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Histopathology of Neoplasia

Definitions

Classification

Nomenclature

Characteristics off benign and malignant

Factors affecting incidence of cance

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Nomenclature

- All tumors have two basic components

Proliferating neoplastic cells that constitutetheir parenchyma

Supportive stroma made up of connectivetissue & blood vessels

- The growth & evolution of neoplasms are

critically dependent on their stroma.- The nomenclature of tumors is based on the

parenchymal component

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Neoplasms are named based upon two factors

On the histologic types : mesenchymal and

epithelial On behavioral patterns : benign and

malignant neoplasms

Nomenclature

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- Benign tumors of mesenchymal cells are

designated by attaching the suffix oma to

the cell of origin

- Malignant tumors arising in mesenchymal

tissue are usually called sarcoma

Nomenclature

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Tumors of mesenchymal originConnective tissue and derivatives

Benign Malignant

Fibrous tissue Fibroma Fibrosarcoma

Fat tissue Lipoma Liposarcoma

Cartilage Chondroma Chondrosarcoma

Bone Osteoma Osteosarcoma

Nomenclature

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Endothelial and related tissues

Benign Malignant

Blood vessels Hemangioma Angiosarcoma

Lymph vessels Lymphangioma Lymphangiosarcoma

Synovium Synovial sarcoma

Nomenclature

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Muscle

Benign Malignant

Smooth Leiomyoma Leiomyosarcoma

Striated Rhabdomyoma Rhabdomyosarcoma

Nomenclature

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- Benign epithelial tumors are variously

classified, some based on

Cell of origin ,

Microscopic architecture &

Macroscopic patterns

Nomenclature

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Adenoma the term applied for benign

epithelial neoplasm that form glandular

pattern

Nomenclature

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Papillomas - benign neoplasmsproducing microscopically or

macroscopically visible finger like

projection or warty projection from

epithelial surface

Nomenclature

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- Benign tumors that form large cystic masses are

referred as cystadenoma. Some tumors produce

papillary patterns that protrude into cystic

spaces are called papillary cystadenoma

- When tumor produces macroscopically visible

projection above a mucosal surface , it is termed

polyp- Malignant neoplasms of epithelial cell origin are

called carcinomas

Nomenclature

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Teratomas are made up of a variety of

parenchymal cell types representative of

more than one germ layer

- They arise from totipotent cells.

- So mostly are found in gonads

Nomenclature

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Characteristics of benign and malignant

neoplasms

A. Differentiation and anaplasia

- Differentiation refers to the extent to which

parenchymal cells resemble comparable normal

cells both morphologically and functionally.

- Thus, well-differentiated tumors cells resemble

mature normal cells of tissue of origin. Poorly

differentiated or undifferentiated tumors haveprimitive appearing, unspecialized cells.

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- In general, benign neoplasms are welldifferentiated.

- Malignant neoplasms in contrast, range fromwell differentiated, moderatelydifferentiated to poorly differentiate types.

- Malignant neoplasm composed of

undifferentiated cells are said to beanaplastic,

- literally anaplasia means to form backward.


neoplasms

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Morphologic changes which mark anaplasia

Pleomorphism both cells & nuclei show

variation in size & shapeAbnormal nuclear morphology the nuclei

contain abundant chromatin & are extremely

dark staining (hyperchromatic), high nuclear

cytoplasmic ratio 1:1(normally 1:4 to 1:6)


neoplasms

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The cell usually reveals large nucleoli with

high number and often abnormal mitoses

Tumor giant cellsNecrosis (in many anaplastic tumors, large

central areas undergo ischemic necrosis.)


neoplasms

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- Anaplastic tumor of the skeletal muscle (rhabdomyosarcoma). Notethe marked cellular and nuclear pleomorphism, hyperchromaticnuclei, and tumor giant cells

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Dysplasia

- Disordered growth

- It is characterized by changes that include a loss

in the uniformity of the individual cells as well asa loss in their architectural orientation

- When dysplastic changes are marked & involve

the entire thickness of the epithelium but the

lesion remains confined to the normal tissue ,it is

considered preinvasive neoplasm & is referred toas Carcinoma in situ


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The better the differentiation of the

transformed cell, the more completely it

retains the functional capabilities found in its

normal counterparts.

Thus, benign neoplasms and well-

differentiated carcinomas of endocrine glands

frequently elaborate the hormones

characteristic of their origin

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Highly anaplastic undifferentiated cells, lose their

resemblance to the normal cells from which they

have arisen.

In some instances, new and unanticipated

functions emerge.

Some tumors may elaborate fetal proteins

(antigens) not produced by comparable cells inthe adult.

Carcinomas of non-endocrine origin may

produce a variety of hormones, often calledectopic hormones.

For example, bronchogenic carcinomas may

produce corticotropin, parathyroid-like hormone,

insulin, and glucagons, as well as others

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neoplasms

B. Rate of growth

The rate of growth of a tumor is determined

by three main factors: the doubling time of tumor cells,

the fraction of tumor cells that are in the

replicative pool, and

the rate at which cells are shed and lost in the

growing lesion.

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- Most benign tumors grow slowly whereas;

most malignant tumors grow rapidly

sometimes, at erratic pace

- In general, the growth rate of neoplasms

correlate with their level of differentiation

and thus, most malignant neoplasms grow

more rapidly than do benign neoplasms.


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C. Local invasion- Nearly all benign neoplasms grow as cohesive

expansile masses thatremains localizedto

their site of origin and do nothave the

capacity to infiltrate , invade or metastasize as

malignant tumors.

- Because they expand & grow slowly, they

usually develop a rim of compressedconnective tissue, called fibrous capsule


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C. Local invasion- Such encapsulations tend to contain the benign

neoplasms as a discrete, palpable and easily

movable masses that can be easily surgically

enucleated(removed).

- Hemangiomas and neurofibromas are

exceptions.


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C. Local invasion

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)


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C. Local invasion

Next to the development of metastasis,

invasiveness is the most reliable feature that

differentiates malignant from benign

neoplasms.


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Most carcinomas begin as localized growth

confined to the epithelium in which they

arise. As long as this early cancers do not

penetrate the basement membrane on which

the epithelium rests such tumors are

called carcinoma in-situ.


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D. Metastasis

Metastasis are tumor implants discontinuouswith the primary tumor

Metastasis unequivocally marks a tumor asmalignant because benign neoplasms dontmetastasize

The invasiveness of cancers permits them topenetrate into blood vessels, lymphatics &body cavities , providing the opportunity tospread


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D. Metastasis

With few exception, all cancers can

metastasize.T

he major exception aregliomas & basal cell carcinomas of the skin.

The more aggressive, the more rapidly

growing, & the larger the primary

neoplasms , the greater the likelihood that

it will metastasize


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Pathway of spread

Seeding of body cavities & surfaces(transcoelomic spread)

- It may occur whenever a malignant neoplasmpenetrates into a natural open field

- Most often involved is the peritoneal cavity

but other cavities - pleural, pericardialsubarachinoid & joint space may be affected

- It is often characteristic of ovarian carcinoma


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Pathway of spread

Lymphatic spread

- Lymphatic route is the most common pathwayfor the initial dissemination of carcinomas

- The pattern of lymph node involvement

follows the natural routes of drainage.


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For example carcinomas of the breast usually

arise in the upper outer quadrants, they

generally disseminate first to the axillary

lymph nodes.

Cancers of the inner quadrant may drain

through lymphatics to the nodes within the

chest along the internal mammary arteries.

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Pathway of spread

Hematogenous spread

- It is typical for sarcoma but is also seen withcarcinoma

- Liver & lung are most frequently involved in

hematogenous spread


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Arteries, with their thicker walls, are less readilypenetrated than are veins.

With venous invasion, the blood-borne cells

follow the venous flow draining the site of theneoplasm.

Understandably the liver and lungs are mostfrequently involved secondarily in such

hematogenous dissemination. All portal area drainage flows to the liver, and all

caval blood flows to the lungs.

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Characterstics Benign Malignant

Differentiation/anaplasia Well differentiated;

structure may be typical of

tissue of origin

Some lack of differentiation with

anaplasia; structure is often

atypical

Rate of growth Usually progressive and

slow; may come to a

standstill or regress;

mitotic figures are rare and

normal

Erratic and may be slow to rapid;

mitotic figures may be numerous

and

abnormal

Local invasion Usually cohesive and

expansile well-demarcated

masses that do not

invade or infiltrate

surrounding normal tissues

Locally invasive, infiltrating the

surrounding normal tissues;

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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Geographic factors Specific differences in incidence rates of

cancers are seen worldwide.

For exampleStomach carcinoma - Japan

Lung cancer - USA

Skin cancer - New zeland & Australia

Liver cancer - Ethiopia

Epidemiology

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Epidemiology

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Environmental factors

Asbestos ------- lung cancer, mesothelioma,

Esophagus and, stomach Ca

Vinyl chloride -------- Angiosarcoma of liver

Benzene ------------------ Leukemias

Cigarette smoking----- Brochogenic Ca.

Venereal infection -----Cervical carcinoma

Epidemiology

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Age

- Most cancers in adults occur in those over 55

years of age.

- Children under 15 years of age however, aresusceptible to acute leukemia, central

nervous system tumors, neuroblastoma,

wilm's tumour, retinoblastoma,

rhabdomyosarcoma and etc..

Epidemiology

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Genetic predisposition to cancer

- It can be divided into

Autosomal dominant inherited cancer

syndromes- It includes several well-defined cancers in

which inheritance of a single mutant gene

greatly increases the risk of developing atumor.

- Eg familial retinoblastoma

Epidemiology

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Defective DNA repair syndromes

- A group of cancer predisposing conditions is

collectively characterized by defects in DNA

repair & resultantDNA instability

- These conditions include Xeroderma

pigmentosum, ataxia- telangectasia & Bloom

syndrome

Epidemiology

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Familial cancers

- Cancers may occur at higher frequency in certainfamilies without a clearly defined pattern oftransmission.

- These include carcinoma of colon, breast, ovary& brain , melanoma

- Features that characterize familial cancers

include early age at onset, tumors arising in twoor more close relatives of the index case &sometimes , multiple or bilateral tumors.

Epidemiology

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onhereditary predisposing conditions

Precancerous conditions

These are non neoplastic conditions with welldefined association with cancer

Epidemiology

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Regenerative, hyperplasic and dysplasticproliferations are fertile soil for the origin ofmalignant neoplasm.

- Endometrial hyperplasia -- endometrialcarcinoma

- Cervical dysplasia - - cervical cancer

- Bronchial dysplasia - - bronchogeniccarcinoma

- Regenerative nodules -- liver cancer

Epidemiology

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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 andpenis - squamous cell carcinoma

Epidemiology

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Large cumulative experiences indicate that

most benign neoplasms do not become

malignant however, it can constitute

pre neoplastic conditions including

- Villous colonic adenoma - colonic cancer

- Carcinoma arising in pleomorphic adenoma

Epidemiology

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Molecular basis of cancer

- The fundamental principles in cancer genetics

include

Non-lethal genetic damage lies at the heartof 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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A tumor is formed by the clonal

expansion of a single precursor cell that

has incurred the genetic damage(tumors are monoclonal)


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The three classes of normal regulator genes

are the principal targets of genetic damage

The growth promoting proto-oncogenes

- Proto-oncogenes activation gives rise to

oncogenes (cancer causing genes).


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Growth inhibiting tumor suppressor genes

- Its physiologic role is to regulate cell growth

however, the inactivation of tumor suppressor

genes is the key event in cancer genesis


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Genes that regulate programmed celldeath (apoptosis)

Genes that regulate DNA repair

- These genes affect cell proliferation orsurvival indirectly by influencing theability of the organism to repair nonlethal damage in other genes. It

predisposes to mutation & to neoplastictransformation


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CARCINOGENESIS

Carcinogenesis is a multistep process

both at the phenotypic and genotypic levels

-A large number of agents cause genetic damagesand induce neoplastic transformation of cells.They fall into three categories

Chemical carcinogens

Radiant energy

Oncogenic viruses & some other microbs


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A) Chemical carcinogenesis

- Chemical carcinogenic agents fall into twocategories

Direct acting compounds these dont requirechemical transformation for theircarcinogenicity

Indirect acting compounds or procarcinogens ,

which require metabolic conversion to produceultimate carcinogens capable of transformingcells


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These include

Direct-acting alkylating agents

-T

herapeutic agents such as cyclophosphamideused as anticancer agents have been

documented to induce lymphoid neoplasms &

leukemia


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Polycyclic aromatic hydrocarbons

- These agents represent some of the most

potent carcinogens

Eg they are produced in the combustion of

tobacco & contribute to the causation of lung

& bladder cancer


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Aromatic amines & Azo dyes

Nitrosamines & amides

Naturally occurring carcinogens

Eg Aflatoxin B1 is a potent hepatic carcinogen ,

produced by some strains of the fungus

Aspergillus flavus that thrives on improperly

stored food


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b) Radiation carcinogenesis

Radiant energy whether in form of ultraviolet

(UV) sun light or ionizing electromagnetic (X

rays and gamma ( ) rays) and particulates

(, , protons and neutrons) radiation can

transform and induce neoplasm in both

humans and experimental animals.


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UV rays induce an increased incidence of

squamous cell carcinoma, basal cell

carcinoma and possibly malignant melanoma

of skin


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c) Viral and microbial carcinogenesis

Large groups ofDNA and RNA viruses have

proved to be oncogenic and there is an

association between infections by the

bacterium HelicobacterPylori and gastric

lymphoma


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i) DNA oncogenic viruses

This group includes

Human Papilloma Virus (HPV)

Epstein Barr Virus (EBV)

Hepatitis B Virus (HBV)


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Human papilloma Virus (HPV)

HPV definitely causes benign squamous

papilloma (warts) (type 1,2,3,4, 7).

It also implicated in the genesis of squamous

cell carcinomas of cervix and anogenital

region (types 16,18 and also 31,33,35,and 51

found in 85% SCC). It is also linked to the

causation of oral and laryngeal cancers


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Epstein Barr virus (EBV)

Member of the herpes family has been implicated

in the pathogenesis of four tumors.

The African form ofBurkitt'slymphoma,

B- cell lymphomas in immuno suppressed

individuals

some cases of Hodgkins disease

Nasopharyngeal carcinoma.


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ii) RNA oncogenic viruses

only one retrovirus is firmly implicated in

the causation of cancer and it is Human T

cells leukemia/ lymphoma virus type 1

(HTLV-1) .

It is associated with a form ofT-cell

leukemia /lymphoma


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Hepatitis B- virus (HBV) Strong epidemiologic association prevails

between HBV and hepatocellular carcinoma

Helicobacter pylori

-There is an association between gastric infectionswith Helicobacter pylori as a cause of gastriclymphoma. The stronger link is with B celllymphoma of stomach.

-T

reatment of H. pylori with antibiotics results inregression of the lymphoma in most cases.


Cli i l f t f t

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Clinical features of tumors

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 surfaces4. Initiation of acute symptoms caused by either

rupture or infarction

Effects of tumor on host

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Local and hormonal effects

For example pituitary adenoma being located

in critical location can cause serious

endocrinopathies

Analogously cancers arising with or

metastatic to an endocrine organ may cause

an endocrine insufficiency by destroying thegland.


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Benign neoplasms of endocrine origin mayproduce manifestations by elaboration ofhormones.

For example a benign B- cell adenoma ofpancreatic islets less than 1 cm in diameter mayproduce sufficient insulin to cause fatalhypoglycemia

Neoplasms in the gut (both benign andmalignant) may cause obstruction as theyenlarge


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The erosive destructive growth of cancers or

expansile pressure on benign tumor of any

natural surface may cause ulceration,

secondary infection and bleeding.


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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

Reduced food intake has been related to

abnormalities in taste and central control of

appetite.


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Cancer Cachexia

- In patients with cancer, calorie expenditureoften remains high and basal metabolic rate

is increased despite reduced food intake. TNF produced by macrophages and possibly

by some tumor cells is the mediator of thewasting syndrome that accompanies cancer.Other cytokines such as IL-1 andIFN synergize with TNF


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Paraneoplastic syndromes

- It is an aggregate of symptom complexes in

cancer - bearing patients that can not readily be

explained either by the local or distant spread ofthe 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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- The endocrinopathies are frequentlyencountered paraneoplastic syndromes. Becausethe cancer cells are not of endocrine origin, the

functional activity is referred as ectopichormone production .

Cushing syndrome is the most commonendocrinopathy . 50% of the patients have

carcinoma of lung ,chiefly the small cell type. itis caused by excessive production ofcorticotropin


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Paraneoplastic syndromes

Syndrome Mechanism Example

Cushing's Syndrome ACTH-like substance Lung (oat cell) carcinoma

Hypercalcemia Parathormone-like

substance

Lung (squamous cell)

carcinoma

Hyponatremia Inappropriate ADHsecretion

Lung (oat cell) carcinoma

Polycythemia Erythropoietin-like

substance

Renal cell carcinoma

T

rousseau's Syndrome Hypercoagulable state Various carcinomasHypoglycemia Insulin-like substance Various carcinomas and

sarcomas

Carcinoid Syndrome -hydroxy-indoleacetic acid

(5-HIAA

Metastatic malignant

carcinoid tumors

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Grading and staging of cancers

Grading denotes the level of differentiation

whereas, staging expresses the extent of

tumor spread and forecast the clinical

gravity of cancers

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Grading of a cancer is based on the degree of

differentiation of tumor cells and the number

of mitoses within the tumor and presumably

correlates to aggressive character of theneoplasm

Cancers are classified into grades Ito IV with

increasing anaplasia. Criteria for individualgrades vary with each form of neoplasm

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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-borne metastases


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Two major staging systems are currently in use

1. Union internationale contre cancer (UICC)

which utilizes the so- calledTNM system Tfor

primary tumor N for regional lymph node

involvement and M for metastasis


G di d t i f

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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 added to

indicate an in - situ lesion.


G di d t i f

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N0for no nodal involvement whereas, N1 -N3

wound denote involvement of an increasing

number and range of nodes.

M0signifies no distant metastasis whereas

M1 or sometimes M2 indicates the presence of

blood born metastasis


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2. The American joint committee (AJC) employs a

some what different nomenclature and divides

all cancers into stages Ito IV incorporating

within each of these stages the size of theprimary lesion as well as the presence of nodal

spread and the distant metastasis


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The staging of neoplastic disease has assumed

great importance in the selection of the best

form of therapy for the patient. Indeed staging

has proved to be of greater clinical value thangrading.


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Laboratory diagnosis of cancer

Histologic and cytologic methods

Several sampling approaches are available

1. Excision or biopsy

2. Fine needle aspiration

3. Cytologic smears

PAPsmearFluid cytology

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Advanced techniques:-

Immunohistochemistry

Molecular diagnosis

Flow cytometry

Tumor markers

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Immunohistochemistry

- The availability of specific monoclonal

antibodies has greatly facilitates the

identification of cell products and surface

markers


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Flow cytometery

Identification of cell surface antigens by flowcytometery is widely used in the classification

of leukemias and lymphomas Flow cytometery is used for detection of

aneuploidy which is also associated withpoorer prognosis in early stage breast cancer

carcinomas of the urinary bladder lungcancer colorectal cancer, and prostate cancer


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Tumour markers

- Tumour markers are biochemical indicators ofthe presence of a tumor . They include cell

surface antigens, cytoplasmic proteins,enzymes and hormones.

- Tumor markers can not be considered asprimary modalites for the diagnosis of cancerand thus, act as supportive laboratory tests.


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Selected tumor markers

Markers Associated CancersHormones

Human chorionic gonadotropin Trophoblastic tumors, nonseminomatous

testicular tumors

Calcitonin Medullary carcinoma of thyroid

Catecholamine and metabolites Pheochromocytoma and related tumors

Ectopic hormones Paraneoplastic Syndromes

Oncofetal Antigens

a-Fetoprotein Liver cell cancer, nonseminomatous germ

cell tumors of testis

Carcinoembryonic antigen Carcinomas of the colon, pancreas, lung,

stomach, and heart

Isoenzymes

Prostatic acid phosphatase Prostate cancer

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SpecificProteins

Immunoglobulins Multiple myeloma and other

gammopathies

Mucins and Other Glycoproteins

CA-125 O

varian cancer

Selected tumor markers

Documents

Neoplasm 2