbouring tissues, the
defining property of invasive carcinoma.
7) Acquistion of ability to metastases at distant sites, the
classical property of malignant tumors.
Classification of Tumors:
Since development of tumor is possible in any region or
organ of the body with dividing cell, tumors were broadly
classified into 3 basic types based upon the embryonic origin
of the tissues involved in the formation of tumor.
They are :
1. CARCINOMAS
2. SARCINOMAS
3. LEUKEMIA
1.Carcinomas
• Developed from cells of ectodermal or endodermal origin.
• They invade surrounding tissues and organs and may
metastasize, or spread, to lymph nodes and other sites.
• Based upon the histopathological appearance they can be
differentiated into “Aden carcinoma” and “squamous cell
carcinoma” to reflect the involvement of glandular or squamous
cells in tumor formation.
• Approximately 90% of human cancers are malignancies of
epithelial cells.
2.Sarcomas (From the Greek ‘sarx” meaning “flesh”)
• Developed from connective tissue or mesoderm.
•Cancers of breast, colon, pancreas bones etc. comes under
this type.
• Sarcomas are rare in humans; about 2% of human cancers
come under this category.
3.Leukemia (Greek leukos “white” ; aima “blood”)
•Developed from bone marrow tissue or in blood.
•Characterized by an abnormal proliferation of blood cells, usually
white blood cells (leukocytes).
•Leukemia tumor is subdivided into lymphoblastic or
lymphocytic leukemia and myeloid or myelogenous leukemia
according to the blood cells affected.
To make it understandable to a common man, tumors were generally
named after the organ or tissue from which it has been developed. For
example, cancer developed in breast tissue is referred as breast cancer.
Similarly, lung cancer, colon Cancer, gastric cancer, skin cancer etc.
William Williams Keen
Different theories to explain cancer development :
From the earliest times, physicians have wondered about
the cause of cancer.
 The Egyptians blamed Gods for the development of
cancers.
Several theories were proposed by different scientists to
explain the cause for cancers. Some of them are as follows :
1. HUMORAL THEORY
2. LYMPH THEORY
3. BLASTEMA THEORY
4. CHRONIC IRRITATION THEORY
5. TRAUMA THEORY
6. PARASITE THEORY
Humoral theory:
 Hippocrates believed that the body contained four humors (Body
fluids) – blood, phlegm, yellow bile, and black bile.
 A balance of these fluids resulted in a state of health. Any excesses
or deficiencies caused disease
 An excess of black bile collecting in various body sites was
thought to cause cancer.
This theory of cancer was passed on by the Romans and was
embraced by the influential doctor Galen”s medical teaching, which
remained unchallenged through the middle Ages for over 1300 years.
During this period of the body, including autopsies, was
prohibited for religious reasons, thus limiting knowledge
Lymph Theory:
 Among the theories that replaced the humoral theory of cancer
was cancer’s formation by another fluid – lymph.
Stahl and Hofman theorized that the cancer was composed of
fermenting and degenerating lymph varying in density, acidity and
alkalinity.
 The theory gained rapid support. John Hunter(1723-1792) agreed
that tumors grow from lymph constantly thrown out by the blood.
Blastema Theory:
In 1838, German pathologist Johannes Muller demonstrated that
cancer is made up of cell and not lymph. But he was of the opinion
that cancer cells did not arise from normal cells.
 Muller proposed that cancer cells arose from budding elements
(Blastema) between normal tissues.
Muller’s students Rudolph including cancer cells, are derived from
other cells.
Chronic Irritation Theory:
Virchow proposed chronic irritations as the cause of cancer, but he
falsely believed that cancers “spread like a liquid.”
 A German surgeon, Karl Thiersch, showed that cancers
metastasize through the spread of malignant cells and not through
some unidentified fluid.
Trauma Theory:
Despite advances in the understanding of cancer, from the late
1800s until the 1920s, cancer was thought by some to be caused
trauma.
Parasite Theory:
In the 17th and 18th centuries, some believed that cancer was
contagious. In fact, the first cancer hospital in France was forced to
move from the city in 1779 because of the fear of the spread of cancer
throughout the city.
Reasons for tumor formation:
Oncogenes, activate cell division and influence embryonic
development and tumor suppressor genes halt cell division.
Since these two genes are typically found in normal human
cells, certain mutations in them may transform their normal
function resulting in the conversion of normal cells into
tumor cells. Either inherited defects or acquired mutations
due to exposure to carcinogens may cause conversion of
normal cell into a tumor cell.
How mutations cause Tumor: Due to mutations, some of the
regular genes may fail to code proteins essential for regulation
of cell cycle, Synthesis of proteins involved in the regulation
of cell cycle are essential to stop access of defective or altered
DNA to the daughter cells. Failure in regulation of cell cycle
results in accumulation of mutations or abnormal characters
in the daughter cells. The normal gene gradually lost its
original characters and become a tumor gene and its modified
tumor gene is known as “Proto-oncogene”. After several
divisions the cell with Proto-oncogene produces tumor.
Mutations may also suppress the efficiency of certain tumor
suppressor genes, as a result chances for tumor development
increases.
Of the many known oncogenes some are derived from normal
Proto-oncogenes. For example the Ros gene that encodes a
protein essential for intracellular signal transduction in
normal cells becomes an oncogene due to mutations and
starts encoding a protein that acts as a signaling molecule for
excessive or uncontrolled growth of cells. An oncopotein
encoded by an oncogene may be similar to the normal
protein but excessive production may alter the character of
normal cells and induces conversion of a normal cell into a
tumor cell.
Others things that may increase the chance of
developing tumors are-
1. Radiation: High- frequency radiation, such as ultraviolet
and ionizing radiation, damages the genetic material DNA,
possibly inducing genetically transferable abnormalities.
2. Viruses: Some human retroviruses and papilloma viruses
exhibit carcinogen gene sequence potential. Retrovirus may
convert proto-oncogenes into oncogenes either by altering or
condensing, to code proteins with abnormal activity or
controlling with powerful regulators to induce the
production in excess or in inappropriate circumstances.
3. Hormones: The role of hormones in carcinogenesis is still
controversial, but it seems that, excessive use of some
hormones, especially estrogen, produces cancer in animals.
4. Chemical substances: Some of the chemical substances
that can induce carcinogens include:
Alkylating agents-leukemia,
Aromatic hydrocarbons and benzopyrene ( From polluted
air) - lung cancer,
Tobacco – cancer of the Lung, oral cavity etc
Repair and Anti-cancer mechaniSM of body
Cell shredding: The body simply shreds some types of cells
that are particularly exposed to environmental carcinogens.
For example, intestinal epithelial cells are shed frequently, so
that any mutations do not get a chance to reproduce. Cell
shedding generally occurs in the stomach, colon, skin, and
other areas.
Cell division limits: Telomeres limit the number of cell
divisions that a single cell can under go, this character helps in
the inhibition of the growth of tumor cells. If a normal cell
becomes cancerous, its clones often die out to telomeric
restriction before producing significant tumor.
Carcinogens neutralization: Carcinogenic substances are
quickly metabolized into harmless substances by the gut and
liver in healthy individuals.
Run away mechanisms of tumor cells:
• Sneaking Through: Newly formed tumor cells escape
immune system’s attack by sneaking, till they increase their
number to resist the immunological response
Some tumors posses weak immunogenicity.
• Modulating Tumor Ags: Here the tumor cells pull the
newly formed Ags to interior(Cytoplasm) or stop expressing
in surface Ags. In the absence of these Ags immune system
fails to enforce any action against the tumor cells.
• Masking Tumor Ags: Certain tumor cells produce
mucoproteins coat known as Sialomucin coat to hide their
new Ags.
• Tumor induced tolerance: Certain tumor cells induce
tolerance through synthesizing different immuno
suppressants to suppress or activate TS-cells which in turn
inhibit the activity of TC ,TD and B-cells activity.
 Production of blocking agents: Producing auto
antibodies known as “blocking antibodies” against their own
antigen.
 Alternation of cell adhesion molecules: Newly formed
tumor cells alter their expression of cell adhesion molecules
to reduce stable contact formation with cytotoxic cells.
DIAGNOSIS:
•Surgery: benign tumors can be removed entirely by
surgery.
•Chemotherapy: by using suitable drugs.
•Radiation Therapy: using ionizing radiation to kill
tumor cells.
•Hormonal Therapy: inhibiting by hormones – breast,
prostate.
•Targeted therapy: interfering with specific molecules
needed for carcinogenesis
Conclusion
 Tumors are uncontrolled growth of cells occurs due to
mutation in different stages of cell cycle
 Two types- Benign and Malignant
 Tumors can occur due to mutation, radiation,
chemicals, viruses etc.
 Although some tumors are mostly fatal we can get rid
of certain tumors through different diagnosis like
surgery, chemotherapy etc.
REFERENCE
 THE ELEMENTS OF IMMUNOLOGY – Fahim
Halim Khan
 A TEXTBOOK OF IMMUNOLOGY – Dr. P.
Madhavee Latha, S Chand publication
 medicalnews.com
 macmillan.org.uk
THANK YOU
Fight cancer with a smile

Weitere ähnliche Inhalte

Was ist angesagt?

2 antigens, immunogens, epitopes, and haptens
2 antigens, immunogens, epitopes, and haptens2 antigens, immunogens, epitopes, and haptens
2 antigens, immunogens, epitopes, and haptens
taha244ali
 
Immunologic tolerance
Immunologic toleranceImmunologic tolerance
Immunologic tolerance
Robin Gulati
 
B CELL RECEPTOR final.pptx
B CELL RECEPTOR final.pptxB CELL RECEPTOR final.pptx
B CELL RECEPTOR final.pptx
BinteHawah1
 

Was ist angesagt? (20)

Antibody diversity presentation
Antibody diversity presentationAntibody diversity presentation
Antibody diversity presentation
 
2 antigens, immunogens, epitopes, and haptens
2 antigens, immunogens, epitopes, and haptens2 antigens, immunogens, epitopes, and haptens
2 antigens, immunogens, epitopes, and haptens
 
Polyclonal and monoclonal antibody production
Polyclonal and monoclonal antibody productionPolyclonal and monoclonal antibody production
Polyclonal and monoclonal antibody production
 
IMMUNE RESPONSE TO TUMORS
IMMUNE RESPONSE TO TUMORSIMMUNE RESPONSE TO TUMORS
IMMUNE RESPONSE TO TUMORS
 
Immunologic tolerance
Immunologic toleranceImmunologic tolerance
Immunologic tolerance
 
Autoimmunity and Tolerance
Autoimmunity and ToleranceAutoimmunity and Tolerance
Autoimmunity and Tolerance
 
ORGANS OF IMMUNE SYSTEM PRIMARY AND SECONDARY LYMPHOID ORGANS
ORGANS OF IMMUNE SYSTEM PRIMARY AND SECONDARY LYMPHOID ORGANSORGANS OF IMMUNE SYSTEM PRIMARY AND SECONDARY LYMPHOID ORGANS
ORGANS OF IMMUNE SYSTEM PRIMARY AND SECONDARY LYMPHOID ORGANS
 
Cells of the immune system
Cells of the immune systemCells of the immune system
Cells of the immune system
 
Transplantation immunology
Transplantation immunologyTransplantation immunology
Transplantation immunology
 
Isotypes allotypes and idiotypes
Isotypes allotypes and idiotypesIsotypes allotypes and idiotypes
Isotypes allotypes and idiotypes
 
Tumour immunology
Tumour immunologyTumour immunology
Tumour immunology
 
B CELL RECEPTOR final.pptx
B CELL RECEPTOR final.pptxB CELL RECEPTOR final.pptx
B CELL RECEPTOR final.pptx
 
Haptens
HaptensHaptens
Haptens
 
Antibody: Structure and Function
Antibody: Structure and FunctionAntibody: Structure and Function
Antibody: Structure and Function
 
Nucleic acid probes
Nucleic acid probesNucleic acid probes
Nucleic acid probes
 
B cell(Immunology)
B cell(Immunology)B cell(Immunology)
B cell(Immunology)
 
Immunodiffusion
Immunodiffusion Immunodiffusion
Immunodiffusion
 
Organ specific autoimmune disorders
Organ specific autoimmune disordersOrgan specific autoimmune disorders
Organ specific autoimmune disorders
 
Antigens
AntigensAntigens
Antigens
 
Immune response to infection by Virus
Immune response to infection by VirusImmune response to infection by Virus
Immune response to infection by Virus
 

Ähnlich wie Tumour immunology

Cancer Genes And Growth Factors
Cancer Genes And Growth FactorsCancer Genes And Growth Factors
Cancer Genes And Growth Factors
alaa essa
 

Ähnlich wie Tumour immunology (20)

Cancer.pptx
Cancer.pptxCancer.pptx
Cancer.pptx
 
neoplasm2. pptx
neoplasm2.                            pptxneoplasm2.                            pptx
neoplasm2. pptx
 
Cancer, Etiology, Classification and Pathophysiology
Cancer, Etiology, Classification and PathophysiologyCancer, Etiology, Classification and Pathophysiology
Cancer, Etiology, Classification and Pathophysiology
 
Assignment on NEOPLASIA
Assignment on NEOPLASIA Assignment on NEOPLASIA
Assignment on NEOPLASIA
 
CANCER
CANCERCANCER
CANCER
 
Nursing care of client with cancer
Nursing care of client with cancerNursing care of client with cancer
Nursing care of client with cancer
 
Cancer
CancerCancer
Cancer
 
Cancer
CancerCancer
Cancer
 
Cancer biology.pdf
Cancer biology.pdfCancer biology.pdf
Cancer biology.pdf
 
biology of cancer
biology of cancerbiology of cancer
biology of cancer
 
Cancer Genes And Growth Factors
Cancer Genes And Growth FactorsCancer Genes And Growth Factors
Cancer Genes And Growth Factors
 
Tumors
TumorsTumors
Tumors
 
Cancer akanksha dubey
Cancer  akanksha dubeyCancer  akanksha dubey
Cancer akanksha dubey
 
Cancer Biology
Cancer Biology Cancer Biology
Cancer Biology
 
Cancer
CancerCancer
Cancer
 
Cancer
Cancer Cancer
Cancer
 
ANTI CANCER DRUGS(ANTI NEOPLASTIC AGENTS) BY P.RAVISANKAR
ANTI CANCER DRUGS(ANTI NEOPLASTIC AGENTS) BY P.RAVISANKARANTI CANCER DRUGS(ANTI NEOPLASTIC AGENTS) BY P.RAVISANKAR
ANTI CANCER DRUGS(ANTI NEOPLASTIC AGENTS) BY P.RAVISANKAR
 
Neoplasia
Neoplasia Neoplasia
Neoplasia
 
cancer genetics familial cancer.pdf
cancer genetics familial cancer.pdfcancer genetics familial cancer.pdf
cancer genetics familial cancer.pdf
 
RECENT DEVELOPMENT IN CANCER PHYTOTHERAPY.
RECENT DEVELOPMENT IN CANCER PHYTOTHERAPY.RECENT DEVELOPMENT IN CANCER PHYTOTHERAPY.
RECENT DEVELOPMENT IN CANCER PHYTOTHERAPY.
 

Mehr von Ashish Pratim Mahanta

Mehr von Ashish Pratim Mahanta (19)

How to WRITE AN ARTICLE REVIEW.
How to WRITE AN ARTICLE REVIEW.How to WRITE AN ARTICLE REVIEW.
How to WRITE AN ARTICLE REVIEW.
 
Ligbuilder V2: overview and tutorial.
Ligbuilder V2: overview and tutorial.Ligbuilder V2: overview and tutorial.
Ligbuilder V2: overview and tutorial.
 
Quiz-O-Pedia finals
Quiz-O-Pedia finalsQuiz-O-Pedia finals
Quiz-O-Pedia finals
 
Quiz-O-Pedia Prelims
Quiz-O-Pedia Prelims Quiz-O-Pedia Prelims
Quiz-O-Pedia Prelims
 
Bone marrow transplant
Bone marrow transplantBone marrow transplant
Bone marrow transplant
 
solid waste management
solid waste managementsolid waste management
solid waste management
 
Nano bots
Nano botsNano bots
Nano bots
 
Treatment of chronic migraine
Treatment of chronic migraineTreatment of chronic migraine
Treatment of chronic migraine
 
Animal cell culture technique : overview & procedures
Animal cell culture technique : overview & proceduresAnimal cell culture technique : overview & procedures
Animal cell culture technique : overview & procedures
 
Milk : good / bad
Milk : good / badMilk : good / bad
Milk : good / bad
 
Dna replication in prokaryotes
Dna replication in prokaryotesDna replication in prokaryotes
Dna replication in prokaryotes
 
Translation in prokaryotes and eukaryotes
Translation in prokaryotes and eukaryotesTranslation in prokaryotes and eukaryotes
Translation in prokaryotes and eukaryotes
 
EXTRA CHROMOSOMAL INHERITANCE
EXTRA CHROMOSOMAL INHERITANCEEXTRA CHROMOSOMAL INHERITANCE
EXTRA CHROMOSOMAL INHERITANCE
 
Methanogens and chemolithotrophy
Methanogens and chemolithotrophyMethanogens and chemolithotrophy
Methanogens and chemolithotrophy
 
INCOMPLETE DOMINANCE VS CO-DOMINANCE
INCOMPLETE DOMINANCE VS CO-DOMINANCEINCOMPLETE DOMINANCE VS CO-DOMINANCE
INCOMPLETE DOMINANCE VS CO-DOMINANCE
 
CRISPR CAS9 technique
CRISPR CAS9 techniqueCRISPR CAS9 technique
CRISPR CAS9 technique
 
Preparation of alcohol
Preparation  of alcoholPreparation  of alcohol
Preparation of alcohol
 
Structural organization of eukaryotic cells 1 (1)
Structural organization of eukaryotic cells 1 (1)Structural organization of eukaryotic cells 1 (1)
Structural organization of eukaryotic cells 1 (1)
 
Digestion of lipids
Digestion of lipidsDigestion of lipids
Digestion of lipids
 

Kürzlich hochgeladen

Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in DelhiRussian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
kauryashika82
 
BASLIQ CURRENT LOOKBOOK LOOKBOOK(1) (1).pdf
BASLIQ CURRENT LOOKBOOK  LOOKBOOK(1) (1).pdfBASLIQ CURRENT LOOKBOOK  LOOKBOOK(1) (1).pdf
BASLIQ CURRENT LOOKBOOK LOOKBOOK(1) (1).pdf
SoniaTolstoy
 
1029-Danh muc Sach Giao Khoa khoi 6.pdf
1029-Danh muc Sach Giao Khoa khoi  6.pdf1029-Danh muc Sach Giao Khoa khoi  6.pdf
1029-Danh muc Sach Giao Khoa khoi 6.pdf
QucHHunhnh
 
Beyond the EU: DORA and NIS 2 Directive's Global Impact
Beyond the EU: DORA and NIS 2 Directive's Global ImpactBeyond the EU: DORA and NIS 2 Directive's Global Impact
Beyond the EU: DORA and NIS 2 Directive's Global Impact
PECB
 

Kürzlich hochgeladen (20)

Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in DelhiRussian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
 
Measures of Central Tendency: Mean, Median and Mode
Measures of Central Tendency: Mean, Median and ModeMeasures of Central Tendency: Mean, Median and Mode
Measures of Central Tendency: Mean, Median and Mode
 
Web & Social Media Analytics Previous Year Question Paper.pdf
Web & Social Media Analytics Previous Year Question Paper.pdfWeb & Social Media Analytics Previous Year Question Paper.pdf
Web & Social Media Analytics Previous Year Question Paper.pdf
 
Key note speaker Neum_Admir Softic_ENG.pdf
Key note speaker Neum_Admir Softic_ENG.pdfKey note speaker Neum_Admir Softic_ENG.pdf
Key note speaker Neum_Admir Softic_ENG.pdf
 
9548086042 for call girls in Indira Nagar with room service
9548086042  for call girls in Indira Nagar  with room service9548086042  for call girls in Indira Nagar  with room service
9548086042 for call girls in Indira Nagar with room service
 
BASLIQ CURRENT LOOKBOOK LOOKBOOK(1) (1).pdf
BASLIQ CURRENT LOOKBOOK  LOOKBOOK(1) (1).pdfBASLIQ CURRENT LOOKBOOK  LOOKBOOK(1) (1).pdf
BASLIQ CURRENT LOOKBOOK LOOKBOOK(1) (1).pdf
 
A Critique of the Proposed National Education Policy Reform
A Critique of the Proposed National Education Policy ReformA Critique of the Proposed National Education Policy Reform
A Critique of the Proposed National Education Policy Reform
 
Sports & Fitness Value Added Course FY..
Sports & Fitness Value Added Course FY..Sports & Fitness Value Added Course FY..
Sports & Fitness Value Added Course FY..
 
Sanyam Choudhary Chemistry practical.pdf
Sanyam Choudhary Chemistry practical.pdfSanyam Choudhary Chemistry practical.pdf
Sanyam Choudhary Chemistry practical.pdf
 
Advance Mobile Application Development class 07
Advance Mobile Application Development class 07Advance Mobile Application Development class 07
Advance Mobile Application Development class 07
 
Measures of Dispersion and Variability: Range, QD, AD and SD
Measures of Dispersion and Variability: Range, QD, AD and SDMeasures of Dispersion and Variability: Range, QD, AD and SD
Measures of Dispersion and Variability: Range, QD, AD and SD
 
General AI for Medical Educators April 2024
General AI for Medical Educators April 2024General AI for Medical Educators April 2024
General AI for Medical Educators April 2024
 
Mattingly "AI & Prompt Design: Structured Data, Assistants, & RAG"
Mattingly "AI & Prompt Design: Structured Data, Assistants, & RAG"Mattingly "AI & Prompt Design: Structured Data, Assistants, & RAG"
Mattingly "AI & Prompt Design: Structured Data, Assistants, & RAG"
 
APM Welcome, APM North West Network Conference, Synergies Across Sectors
APM Welcome, APM North West Network Conference, Synergies Across SectorsAPM Welcome, APM North West Network Conference, Synergies Across Sectors
APM Welcome, APM North West Network Conference, Synergies Across Sectors
 
1029-Danh muc Sach Giao Khoa khoi 6.pdf
1029-Danh muc Sach Giao Khoa khoi  6.pdf1029-Danh muc Sach Giao Khoa khoi  6.pdf
1029-Danh muc Sach Giao Khoa khoi 6.pdf
 
Mattingly "AI & Prompt Design: The Basics of Prompt Design"
Mattingly "AI & Prompt Design: The Basics of Prompt Design"Mattingly "AI & Prompt Design: The Basics of Prompt Design"
Mattingly "AI & Prompt Design: The Basics of Prompt Design"
 
Beyond the EU: DORA and NIS 2 Directive's Global Impact
Beyond the EU: DORA and NIS 2 Directive's Global ImpactBeyond the EU: DORA and NIS 2 Directive's Global Impact
Beyond the EU: DORA and NIS 2 Directive's Global Impact
 
Introduction to Nonprofit Accounting: The Basics
Introduction to Nonprofit Accounting: The BasicsIntroduction to Nonprofit Accounting: The Basics
Introduction to Nonprofit Accounting: The Basics
 
Arihant handbook biology for class 11 .pdf
Arihant handbook biology for class 11 .pdfArihant handbook biology for class 11 .pdf
Arihant handbook biology for class 11 .pdf
 
Paris 2024 Olympic Geographies - an activity
Paris 2024 Olympic Geographies - an activityParis 2024 Olympic Geographies - an activity
Paris 2024 Olympic Geographies - an activity
 

Tumour immunology

  • 2. CONTENTS  INTRODUCTION  PROPERTIES  CLASSIFICATION  THEORIES  REASONS FOR MUTATION  HOW MUTATIONS CAUSE TUMOR  REPAIR AND ANTI CANCER MECHSNISM  RUNAWAY MECHANISM AND DIAGNOSIS  CONCLUSION  REFERENCE
  • 3. What is a tumor ? In spite of several check points in a cell cycle to check any modifications in DNA before its transfer to next generation, certain mutations takes place in DNA leading to loss of certain characters and control over its multiplication rate. The consequences of these modification result in pathological over growth of modified tissues generally referred as TUMOR or Neoplasia (meaning new formation) or “cancer”. There are two types of Tumors : Benign tumors and Malignant Tumors.
  • 4. BENIGN TUMORS : • Benign tumors are generally not harmful due to their well- defined growth with smooth boundaries. • Simply grow in diameter and restricted to one place but can be harmful if the tumor compresses the surrounding tissue against a hard surface in the body. • Usually grows at a relatively slow pace and may stop growing for a time when it reaches a certain size. • A complete cure can usually be achieved by removing the abnormally grown tissue mass.
  • 5. MALIGNANT TUMORS : • The Malignant tumors are dreadful because their growth is not restricted to one place. • Their metastasis nature helps their spread from one place to other locations in the body via lymph or blood. •Unlike benign malignant tumors are properly referred to as “Cancers”.  The origin of the word cancer is credited to the Greek physician Hippocrates (460-370 B.C.). In Greek cancer refers to a crab. It is most likely applied to the disease to mind the shape of a crab, because of finger – like projections spreading from a cancer tissue mass resembles the structure of crab more over the spread of cancer
  • 6. Altered biological properties of cancer cells 1) Acquistion of self-sufficiency in growth signals. 2) Loss of sensitivity to anti-growth signals. 3) Loss of apoptosis, in order to allow growth despite genetic errors and external anti-growth signals. 4) Loss of senescence, leading to limitless replicative potential (Immortality). 5) Acquistion of sustained “angiogenesis” (Growth of new blood vessels from pre-existing vessels). 6) Acquistion of ability to invade neighbouring tissues, the defining property of invasive carcinoma. 7) Acquistion of ability to metastases at distant sites, the classical property of malignant tumors.
  • 7. Classification of Tumors: Since development of tumor is possible in any region or organ of the body with dividing cell, tumors were broadly classified into 3 basic types based upon the embryonic origin of the tissues involved in the formation of tumor. They are : 1. CARCINOMAS 2. SARCINOMAS 3. LEUKEMIA
  • 8. 1.Carcinomas • Developed from cells of ectodermal or endodermal origin. • They invade surrounding tissues and organs and may metastasize, or spread, to lymph nodes and other sites. • Based upon the histopathological appearance they can be differentiated into “Aden carcinoma” and “squamous cell carcinoma” to reflect the involvement of glandular or squamous cells in tumor formation. • Approximately 90% of human cancers are malignancies of epithelial cells.
  • 9. 2.Sarcomas (From the Greek ‘sarx” meaning “flesh”) • Developed from connective tissue or mesoderm. •Cancers of breast, colon, pancreas bones etc. comes under this type. • Sarcomas are rare in humans; about 2% of human cancers come under this category.
  • 10. 3.Leukemia (Greek leukos “white” ; aima “blood”) •Developed from bone marrow tissue or in blood. •Characterized by an abnormal proliferation of blood cells, usually white blood cells (leukocytes). •Leukemia tumor is subdivided into lymphoblastic or lymphocytic leukemia and myeloid or myelogenous leukemia according to the blood cells affected. To make it understandable to a common man, tumors were generally named after the organ or tissue from which it has been developed. For example, cancer developed in breast tissue is referred as breast cancer. Similarly, lung cancer, colon Cancer, gastric cancer, skin cancer etc.
  • 12. Different theories to explain cancer development : From the earliest times, physicians have wondered about the cause of cancer.  The Egyptians blamed Gods for the development of cancers. Several theories were proposed by different scientists to explain the cause for cancers. Some of them are as follows : 1. HUMORAL THEORY 2. LYMPH THEORY 3. BLASTEMA THEORY 4. CHRONIC IRRITATION THEORY 5. TRAUMA THEORY 6. PARASITE THEORY
  • 13. Humoral theory:  Hippocrates believed that the body contained four humors (Body fluids) – blood, phlegm, yellow bile, and black bile.  A balance of these fluids resulted in a state of health. Any excesses or deficiencies caused disease  An excess of black bile collecting in various body sites was thought to cause cancer. This theory of cancer was passed on by the Romans and was embraced by the influential doctor Galen”s medical teaching, which remained unchallenged through the middle Ages for over 1300 years. During this period of the body, including autopsies, was prohibited for religious reasons, thus limiting knowledge
  • 14. Lymph Theory:  Among the theories that replaced the humoral theory of cancer was cancer’s formation by another fluid – lymph. Stahl and Hofman theorized that the cancer was composed of fermenting and degenerating lymph varying in density, acidity and alkalinity.  The theory gained rapid support. John Hunter(1723-1792) agreed that tumors grow from lymph constantly thrown out by the blood. Blastema Theory: In 1838, German pathologist Johannes Muller demonstrated that cancer is made up of cell and not lymph. But he was of the opinion that cancer cells did not arise from normal cells.  Muller proposed that cancer cells arose from budding elements (Blastema) between normal tissues. Muller’s students Rudolph including cancer cells, are derived from other cells.
  • 15. Chronic Irritation Theory: Virchow proposed chronic irritations as the cause of cancer, but he falsely believed that cancers “spread like a liquid.”  A German surgeon, Karl Thiersch, showed that cancers metastasize through the spread of malignant cells and not through some unidentified fluid. Trauma Theory: Despite advances in the understanding of cancer, from the late 1800s until the 1920s, cancer was thought by some to be caused trauma. Parasite Theory: In the 17th and 18th centuries, some believed that cancer was contagious. In fact, the first cancer hospital in France was forced to move from the city in 1779 because of the fear of the spread of cancer throughout the city.
  • 16. Reasons for tumor formation: Oncogenes, activate cell division and influence embryonic development and tumor suppressor genes halt cell division. Since these two genes are typically found in normal human cells, certain mutations in them may transform their normal function resulting in the conversion of normal cells into tumor cells. Either inherited defects or acquired mutations due to exposure to carcinogens may cause conversion of normal cell into a tumor cell.
  • 17. How mutations cause Tumor: Due to mutations, some of the regular genes may fail to code proteins essential for regulation of cell cycle, Synthesis of proteins involved in the regulation of cell cycle are essential to stop access of defective or altered DNA to the daughter cells. Failure in regulation of cell cycle results in accumulation of mutations or abnormal characters in the daughter cells. The normal gene gradually lost its original characters and become a tumor gene and its modified tumor gene is known as “Proto-oncogene”. After several divisions the cell with Proto-oncogene produces tumor. Mutations may also suppress the efficiency of certain tumor suppressor genes, as a result chances for tumor development increases. Of the many known oncogenes some are derived from normal Proto-oncogenes. For example the Ros gene that encodes a protein essential for intracellular signal transduction in
  • 18. normal cells becomes an oncogene due to mutations and starts encoding a protein that acts as a signaling molecule for excessive or uncontrolled growth of cells. An oncopotein encoded by an oncogene may be similar to the normal protein but excessive production may alter the character of normal cells and induces conversion of a normal cell into a tumor cell. Others things that may increase the chance of developing tumors are- 1. Radiation: High- frequency radiation, such as ultraviolet and ionizing radiation, damages the genetic material DNA, possibly inducing genetically transferable abnormalities. 2. Viruses: Some human retroviruses and papilloma viruses exhibit carcinogen gene sequence potential. Retrovirus may convert proto-oncogenes into oncogenes either by altering or condensing, to code proteins with abnormal activity or
  • 19. controlling with powerful regulators to induce the production in excess or in inappropriate circumstances. 3. Hormones: The role of hormones in carcinogenesis is still controversial, but it seems that, excessive use of some hormones, especially estrogen, produces cancer in animals. 4. Chemical substances: Some of the chemical substances that can induce carcinogens include: Alkylating agents-leukemia, Aromatic hydrocarbons and benzopyrene ( From polluted air) - lung cancer, Tobacco – cancer of the Lung, oral cavity etc
  • 20. Repair and Anti-cancer mechaniSM of body Cell shredding: The body simply shreds some types of cells that are particularly exposed to environmental carcinogens. For example, intestinal epithelial cells are shed frequently, so that any mutations do not get a chance to reproduce. Cell shedding generally occurs in the stomach, colon, skin, and other areas. Cell division limits: Telomeres limit the number of cell divisions that a single cell can under go, this character helps in the inhibition of the growth of tumor cells. If a normal cell becomes cancerous, its clones often die out to telomeric restriction before producing significant tumor. Carcinogens neutralization: Carcinogenic substances are quickly metabolized into harmless substances by the gut and liver in healthy individuals.
  • 21. Run away mechanisms of tumor cells: • Sneaking Through: Newly formed tumor cells escape immune system’s attack by sneaking, till they increase their number to resist the immunological response Some tumors posses weak immunogenicity. • Modulating Tumor Ags: Here the tumor cells pull the newly formed Ags to interior(Cytoplasm) or stop expressing in surface Ags. In the absence of these Ags immune system fails to enforce any action against the tumor cells. • Masking Tumor Ags: Certain tumor cells produce mucoproteins coat known as Sialomucin coat to hide their new Ags. • Tumor induced tolerance: Certain tumor cells induce
  • 22. tolerance through synthesizing different immuno suppressants to suppress or activate TS-cells which in turn inhibit the activity of TC ,TD and B-cells activity.  Production of blocking agents: Producing auto antibodies known as “blocking antibodies” against their own antigen.  Alternation of cell adhesion molecules: Newly formed tumor cells alter their expression of cell adhesion molecules to reduce stable contact formation with cytotoxic cells.
  • 23. DIAGNOSIS: •Surgery: benign tumors can be removed entirely by surgery. •Chemotherapy: by using suitable drugs. •Radiation Therapy: using ionizing radiation to kill tumor cells. •Hormonal Therapy: inhibiting by hormones – breast, prostate. •Targeted therapy: interfering with specific molecules needed for carcinogenesis
  • 24. Conclusion  Tumors are uncontrolled growth of cells occurs due to mutation in different stages of cell cycle  Two types- Benign and Malignant  Tumors can occur due to mutation, radiation, chemicals, viruses etc.  Although some tumors are mostly fatal we can get rid of certain tumors through different diagnosis like surgery, chemotherapy etc.
  • 25. REFERENCE  THE ELEMENTS OF IMMUNOLOGY – Fahim Halim Khan  A TEXTBOOK OF IMMUNOLOGY – Dr. P. Madhavee Latha, S Chand publication  medicalnews.com  macmillan.org.uk
  • 26. THANK YOU Fight cancer with a smile