Pujasari Neoplasia Week 3

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NEOPLASIA
Hening P. Syahrin
Basic Science and Fundamental of Nursing Group
Faculty of Nursing Universitas Indonesia
2008
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Sub topics to cover today

The concepts of cell growth &
differentiation
Characteristics of benign & malign
neoplasm
Carcinogenesis & cause of cancer
Cancer
is the 2nd leading cause of death in US

after cardiovascular disease
affects all age groups, any organ, female
& male
most common site in maleprostate, in
femalebreast
results from altered cell differentiation &
growth
its cell growth is uncoordinated &
relatively autonomous
is not a single disease
Definition
Neoplasia: neo (new) + plasia (form)

the process of new growth
Neoplasm: the new growth; can be benign or
malignant
Tumor= tumere (to swell); historically referred to
any swelling, now synonymous with neoplasm
Oncology=oncos (mass, bulk) + logos (reason);
the study of neoplasia
Oncogenesis = oncos + genesis (production); the
causation or production of neoplasia
Cancer = karkinos (crab) the common term for all
malignant neoplasms (used more frequently in
human)
Definition
it is called cancer as it has similar characteristics

with a cancer/crab
eg. adhere in obstinate manner like a crab,
infiltrative, erosive growth that extent crab-like
feet
some inconsistencies in classifying & naming
suffix oma is almost always present (from
onkoma = swelling)
naming should indicate benign vs malignant,
mesenchymal vs epithelial
plus mixed tumor: contains more than one cell
type but they are derived from one germ layer
Classification & Naming of Neoplasm

Benign
Mesenchymal (structural
tissue, blood vessels,
lymphatics)
- lipoma,
- fibroma,
- osteoma.
Epithelial:
- pituitary adenoma
- hepatocellular adenoma
Malignant
Mesenchymal:
- liposarcoma,
- fibrosarcoma,
- osteosarcoma
Epithelial:
- pituitary carcinoma
- hepatocellular carcinoma
Classification of Neoplasm
Classification of Neoplasm
Example of Inconsistency in Tumor

Naming
lymphoma (or lymphosarcoma): a
neoplastic disorder, usually malignant, of
lymphoid tissue
leukemia: malignant neoplasm of bloodforming tissues
melanoma: malignant tumor of
melanocytes
melanocytoma: a benign tumor of
melanocytes
Benign vs Malignant Neoplasm

Benign, most benign tumor are:

composed of well differentiated cells that closely
resemble their normal counterparts, often
including the same architecture arrangement
eg. a uterine leiomyoma resemble uterine
smooth muscle cells
grow as cohesive expansive masses that remain
localized to their site of origin
grow & expand slowly with comprehensive
atrophy of adjacent parenchymal cells & many
have a well-defined fibrous capsule formed from
the surrounding compressed stroma
fail to metastasize to distant sites

Benign, some benign tumor:
are spontaneously regressed
may slowly progress to malignancy
morphologically, may have serious, if not
fatal, consequences
egs. tumors of brains (space-occupying
lesions), some hormone-producing tumors
(tumor of pancreatic islet cells that
produces insulin, causing hypoglycemia)

Malignant tumors
an aggressive & life-threatening tumor
characterized by:
1) anaplasia,
2) rapid rate of growth,
3) local invasion of tissue, &
4) metastasis.
there are: 1) solid tumors & 2) hematologic
cancers
1) Differentiation/Anaplasia
anaplasia (loss of differentiation)

characterized malignancy
morphology anaplasia includes:
a) pleomorphism: variation in
size & shape both cells
(anisocytosis) & nuclei
(anisokaryosis)
b) abnormal nuclei: large,
coarsely clumped, marginalized
chromatin
c) mitoses: increased, tripolar
mitotic figure
d) loss of polarity: no a polarized
orientation
e) single large nucleus/
binucleated/ multinucleated
2) Rate of Growth (Tumor Cell Kinetics)

most malignant tumors grow rapidly than benign
ones
the rate of tissue growth depends on 3 factors:
increased number of cells that are dividing, cells
do not die on schedule, greater ratio of dividing
cells and resting cells (growth fraction), &
decreased length of time taken for total mass of
cells to double (doubling time/Td)
alteratered in contact inhibition (the cessation of
growth after a cell comes in contact with another
cell).
Cell Cycle
3) Local Invasion of Tissue

extensive infiltration (invasion) & destruction of

surrounding tissues
besides metastasis, invasion is the most reliable
indicator of malignancy
can make complete surgical removal difficult
(often necessitates taking wide margins)
seeding of the cancer cells into body cavities
occurs when tumor erodes these spaces
tumor cells secret tumor-angiogenesis factors,
which enables the development of new blood
vessels within tumor (angiogenesis)
4) Metastasis
as a development of secondary tumor in a location

distant from primary tumor
indicates malignancy and is what kills the majority of
human cancer patients
metastatic tumor retains characteristics of the primary
tumor from which they were derived possible to
determine the site of primary tumor from the cellular
characteristics of the metastatic tumor
occasionally, the metastatic tumor is far advanced before
the primary tumor becomes clinically detected
eg. tumor of the kidney is completely
undetected/asymptomatic even when a metastatic lesion
is found in the lung
there is selectivity in organ metastasis, eg. Heart, skin &
skeletal muscle are rarely as a site of metastasis
Tumor Metastasis

Carcinogenic agents
1.
2.
3.
4.
5.
Chemical carcinogens
Oncogenic viruses
Radiation carcinogenesis
Chronic inflammation
(heredity)
Chemical Carcinogens
2-4% cancer death are associated with an exposure to
an occupational hazard
egs. asbestos fiberrisks of lung, laryngeal, & GI Ca;
benzenaleukemia; herbicidenon-Hodgkins
lymphoma
many Ca are associated with lifestyle; smoking, diet,
alcohol consumption
egs. cigarette smoke contains procarcinogen &
promoterrisk of lung & laryngeal cancers
diet contains polycyclic hydrocarbons (from smoked
meat/fish or multiple reused oil), nitrosamines (from
food/vegetables preservative), high fat & protein but low
fibers
the effect of carcinogenic agents is dose & duration
dependent. eg. duration 5-30 years after exposure.
Oncogenic Viruses
an oncogenic virus is
one that can induce
cancer
virus enters a host cell,
incorporates into host
cell DNA, & takes
control of the cellular
machinery for the
purpose of producing
viral proteins
Radiation Carcinogenesis
through the effect of ionizing radiation

egs in atomic bomb survivor, patients
diagnostically exposed, industrial workers,
lab scientistmalignant epitheliomas of
skin & leukemia
the effect depends on dose, sex, age at
exposure
sunlightskin cancer, primarily in the area
that frequently exposed; head, neck, &
arms, higher incident in individual with lack
of UV filtering skin pigment melanin
Chronic Inflammation
the generation of O2 free radicals by
inflammatory cells,
the regeneration of cells to replace
damaged cells at a site of chronic
inflammation may result in genetic
damage progress to neoplastic
transformation
proliferating fibroblast at the chronic
inflammation can secrete growth factors
that contribute to neoplastic transformation
Heredity
there is a genetic predisposition for development

of cancers ( 50 type of cancers)
eg. Breast cancer occurs more frequently in women whose
grandmothers, mothers, aunts, & sisters with breast malignancy
the risk increases 50% in women age 65 who

have multiple family members with breast cancer
2 oncongens: BRCA1 &BRCA2 have been
implicated in a genetic susceptibility to breast
cancer
mutation of p53 tumor suppressor gene places
women at high risk of breast cancer in 20 or 30
of age
40% of retinoblastoma is inherited
Carcinogenesis & Cause of Cancer

as cancer is not a single diseaseit does

not have a single cause
occurs because interaction between multiple
risks factors (carcinogen & heredity) or
repeated exposure to a single
carcinogenic agent
all cancers result from nonlethal genetic
changes that transform a normal cell into
cancerous cell
Carsinogensis/Oncogenesis
is a genetic mechanism whereby normal cells are

transformed into cancer cells
two kinds of gene control normal cell growth & replication:
1. growth-promoting regulatory genesprotooncogens
2. growth-inhibiting regulatory genesanti-oncogenes
(cancer supressor genes)
these genes have been implicated as principal targets of
genetic damage that occurs during the development of
cancer cell
oncogenes are mutations of normal growth-regulating
genes
the mutation of cause proto-oncogen to change into
oncogen results in unregulated cellular proliferation
Oncogenesis
Multiple Steps of Oncogenesis

Transformation of normal cells into cancer cells by

carcinogenic agents is a multiple process, 3 stages:
1. initiation: the exposure of cells to appropriate doses of a
carcinogenic agent that makes them susceptible to
malignant transformationirreversible changes in the
genome
2. Promotion: induction of unregulated accelerated growth
in already initiated cells by various chemical & growth
factorsreversible if the promoter substance is
removed
3. Progression: the process whereby tumor cells acquired
malignant phenotypic changes that allow invasiveness,
metastatic competency, a tendency for autonomous
growth, & increased karyotypic instability
Seven Cellular Traits in Neoplasm

1.
2.
3.
4.
5.
6.
7.
activation of oncogenesis
inactivation of tumor suppressor gen
evasion of apoptosis
defects in DNA repair
limitless replicative potential
sustained angiogenesis
ability to invade and metastasize
Cellular Traits in Neoplasm

Systemic/General Effects of Neoplasm

1. impairment of function at the primary site of involvement, caused by

destruction & replacement of parenchymal tissue by neoplastic
growth, eg. lung cancer will impair respiratory function,
as the tumor grows & metastasizes, other body structures become
affected
2. compression of adjacent vital structures
the growth of brain tumor can compress adjacent vital structure
3. bleeding & hemorrhage, related to compression of blood vessel
eg. colorectal cancer--blood in the stool
4. obstruction of hollow viscera & rupture of tubular organ as a result of
expansive growth of tumor with compression & invasion
5. ulceration, necrosis & infection of tumor area, related to ischemia
associated with rapid growth, with subsequent bacterial infection
cancers may produce enzymes & metabolic toxins that destruct
surrounding tissues
Systemic/General Effects of Neoplasm

6. effusion in serous cavity, due to impaired lymph flow or erosion of

tumor into the cavity
7. pain (that does not heal is a second warning signal of cancer)-liberation of pain mediator by the tumor, compression, or ischemia of
the structure
8. cachexia; lost of muscle mass & fat store as a result from the action
of cytokines (anorexigenic) produced by tumor cell & TNF (Tumor
Necrosis Factor released by macrophage
9. anemia, caused be bleeding and depression of erythrocytes
production
10. inappropriate hormone production
eg. uncontrolled corticosteroid production of adrenal cortex tumor
production of hormone-like substances that are not regulated by
normal feedback mechanisms
11. paraneoplastic syndromes; manifestation in sites that are nor
directly affected by disease.
eg. cancer may produce procoagulation factors that contribute to
increased risk of venous thrombosis
Staging & Grading of Tumors

Two basic methods of classifying cancer are:

1. staging according to clinical stage of the disease, &
2. grading according to histologic & cellular
characteristics of tumors.
Both methods are useful to determine the course of the
disease & to aid in selecting appropriate treatments
1. Staging
to determine progress & spread
classify tumors based according to their progression
TNM system is based on:

- assessment of the size of the primary tumor (T)
- involvement of regional lymph nodes (N)
- presence or absence of distant metastasis (M)
Staging & Grading of Tumors

2. Grading
to determine level of differentiation & number of
mitoses
involves microscopic examination
quantify characteristic of tumors as a means of
predicting their outcomes:
- degree of differentiation
- size of nuclei
- mitotic activity
- degree of vascularization
- presence or absence of necrosis cancers
classified as grade I, II, III, & IV with increasing
anaplasia & lack of differentiation

Pujasari Neoplasia Week 3

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Sub topics to cover today

is the 2nd leading cause of death in US

Neoplasia: neo (new) + plasia (form)

it is called cancer as it has similar characteristics

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Classification & Naming of Neoplasm

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Example of Inconsistency in Tumor

Benign vs Malignant Neoplasm

Benign, most benign tumor are:

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Benign vs Malignant Neoplasm

Benign vs Malignant Neoplasm

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anaplasia (loss of differentiation)

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2) Rate of Growth (Tumor Cell Kinetics)

3) Local Invasion of Tissue

extensive infiltration (invasion) & destruction of

as a development of secondary tumor in a location

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Benign vs Malignant Neoplasm

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through the effect of ionizing radiation

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there is a genetic predisposition for development

the risk increases 50% in women age 65 who

Carcinogenesis & Cause of Cancer

as cancer is not a single diseaseit does

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is a genetic mechanism whereby normal cells are

Multiple Steps of Oncogenesis

Transformation of normal cells into cancer cells by

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Seven Cellular Traits in Neoplasm

Cellular Traits in Neoplasm

Systemic/General Effects of Neoplasm

1. impairment of function at the primary site of involvement, caused by

Systemic/General Effects of Neoplasm

6. effusion in serous cavity, due to impaired lymph flow or erosion of

Staging & Grading of Tumors

Two basic methods of classifying cancer are:

to determine progress & spread

classify tumors based according to their progression

TNM system is based on:

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Staging & Grading of Tumors

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