DR.MYM neoplasia Unit 9-1.pptx

Samara University
Biomedical Sciences Department
Pathology of Neoplasia
DR. Mohammed Yassin(MD)

Learning objectives:
 At the end of this chapter, students are expected to:
 Differentiate neoplastic lesions from non-neoplastic ones.
 Contrast benign from malignant tumors.
 Describe methods and mechanisms of metastasis.
 List the etiologic factors in carcinogenesis.
 Understand clinical effects of neoplasms.
 Know the diagnostic modalities for cancers
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Definition
 Literally, neoplasia means “new growth” and
 Technically, it is defined as abnormal mass of tissues the
growth of which exceeds and is uncoordinated with that of the
normal tissues and persists in the same excessive manner after
cessation of the stimulus, evoking the transformation.
 Oncology (Greek oncos = tumor) is the study of tumors or
neoplasms
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Definition Cont’d…
 " Fundamental to the origin of all neoplasms are heritable (genetic)
changes that allow excessive and unregulated proliferation that is
independent of physiologic growth-regulatory stimuli.
 Neoplasms therefore enjoy a certain degree of autonomy and
more or less steadily increase in size regardless of their local
environment and the nutritional status of the host.
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Nomenclature
 Neoplasms are named based upon two factors
1. On the histologic types : Mesenchymal and Epithelial
2. On behavioral patterns : Benign and Malignant neoplasms
 Th us, the suffix -oma denotes a benign neoplasm.
 Benign mesenchymal neoplasms
 Muscle…….. Rhabdomyoma, Bone………… osteoma,
 Fat……………. lipoma, Blood vessel .. Hemangioma
 Nerve…………… neuroma, Fibrous tissue … fibroma
 Cartilages……… chondroma.
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Nomenclature Cont’d…
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 Benign epithelial neoplasms are classified on the basis of cell of
origin.
 Adenoma is the term for benign epithelial neoplasm that form
glandular pattern or on basis of microscopic or macroscopic
patterns for example visible finger like or warty projection from
epithelial surface are referred to as papilloma's.
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 Exceptional nomenclature
 Non-neoplastic misnomers :- E.g. Hematoma, Granuloma,
Hamartoma, mycetoma, tuberculoma, atheroma.
 Malignant misnomers :- E.g. Melanoma, Lymphoma,
Seminoma, Glioma, Hepatoma.
 The suffix for neoplastic disorders of blood cells is 'aemia', as
in leukemia; but again, exceptions exist. For example, anemia is
not a neoplastic disorder.
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 Malignant neoplasms arising from mesenchymal tissues are called
sarcomas(Fleshy).
 These neoplasms are named as fibrosarcoma, liposarcoma,
osteosarcoma, hemangiosarcoma etc.
 Malignant neoplasms of epithelial cell origin derived from any of
the three germ layers are called carcinomas.
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 Malignant neoplasms of epithelial cell origin derived from any of
the three germ layers.
 Ectodermal origin:
• Skin… epidermis (squamous cell carcinoma, basal cell
carcinoma).
 Mesodermal origin:
• Renal tubules…….. renal cell carcinoma
 Endodermal origin:
• Linings of the gastrointestinal tract ……..colonic carcinoma
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 Malignant neoplasms of epithelial cell origin.
– Those producing glandular microscopic pictures are called
Adeno carcinomas .e.g renal cell adenocarcinoma.
– Those producing recognizable squamous cells are designated as
squamous cell carcinoma.
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 Tumors that arise from more than tissue components:
 Teratomas: contain representative of parenchyma cells of more
than one germ layer, usually all three layers.
• They arise from tot potential cells and so are principally
encountered in ovary and testis.
 Mixed tumors: containing both epithelial and mesenchymal
components
• Examples include pleomorphic adenoma and fibro
adenoma
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Carcinoma in situ
 It refers to an epithelial neoplasm exhibiting all the cellular
features associated with malignancy, but which has not yet
invaded through the epithelial basement membrane separating
it from potential routes of metastasis-blood vessels and lymphatics.
 Detection of the lesion Is used in population screening
programmes for cervical, breast and some other carcinomas.
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Characteristics of Benign and
Malignant Neoplasms
 The difference in characteristics of these neoplasms can be
conveniently discussed under the following features:
1. Differentiation & anaplasia
2. Rate of growth
3. Local invasion
4. Metastasis
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Characteristics Cont’d…
1. Differentiation and Anaplasia
 Differentiation refers to the extent to which neoplastic
parenchymal cells resemble the corresponding normal parenchymal
cells, both morphologically and functionally; lack of
differentiation is called anaplasia.
 In general,
Benign tumors are well differentiated.
 Malignant neoplasms – could be well differentiated to
undifferentiated.
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 Dysplasia:
 a term used to describe disorderly but non-neoplastic
proliferation.
 Dysplasia is encountered principally in the epithelia.
 It is a loss in the uniformity of individual cells and in their
architectural orientation.
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2. Rate of Growth
 The growth rate of tumors correlates with their level of
differentiation, and thus most malignant tumors grow more rapidly
than do benign lesions.
 There are, however, many exceptions to such an
oversimplification.
 Some benign tumors have a higher growth rate than
malignant tumors.
 Factors such as hormonal stimulation, adequacy of blood
supply, and unknown influences may affect their growth.
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3. Local Invasion
 Nearly all benign tumors grow as cohesive expansile masses
that remain localized to their site of origin and do not have the
capacity to infiltrate, invade, or metastasize to distant sites, as
do malignant tumors.
 Benign tumors grow and expand slowly, they usually develop a
rim of compressed connective tissue, sometimes called a fibrous
capsule, which separates them from the host tissue.
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Schematic depiction of phenotypic transition of epithelial cells from hyperplasia to invasive carcinoma
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 The growth of malignant neoplasms is accompanied by
progressive infiltration, invasion and destruction of the
surrounding tissue.
 Generally, they are poorly demarcated from the surrounding
normal tissue (and a well-defined cleavage plane is lacking).
 Next to the development of metastasis, invasiveness is the most
reliable feature that differentiates malignant from benign
neoplasms.
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 Fibroadenoma of the breast. The tan-colored, encapsulated small
tumor is sharply demarcated from the whiter breast tissue.
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Malignant Tumors
Osteogenic sarcoma of femur
Rhabdomyosarcoma of foot
Adenocarcinoma of colon
Squamous cell carcinoma of bronchus
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4. Metastasis
 It is defined as a transfer of malignant cells from one site to another
not directly connected with it.
 Metastasis is the most reliable sign of malignancy.
The invasiveness of cancers permits them to penetrate in to the
blood vessel, lymphatic and body cavities providing the
opportunity for spread.
 Most malignant neoplasm metastasies except few such as gliomas in
the CNS, basal cell carcinoma (Rodent ulcer) in the skin and
dermatofibrosarcoma in soft tissues.
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 Organs least favoured for metastatic spread include striated
muscles and spleen.
 Approximately 30% of newly diagnosed patients with solid
tumors (excluding skin cancers other than melanoma) present
with metastasis.
 In general, the more aggressive, the more rapidly growing, and
the larger the primary neoplasm, the greater the likelihood that
it will metastasize or already has metastasized.
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Benign Malignant
Differentiation/
anaplasia
Well differentiated; structure
sometimes typical of tissue of
origin
Some lack of differentiation with
anaplasia; structure often atypical
Rate of growth Usually progressive and slow;
may come to a standstill or
regress; mitotic figures rare and
normal
Erratic and may be slow to rapid;
mitotic figures may be numerous and
abnormal
Local invasion Usually cohesive expansile
well-demarcated masses that do
not invade or infiltrate
surrounding normal tissues
Locally invasive, infiltrating
surrounding tissue; sometimes may be
seemingly cohesive and expansile
Metastasis Absent Frequently present; the larger and more
undifferentiated the primary, the more
likely are metastases
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Pathways of Spread
 Dissemination of cancers may occur through one of three
pathways:
i. Direct seeding of body cavities or surfaces/trans coelomic
spread)
ii. Lymphatic spread, and
iii. Hematogenous spread.
 Although direct transplantation of tumor cells, as for example
on surgical instruments, may theoretically occur.
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Pathways of Spread
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Routes of metastasis
exemplified by a
carcinoma of the bowel.
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1. Direct seeding of body cavities or surfaces, .
 Seeding of body cavities and surfaces may occur whenever a
malignant neoplasm penetrates into a natural “open field.”
 Most often involved is the peritoneal cavity, but any other
cavity—pleural, pericardial, subarachnoid, and joint space—
may be affected.
 Such seeding is particularly characteristic of carcinomas arising
in the ovaries.
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Direct seeding Cont’d…
 Examples are:
 Krukenberg tumor:- Mucin producing signet ring
adenocarcinomas arising from gastrointestinal tract, pancreas,
breast, and gall bladder spread to one or both ovaries and the
peritoneal cavities.
 Pseudomyxoma peritoni which are mucus secreting
adrocarcinoma arising either from ovary or appendix.
These carcinomas fill the peritoneal cavity with a gelatinous
soft, translucent neoplastic mass.
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2. Lymphatic spread
 Transport through lymphatics is the most common pathway for the
initial dissemination of carcinomas, and sarcomas may also use this
route.
For Instance:-
 Carcinoma of Breast (Common in outer Quadrants)->
Metastasize to Axilary Lymph nodes
 Cancers of Breast of Inner Quadrant -> Internal
Mammary arteries.
 The pattern of lymph node involvement follows the natural routes
of lymphatic drainage.
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2. Lymphatic spread Cont’d…
 A "sentinal lymph node" is defined as the first lymph node in a
regional lymphatic basin that receives lymph flow from a primary
tumor.
 Drainage of tumor cell debris or tumor antigens, or both, also
induces reactive changes within nodes.
 Enlargement of nodes may be caused by
I. The spread and growth of cancer cells or
II. Reactive hyperplasia
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A nodular and hyperkeratotic lesion
occurring on the ear, unfortunately
with early metastasis to a prominent
postauricular lymph node (arrow).
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2. Lymphatic spread Cont’d…

3. Hematogenous spread
 is typical of sarcomas but is also seen with carcinomas.
 Arteries, with their thicker walls, are less readily penetrated
than are veins.
 The spread appears to be selective with seed and soil
phenomenon.
 Lung & liver are common sites of metastasis because they receive
the systemic and venous out flow respectively. Other major sites
include brain and bones.
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3. Hematogenous spread Cont’d…
 Some hematogenous spread preferential sites
 Renal cell carcinoma -> invades the branches of the renal vein
-> inferior vena cava, sometimes -> right side of the heart.
 Hepatocellular carcinomas -> Portal and hepatic venules.
 Breast carcinoma -> Bone
 Bronchogenic carcinomas -> Adrenals and the brain
 Neuroblastomas -> Liver and bones.
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A liver studded with
metastatic cancer
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3. Hematogenous spread Cont’d…

Cancer Epidemiology
 The only certain way to avoid cancer is not to be born, to live is
to incur the risk.
 Over the years cancer incidence increased in males while it
slightly decreased in females due to largely screening
Procedures-cervical, breast.
 The most common tumors in
Men - arise in the prostate, lung, and colorectum.
 Women - cancers of the breast, lung, and colon and rectum.
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Age
• Most cancers in adults occur in those over 55
years of age.
• Children under 15 years of age however, are
susceptible to
– Acute leukemia, central nervous system tumours,
– Neuroblastoma, wilm's tumour,
– Retinoblastoma, rhabdomyosarcoma.
– Acute leukemias and neoplasms of the central
nervous system accounts for about 60% of the deaths.
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Cancer incidence and mortality
by site and sex.
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Geographic Variables
• Nearly all the evidence
indicates that these
geographic differences are
environmental rather than
genetic in origin.
– Stomach carcinoma - Japan
– Lung cancer - USA
– Skin cancer - New zeland &
Australia
– Liver cancer - Ethiopia
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Environmental factors
• Environmental factors (occupational hazards) include:
– Asbestos -> Lung cancer, mesothelioma, esophagus and,
stomach carcinomas;
– Vinyl chloride -> Angiosarcoma of liver
– Benzene -> Leukemias
– Cadmium and cadmium compounds -> prostatic ca
– Cigarette smoking -> Brochogenic carcinomas
– Venereal infection (HPV) -> Cervical carcinoma
– Radon and its decay products -> Lung ca
– Ethylene oxide -> Leukemia
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Premalignant disorders
A. Heredity premalignant disorders
• Categorized in to three groups:
1. Inherited cancer syndromes (Autosomal
dominant)
– Familial retinoblastomas usually bilateral, and a second
cancer risk particularly osteogenic sarcoma.
– Oncosupressor gene is the basis for this carcinogenesis
– Familial adenomatous polyps of the colon……. virtually
all cases are fatal to develop carcinoma of the colon by
the age of 50.
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Premalignant disorders Cont’d…
2. Familial cancers
• E.g. Breast, ovarian, colonic, and brain cancers
3. Autosmal recessive syndromes of defective
DNA repair
– Characterized by chromosomal or DNA instability
– Examples..
• xeroderma pigmentosium,
• Ataxia telaangietasia,
• Bloom syndrome and
• Fanconi anemia
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B. Acquired preneoplastic disorders
• Regenerative, hyperplasic and dysplastic
proliferations
– Endometrial hyperplasia -> Endometrial
carcinoma
– Cervical dysplasia -> Cervical cancer
– Bronchial dysplasia -> Bronchogenic carcinoma
– Regenerative nodules -> Liver cancer
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• Certain non-neoplastic disorders may
predispose to cancers.
– Chronic atrophic gastritis -> Gastric cancer
– Solar keratosis of skin -> Skin cancer
– Chronic ulcerative colitis -> Colonic cancer
– Leukoplakia of the oral cavity, vulva and penis ->
Squamous cell carcinoma
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• Certain types of benign neoplasms
• Some benign neoplasms can constitute
premalignant conditions.
• E.g Villous colonic adenoma - Colonic cancer
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Molecular Basis of Cancer
(Carcinogenesis)
• Basic principles of carcinogenesis:
• The fundamental principles in carcinogenesis
include
1. Non-lethal genetic damage lies at the heart of
carcinogenesis.
– Such genetic damage (mutation) may be acquired by
the action of environmental agents such as
chemicals, radiation or viruses or it may be inherited
in the germ line.
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Molecular Basis of Cancer
(Carcinogenesis) Cont’d…
2. The three classes of normal regulatory genes
are:
– A) The growth promoting proto-oncogenes
– B) Cancer suppressor genes (anti-oncogenes)
– C) Genes that regulate apoptosis
– D) Genes that regulate DNA repair
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Carcinogenesis Cont’d…
• A) The growth promoting proto-oncogenes
–Activation of proto-oncogenes activation
gives rise to oncogenes (cancer causing
genes)
• Point mutation
• Chromosomal rearrangements……translocation,
Inversion
• Gene amplification
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• B) Cancer suppressor genes (anti-oncogenes)
– Its physiologic role is to regulate cell growth however, the
inactivation of cancer suppressor genes is the key event in
cancer genesis
– Examples of tumour suppressor genes include-Rb, P53,
APC and NF-1&2 genes
• C) Genes that regulate apoptosis
– Genes that prevent or induce programmed cell death are
also important variables in the cancer equation.
– bcl-2……… inhibits apoptosis
– Bax, Bad, and bcl-x5………. favour programmed cell death.
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• D) Genes that regulate DNA repair
– Inability to DNA repair can predispose to
mutations in the genome and hence,to neoplastic
transformations.
• 3) Carcinogenesis is a multifactorial process
at both the phenotypic and genotypic levels.
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Major categories of
carcinogens.
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Types of carcinogenesis:
• A large number of agents cause genetic damages
and induce neoplastic transformation of
cells.
• They fall into the following three categories:
I. Chemical carcinogenesis
II. Radiation carcinogenesis
III. Viral carcinogenesis
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I. Chemical carcinogens
• No common structural features
• Most require metabolic conversion into active
carcinogens
• Major classes include polycyclic aromatic
hydrocarbons, aromatic amines, nitrosamines,
azo dyes, alkylating agents
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Chemical carcinogens Cont’d…
• Chemical carcinogenic agents fall into two categories
• 1. Directly acting compound
– These are ultimate carcinogens and have one property in
common:
– They are highly reactive electrophiles (have electron
deficient atoms) that can react with nucleophilic (electron-
rich) sites in the cell.
• This result in electrophilic reactions may attack several electron-
rich sites in the target cells including DNA, RNA, and proteins.
– Only a few alkylating and acylating agents are directly
acting carcinogens.
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Chemical carcinogens Cont’d…
• 2. Indirect acting compounds (or pro-carcinogens)
– Requires metabolic conversion in vivo to produce ultimate
carcinogens capable of transforming cells.
– Most known carcinogens are metabolized by cytochrome
p-450 dependent monooxygenase.
• Examples of this group include polycyclic and heterocyclic
aromatic hydocarbones, and aromatic amines etc….
– These chemical carcinogens lead to mutations in cells by
affecting the functions of oncogenes, onco-suppressor
genes and genes that regulate apoptosis.
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Summary of some metabolic pathways for conversion of chemical
procarcinogens into the active ultimate carcinogens
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Examples of proven or
suspected chemical carcinogens
Chemical Tumour Comments
Polycyclic aromatic
hydrocarbons e.g. 3,4-
benzpyrene
Lung cancer Strong link with smoking
Skin cancer Following repeated
exposure to mineral oils
Aromatic amines e.g. β-
naphthylamine
Bladder cancer In rubber and dye workers
Nitrosamines Gut cancers Proven in animals
Azo dyes e.g. 2-
acetylaminofluorene
Bladder and liver cancer Proven in animals
Alkylating agents e.g.
cyclophosphamide
Leukaemia Small risk in humans
Other organic chemicals e.g.
vinyl chloride
Liver angiosarcoma Used in PVC manufacture
Arsenical compounds Skin cancer No longer a common event
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II. Radiation carcinogenesis
• Radiant energy whether in form of ultraviolet
(UV) sun light or ionizing electromagnetic (X
rays and gamma (δ ) rays) and particulates (α,β,
protons and neutrons) radiation can transform
and induce neoplasm.
• Two types of radiation injuries are recognized:
a) Ultraviolet rays (UV light)
b) Ionizing radiation
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Radiation carcinogenesis Cont’d…
a. Ultraviolet rays (UV light)
– Non-ionizing radiation that cause vibration and rotation of atoms in
biologic molecules.
– Induce an increased incidence of squamous cell carcinoma, basal cell
carcinoma and possibly malignant melanoma of skin.
– Risk factors for developing UV rays related disorders depend on
• Type of UV rays – UV type B
• Intensity of exposure
• Quality of light absorbing “protective mantle” of melanin in the skin
Ex. Australians (queen's land etc.)
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• UV rays’ effects on cell nucleus are:
– The carcinogenesis of UV type B rays is
attributable to its formation of pyrimidine
dimmers in DNA.
– However, UV rays can also cause inhibition of cell
division, inactivation of enzymes, Induction of
mutation and sufficient dose kill cells.
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b. Ionizing radiation
– Electromagnetic (x-rays, γ rays) and particulate (α
particles, β particles, protons, neutrons) radiations
are all carcinogenic.
– Ionizing radiations are of short wave lengh and high
frequency which can ionize biologic target molecules
and eject electrons
– Electromagnetic and particulate radiations in forms
of therapeutic, occupational or atomic bomb incidents
can be carcinogenic.
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• Occupational hazards include:
– Roentgen rays -> skin cancers
– Miners for radioactive elements -> lung cancer
– Childhood & infancy irradiation (9%) -> Thyroid
cancer
– Radiation therapy for spondylitis -> a possible
acute leukemia year later.
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• Atomic bonds dropped in Hiroshima and Nagasaki
during the second World war
– Initially…………….acute and chronic mylogenous leukemias.
– After 7 years…….. breast, colon, thyroid and lung cancers
• In contrast, skin, bone and gastrointestinal tract are
relatively resistant to radiation induced neoplasia.
– Nonetheless, the physician dare not forget: practically
any cell can be transformed into a cancer cell by sufficient
exposure to radiant energy.
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3. Microbial Carcinogenesis
• Many RNA and DNA viruses have proved to
be oncogenic.
• Despite intense scrutiny, however, only a few
viruses have been linked with human cancer.
– There is an association between infections by the
bacterium Helicobacter Pylori and gastric
lymphoma.
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Viruses implicated in human tumours
Virus Tumour Comments
Human papillomavirus Common wart (squamous cell
papilloma)
Benign, spontaneously regressing lesion
Cervical carcinoma Strong association with HPV types 16 and
18
Epstein-Barr virus Burkitt's lymphoma Requires a co-factor, probably malaria
Nasopharyngeal cancer In Far East and Africa
Hepatitis B and C
viruses
Hepatocellular carcinoma Strong association
Human herpes virus-8 Kaposi's sarcoma Explains association between venereally-
acquired
Pleural effusion lymphoma AIDS and Kaposi's sarcoma
Human T-cell
lymphotropic virus-1
Adult T-cell leukaemia/lymphoma Endemic in Southern Japan and
Caribbean basin
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Microbial Carcinogenesis Cont’d…
I. DNA oncogenic viruses: this group includes:
• Human Papilloma Virus (HPV) – results in
– HPV (type 1,2,3,4, 7) - > Benign squamous papilloma (warts)
– HPV (types 16,18 and also 31,33,35,and 51 found in 85% SCC)
- > Squamous cell carcinomas of cervix and anogenital region.
– It is also linked to the causation of oral and laryngeal cancers.
• Epstein – Barr virus (EBV)
– The African form of Burkitt's lymphoma, B-cell lymphomas,
Nasopharyngeal and some gastric carcinomas and rare forms
of T cell lymphomas and natural killer (NK) cell lymphomas
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• Hepatitis B- virus (HBV)
– Strong epidemiologic association prevails between
HBV and hepato cellular Carcinoma.
– It is estimated that 70% to 85% of hepatocellular
carcinomas worldwide are due to infection with
HBV or HCV
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II. RNA oncogenic viruses
– Similar to HIV virus. HTLV-1 has tropism for CD4+T
cells -> Human infection requires transmission of
infected T cells through sexual intercourse, blood
products, or breast feedings.
– Leukemia develops after a 20 or 30 years of latency
in about 1% of patients.
– HTLV-1 is also associated tropical spastic Para
paresis.
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Clinical Features of Tumors
• Effects of tumor on the host:
• Both benign and malignant neoplasms may cause
problems because of:
1) Location and impingement on adjacent structures
2) Functional activities such as hormone synthesis
3) Bleeding and secondary infection when they
ulcerate through adjacent natural surfaces
4) Initiation of acute symptoms caused by either
rupture or infarction local and hormonal effects.
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Clinical Features of Tumors Cont’d…
• Cancer cachexia
– Cachexia is a progressive loss of body fat and lean
body mass accompanied by profound weakness,
anorexia and anemia .
– The origin of cancer cachexia are obscure.
– Clinically anorexia is a common problem in patients
with cancer. Reduced food intake has been related to
abnormalities in taste and central control of appetite.
• In patents with cancer, calorie expenditure often remains
high and basal metabolic rate is increased despite reduced
food intake.
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Paraneoplastic syndromes
• is an aggregate of symptom complexes in
cancer – bearing patients that can not readily
be explained either by the local or distant
spread of the tumor or by the elaboration of
hormones indigenous to the tissue from
which the tumor arose.
• Paraneoplastic syndrome occurs in about 10%
of patients with malignant disease.
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• Despite its infrequency, the syndrome is
important for three reasons:
1. They be the earliest manifestation of an occult
neoplasm
2. In affected patients, they may represent
significant clinical problems and may even be
lethal.
3. They may mimic metastatic disease and,
therefore, confound treatment.
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Classification of Paraneoplastic syndromes
Clinical
Syndromes Major Forms of Underlying Cancer Causal Mechanism
Cushing
syndrome
Small lung ca, pancreatic ca ACTH and ACTH like
Substances
IADH
Secretion
Small cell lung Ca ADH or atrial natriuretic
hormones
Hypercalcimia SCC of lungs, breast ca, renal ca,
Adult T-cell leukemia/lymphoma,
Ovarian cancers.
Parathyroid hormone
related peptide TGF -, TNF IL-1
Hypoglycemia Fibrosarcoma other sarcomas
HCC
Insulin or insulin like
substances
Carcinoid
syndrome
Bronchial adenoma, pancreatic
ca, gastric ca
Serotonins, bradykinins
histamine
Polycythemia Renal ca, cerebellar
Hemangioma, liver cancer
Erythropoietin
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Classification of paraneoplastic
syndromes Cont’d...
Clinical Syndromes
Major Forms of
Underlying Cancer Causal Mechanism
Dermatologic disorders such
as acanthosiss nigricans,
dermatomyositis
Gastric, lung & uterine
cancers
? immunologic
Vascular and hematologic Bronchographie ca, breast
ca
? immunologic
Venous thrombosis Pancreatic and
bronchogenic ca
Mucin that activate
clotting
Nonbacterial thrombotic
endocarditis
Advanced cancers Hypercoagulobilty
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Cont’d…
• Hypercalcimia - > the most common
paraneoplastic syndrome.
• Among endocrinopathies - > Cushing
syndrome is the most common variety of
paraneoplastic effect.
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Grading and staging of cancers
• Grading denotes the level of differentiation
• Staging expresses the extent of tumour spread
and forcast the clinical gravity of cancers.
• Cancers are classified into grades I to IV with
increasing anaplasia. Criteria for individual
grades vary with each form of neoplasm.
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Grading and staging of cancers Cont’d…
• The staging of cancers is based on the size of
primary lesions, its extent of spread to regional
lymph nodes and the presence or absence of
blood born metastases.
– Two major staging systems are currently in use are
I. Union internationale contre cancer (UICC) which
utilizes the so- called TNM system
• T for primary tumour N for regional lymph node
involvement and m for metastasis.
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• The TNM staging varies for each specific form
of cancer but there are general principles:
– With increasing size, the primary lesion is
characterized as T1 to T4, T0 is used to indicate an
in - situ lesion.
• No for no nodal involvement whereas, N1 -N3
would denote involvement of an increasing
number and range of nodes.
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Summary of TNM system for
staging of tumours
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• Mo signifies no distant metastasis whereas M1 or
sometimes M2 indicates the presence of blood
born metastasis.
II. The American joint committee (AJC) employs a
somewhat different nomenclature and divides
– All cancers into stages to IV incorporating within
each of these stages the size of the primary lesion as
well as the presence of nodal spread and the distant
metastasis
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Laboratory Diagnosis of Cancer
• Histologic and cytologic methods:
– The laboratory diagnoses of most cancers is not
difficult however, border line cases in no man's
land where wise men trade cautiously pose the
most difficulties.
– The laboratory sample to be diagnosed need to
be adequate, representative and well preserve.
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Laboratory Diagnosis of Cancer Cont’d…
• Several sampling approaches are available:
1. Excisional or incisional biopsy:
2. Cytologic smears:
• Fine needle aspiration
• PAP smear
• Fluid cytology
3. Advanced techniques
• Immunocytochemistry
• Flow cytometry
• Tumour markers
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Laboratory Diagnosis of Cancer Cont’d…
• New advanced techniques
– Immunocytochemistry
• The availability of specific monoclonal antibodies has
greatly facilitates the identification of cell products and
surface markers.
– Flow cytometry
• Identification of cell surface antigens by flow cytometry
is widely used in the classification of leukemias and
lymphomas .
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Quiz 10%
1. Defined Neoplasia?(2point)
2. Write different Characteristics of Benign and
Malignant Neoplasms?(4point)
3. List Pathways of cancer Spread?(2point)
4. Anemia is not a neoplastic disorder. (T or F)(1point)
5. Leukemia is a neoplastic disorder. (T or F)(1 point)
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85

THANK YOU!!!
END OF NEOPLASIA!!!
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DR.MYM neoplasia Unit 9-1.pptx

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