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Department of:

HERE
UNIVERSITY OF MOSUL
COLLEGE OF DENTISTRY

Neoplasia 2020-2021

Lect. IV

Department of:
Oral &
Ass.Prof.Dr.Nadwa Alazzo Maxillofascial
Surgery
Department of: UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY
HERE

Objectives
 Causes of neoplasia

 Molecular basis

 Transformation &progression

 How the tumor escape the immune


surviellence ?

 Treatment of cancer
Causes of Neoplasia
The origin for many neoplasms is obscure. However, there are several theories of origin:

Chemicals Oncogenic viruses


• aniline dyes and bladder cancer • HPV in Squamous cell carcinoma of cervix
• cigarette smoke and lung cancer • Hepatitis B virus in hepatocellular carcioma
• Epestein virus in Burkitt’s lymphoma
• Aflatoxine & hepatocellular
carcinoma
Radiation
Hereditary causes
UV light= skin cancer
Defect in chromosomes as
Ionizing radiation =thyroid, Retinoblastoma defect in
lung,colon and Breast chromosome 13
cancer
Department of: UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY
HERE
Also they are found the incidence of cancers are
increased in older persons

racial predilections (American women have breast


cancer more often than Japanese women; Japanese
men have stomach cancer far more often than
American men).
Carcinogenesis is a multistep process : UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

Initiators
Initiation that lead to irreversible DNA damage(lethal
020-2021
damage)
Example : Alkylating agent like cycophosphamide
Promotors
Lead to proliferation of abnormal (mutagenic cells) but they
there appears to be a "dose-threshold" concentration of
promoter below which neoplasia will not occur
like hormone therapy estrogen(diethylstilbesterol)
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

MOLECULAR BASIS of CANCER


Four classes of normal regulatory genes
Department of:
PROTO-oncogenes
HERE ((gene responsible for cell growth)
Tumor suppressor genes
DNA repair genes
Apoptosis genes
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

Defect (over expression) in proto-oncogene (growth factors) leads to uncontrolled cell


proliferations )
e.g / RAS overexpression in many human cancer

Loss of tumor supprresor genes (P53)


Department of:
HERE
Limitation of apoptotic genes (BCL2)

Defects in DNA repair genes


UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

Oncogenes
 in non-mutant state called proto-oncogenes (stimulate cell growth and
replication)
Department of:
 when turned “on” HERE
by mutation cause uncontrolled growth

 Oncoproteins are encoded by oncogenes generally serve functions similar to their normal
counterparts .
 mutations convert proto-oncogenes into constitutively active cellular oncogenes that are
involved in tumor development
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

Tumor suppressor genes


Failure of growth inhibition is one of the fundamental alterations in the
process of carcinogenesis.
Department of:
HERE

the products of tumor suppressor genes apply brakes to cell proliferation


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UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

TRANSFORMATION & PROGRESSION


Self-sufficiency in growth signals
Insensitivity to growth-inhibiting signals
Evasion of apoptosis
Defects in DNA repair: “Spell checker”
Limitless replicative potential: Telomerase
Angiogenesis
Invasive ability
Metastatic ability
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

EVASION OF APOPTOSIS

Accumulation of Department
neoplastic cells may
of: result not only from activation of growth-promoting
oncogenes or inactivation of growth-suppressing tumor suppressor genes, but also from
HERE
mutations in the genes that regulate apoptosis
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

How do tumor cells


escape immune surveillance?

Mutation, like microbes


↓ MHC molecules on tumor cell of:
Department surface
HERE
Immunosuppressive agents
Antigen masking
Apoptosis of cytotoxic T-Cells (CD8), i.e., the tumor cell KILLS the T-cell!
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

Treatment OF Cancer
Surgical Excision

Radiation
Department of:
HERE

Chemotherapy
UNIVERSITY OF MOSUL

REFERENCES
COLLEGE OF DENTISTRY

020-2021
UNIVERSITY OF MOSUL

COLLEGE OF DENTISTRY

2020-2021

THE END

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