pujasari neoplasia week 3

7/23/2019 Pujasari Neoplasia Week 3

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NEOPLASIA

Hening P. Syahrin

Basic Science and Fundamental of Nursing GroupFaculty 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

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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

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DefinitionNeoplasia: neo (new) + plasia (form)

the process of new growth

Neoplasm: the new growth; can be benign ormalignant

Tumor= tumere (to swell); historically referred toany swelling, now synonymous with neoplasm

Oncology=oncos (mass, bulk) + logos (reason);the study of neoplasia

Oncogenesis = oncos + genesis (production); the

causation or production of neoplasiaCancer = karkinos (crab) the common term for all

malignant neoplasms (used more frequently in

human)

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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-likefeet

some inconsistencies in classifying & naming

suffix oma is almost always present (fromonkoma = 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

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Classification & Naming of Neoplasm

Benign

Mesenchymal (structuraltissue, blood vessels,lymphatics)

- lipoma,

- fibroma,- osteoma.

Epithelial:

- pituitary adenoma- hepatocellular adenoma

Malignant

Mesenchymal:

- liposarcoma,

- fibrosarcoma,

- osteosarcoma

Epithelial:

- pituitary carcinoma- hepatocellular carcinoma

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Benign vs Malignant NeoplasmBenign, most benign tumor are: composed of well differentiated cells that closely

resemble their normal counterparts, often

including the same architecture arrangementeg. a uterine leiomyoma resemble uterinesmooth muscle cells

grow as cohesive expansive masses that remainlocalized to their site of origin grow & expand slowly with comprehensive

atrophy of adjacent parenchymal cells & many

have a well-defined fibrous capsule formed fromthe surrounding compressed stroma fail to metastasize to distant sites

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Benign vs Malignant Neoplasm

Benign, some benign tumor:

are spontaneously regressed

may slowly progress to malignancy

morphologically, may have serious, if not

fatal, consequencesegs. tumors of brains (space-occupyinglesions), some hormone-producing tumors

(tumor of pancreatic islet cells thatproduces insulin, causing hypoglycemia)

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Benign vs Malignant Neoplasm

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) hematologiccancers

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1) Differentiation/Anaplasia anaplasia (loss of differentiation)

characterized malignancy

morphology anaplasia includes:

a) pleomorphism: variation insize & shape both cells(anisocytosis) & nuclei

(anisokaryosis)b) abnormal nuclei: large,coarsely clumped, marginalizedchromatin

c) mitoses: increased, tripolar

mitotic figured) loss of polarity: no a polarizedorientation

e) single large nucleus/

binucleated/ multinucleated



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2) Rate of Growth (Tumor Cell Kinetics)

most malignant tumors grow rapidly than benignones

the rate of tissue growth depends on 3 factors:increased number of cells that are dividing, cellsdo not die on schedule, greater ratio of dividing

cells and resting cells (growth fraction), &decreased length of time taken for total mass ofcells to double (doubling time/Td)

alteratered in contact inhibition (the cessation ofgrowth after a cell comes in contact with another

cell).



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CellCycle


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3) Local Invasion of Tissue

extensive infiltration (invasion) & destruction ofsurrounding tissues

besides metastasis, invasion is the most reliableindicator 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 bloodvessels within tumor (angiogenesis)



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4) Metastasis as a development of secondary tumor in a location

distant from primary tumor

indicates malignancy and is what kills the majority ofhuman cancer patients

metastatic tumor retains characteristics of the primarytumor from which they were derived possible todetermine the site of primary tumor from the cellularcharacteristics of the metastatic tumor

occasionally, the metastatic tumor is far advanced beforethe primary tumor becomes clinically detected

eg. tumor of the kidney is completely

undetected/asymptomatic even when a metastatic lesionis found in the lung

there is selectivity in organ metastasis, eg. Heart, skin &skeletal muscle are rarely as a site of metastasis



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Tu

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gnv

sMalignan

tNeo

plasm


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Carcinogenic agents

1. Chemical carcinogens

2. Oncogenic viruses

3. Radiation carcinogenesis

4. Chronic inflammation5. (heredity)

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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-Hodgkinslymphoma

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 smokedmeat/fish or multiple reused oil), nitrosamines (from

food/vegetables preservative), high fat & protein but lowfibers

the effect of carcinogenic agents is dose & durationdependent. eg. duration 5-30 years after exposure.

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Oncogenic Virusesan oncogenic virus is

one that can inducecancer

virus enters a host cell,

incorporates into hostcell DNA, & takescontrol of the cellular

machinery for thepurpose of producingviral proteins

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Radiation Carcinogenesis

through the effect of ionizing radiation

egs in atomic bomb survivor, patients

diagnostically exposed, industrial workers,lab scientistmalignant epitheliomas ofskin & leukemia

the effect depends on dose, sex, age atexposure

sunlightskin cancer, primarily in the area

that frequently exposed; head, neck, &arms, higher incident in individual with lackof UV filtering skin pigment melanin

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Chronic Inflammation the generation of O2 free radicals by

inflammatory cells,

the regeneration of cells to replacedamaged cells at a site of chronicinflammation may result in geneticdamage progress to neoplastictransformation

proliferating fibroblast at the chronicinflammation can secrete growth factorsthat contribute to neoplastic transformation

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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 whohave multiple family members with breast cancer

2 oncongens: BRCA1 &BRCA2 have beenimplicated in a genetic susceptibility to breastcancer

mutation of p53 tumor suppressor gene placeswomen at high risk of breast cancer in 20 or 30of age

40% of retinoblastoma is inherited

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Carcinogenesis & Cause of Cancer

as cancer is not a single diseaseit doesnot have a single cause

occurs because interaction between multiplerisks factors (carcinogen & heredity) orrepeated exposure to a single

carcinogenic agentall cancers result from nonlethal genetic

changes that transform a normal cell intocancerous cell

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Carsinogensis/Oncogenesisis a genetic mechanism whereby normal cells are

transformed into cancer cells

two kinds of gene control normal cell growth & replication:

1. growth-promoting regulatory genesprotooncogens2. growth-inhibiting regulatory genesanti-oncogenes

(cancer supressor genes)

these genes have been implicated as principal targets of

genetic damage that occurs during the development ofcancer cell

oncogenes are mutations of normal growth-regulatinggenes

the mutation of cause proto-oncogen to change intooncogen results in unregulated cellular proliferation

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Onco

genesis


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Multiple Steps of Oncogenesis

Transformation of normal cells into cancer cells bycarcinogenic agents is a multiple process, 3 stages:

1. initiation: the exposure of cells to appropriate doses of acarcinogenic agent that makes them susceptible to

malignant transformationirreversible changes in thegenome

2. Promotion: induction of unregulated accelerated growthin already initiated cells by various chemical & growth

factorsreversible if the promoter substance isremoved

3. Progression: the process whereby tumor cells acquiredmalignant phenotypic changes that allow invasiveness,metastatic competency, a tendency for autonomousgrowth, & increased karyotypic instability

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Seven Cellular Traits in Neoplasm

1. activation of oncogenesis

2. inactivation of tumor suppressor gen

3. evasion of apoptosis

4. defects in DNA repair5. limitless replicative potential

6. sustained angiogenesis

7. ability to invade and metastasize



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CellularTra

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Systemic/General Effects of Neoplasm1. impairment of function at the primary site of involvement, caused bydestruction & replacement of parenchymal tissue by neoplastic

growth, eg. lung cancer will impair respiratory function,

as the tumor grows & metastasizes, other body structures become

affected2. compression of adjacent vital structures

the growth of brain tumor can compress adjacent vital structure3. 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 ofexpansive growth of tumor with compression & invasion

5. ulceration, necrosis & infection of tumor area, related to ischemiaassociated with rapid growth, with subsequent bacterial infection

cancers may produce enzymes & metabolic toxins that destructsurrounding tissues



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Systemic/General Effects of Neoplasm6. effusion in serous cavity, due to impaired lymph flow or erosion of

tumor into the cavity7. pain (that does not heal is a second warning signal of cancer)--

liberation of pain mediator by the tumor, compression, or ischemia ofthe structure

8. cachexia; lost of muscle mass & fat store as a result from the actionof cytokines (anorexigenic) produced by tumor cell & TNF (TumorNecrosis Factor released by macrophage

9. anemia, caused be bleeding and depression of erythrocytesproduction

10. inappropriate hormone productioneg. uncontrolled corticosteroid production of adrenal cortex tumorproduction of hormone-like substances that are not regulated bynormal feedback mechanisms

11. paraneoplastic syndromes; manifestation in sites that are nor

directly affected by disease.eg. cancer may produce procoagulation factors that contribute toincreased risk of venous thrombosis

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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)


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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


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pujasari neoplasia week 3

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