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NEOPLASIA

-new growth
Neoplasm- abnormal mass of tissue the growth of which exceeds & is
uncoordinated with that of the normal tissues & persists in the same
excessive manner after the cessation of the stimuli which evoked the
change.

state of autonomous cell division

cells are said to be transformed because they continue


toreplicate

behave as parasite and competes with normal cells &


tissues for their metabolic needs

may flourish in patients who are otherwise wasting

increases in size regardless of their local environment & the


nutritional status of the host

depends on the host for its nutrition & blood supply

referred as tumor in common medical usage


Oncology study of tumors (ONCOS)
DIVISION
OF
NEOPLASMS
(based on the potential clinical behavior)

BENIGN

Localized the margins of the tumor are well


defined & cell growth is entirely local

Non-invasive cannot spread to other sites

Amenable to local surgical removal

Patient generally survives

MALIGNANT
o
-collectively referred to as Cancer (crab)
o
-spreading to distant sites (metastasis)
o
-Invasive destroying adjacent structures
TUMOR
NOMENCLATURE
Two Basic Components of Tumors
1) Parenchyma
- made up of transformed or neoplastic cells
- determines the biologic behavior
- the component from which the tumor derives its name
2) Stroma
- non-neoplastic
- carries the blood supply
- provides support for the growth of parenchymal cells
- crucial to the growth of the neoplasm
- does not aid in the separation of benign from
malignant
T UMO

R NOMENC L AT UR E : BE N IGN T U MO R S
Generally designated by attaching the suffix oma to the
cell type or connective tissue from which the tumor arises
A benign tumor arising in fibrous tissue is a FIBROMA; a
benign cartilaginous tumor is a CHONDROMA.

The nomenclature of benign epithelial tumors is MORE


COMPLEX.

They are classified sometimes on the basis of their


microscopic pattern and sometimes on the basis of their
macroscopic pattern. Others are classified by their cells
of origin.

Benign neoplasms of surface epithelia, ex. Skin, are termed


papillomas. This term is preceded by the cell of origin, ex.
Squamos papilloma of the skin . PAPILLOMA produces
microscopic or macroscopic finger-like fronds

ADENOMA- is applied to benign epithelial neoplasms


producing gland patterns and to neoplasms derived from
glands but not necessarily exhibiting gland patterns

POLYP is a mass that projects above a mucosal surface, as


in

the gut, to form a macroscopically visible structure

CYSTADENOMAS -are hollow cystic masses typically seen


in the ovary
TUMOR
NOMENCLATURE:
MALIGNANT
TUMORS

The nomenclature of malignant tumors essentially follows


that of benign tumors, with certain additions and exceptions.

Malignant neoplasms arising in mesenchymal tissue or its


derivatives are called SARCOMAS.

are designated by their histogenesis (i.e., the cell type of


which they are composed

A cancer of fibrous tissue origin is a FIBROSARCOMA, and a


malignant neoplasm composed of chondrocytes is a
CHONDROSARCOMA

Malignant neoplasms of epithelial cell origin are called

carcinomas. Tumors are preceded by the cell type of origin,


ex. Squamos cell carcinoma.

It must be remembered that the epithelia of the body are


derived from all three germ-cell layers; a malignant
neoplasm arising in the renal tubular epithelium (mesoderm)
is a carcinoma, as are the cancers arising in the skin
(ectoderm) and lining epithelium of the gut (endoderm).

Carcinomas that grow in a glandular pattern are called


adenocarcinomas, and those that produce squamous cells
are called squamous cell carcinomas

Sometimes the tumor shows little or no differentiation and


must be called poorly differentiated or undifferentiated
carcinoma.
NOMENCLATURE OF OTHER TUMORS (MIXED TUMORS)

The parenchymal cells in a neoplasm, whether benign or


malignant, resemble each other, as though all had been
derived from a single progenitor

In some instances, however, the tumor cells may undergo


divergent differentiation, creating so-called mixed
tumors

example is mixed tumor of salivary gland which have diverse


elements that are thought to derive from epithelial cells,
myoepithelial cells, or both in the salivary glands, and the
preferred designation of these neoplasms is pleomorphic
adenoma

Fibroadenoma of the female breast is another common


mixed tumor

The multifaceted mixed tumors should not be confused


with a teratoma, which contains recognizable mature or
immature cells or tissues representative of more than one
germ-cell layer and sometimes all three

Teratomas originate from totipotential stem cells such as


those normally present in the ovary and testis and
sometimes abnormally present in sequestered midline
embryonic rests.

Such cells have the capacity to differentiate into any of the


cell types found in the adult body and so, not surprisingly,
may give rise to neoplasms that mimic, in a helter-skelter
fashion, bits of bone, epithelium, muscle, fat, nerve, and
other tissues.
*** Teratoma - is an encapsulated tumor with tissue or organ
components resembling normal derivatives of all three germ
layers. The tissues of a teratoma, although normal in themselves,
may be quite different from surrounding tissues and may be
highly disparate; teratomas have been reported to contain hair,
teeth, bone and, very rarely, more complex organs such as eyes,
[1][2] torso,[3][4] and hands, feet, or other limbs.[5]
NOMENCLATURE
REMINDERS

Some glaring inconsistencies may be noted. For example,


the terms lymphoma, mesothelioma, melanoma, and
seminoma are used for malignant neoplasms. These
inappropriate usages are firmly entrenched in medical
terminology.

There are other instances of confusing terminology:


Hamartoma is a malformation that presents as a mass of
disorganized tissue indigenous to the particular site. One
may see a mass of mature but disorganized hepatic cells,
blood vessels, and possibly bile ducts within the liver, or
there may be a hamartomatous nodule in the lung
containing islands of cartilage, bronchi, and blood vessels

There are other instances of confusing terminology:


choristoma. This congenital anomaly is better described as
a heterotopic rest of cells.

For example, a small nodule of well-developed and normally


organized pancreatic tissue may be found in the submucosa
of the stomach, duodenum, or small intestine.

This heterotopic rest may be replete with islets of


Langerhans and exocrine glands.

The term choristoma, connoting a neoplasm, imparts to the


heterotopic rest a gravity far beyond its usual trivial
significance

** Choristomas,

forms of heterotopia, are closely


related benign tumors. These tumors also
contain normal tissues but are found in
abnormal locations
**Heterotopia (medicine), the displacement of an organ from its
normal position

chromatin is coarse & clumped & nucleeoli may be


astounding size

mitoses are often numerous & atypical


DYSPLASIA, a term used to describe disorderly but nonneoplastic proliferation. loss in the uniformity of individual
cells and in their architectural orientation

When dysplastic changes are marked and involve the entire


thickness of the epithelium, the lesion is referred to as
carcinoma in situ, a pre-invasive stage of cancer

Although dysplastic changes are often found adjacent to foci


of malignant transformation, and long-term studies of
cigarette smokers show that epithelial dysplasia almost
invariably antedates the appearance of cancer, the term
dysplasia without qualifications does not indicate cancer,
and dysplasias do not necessarily progress to cancer
B. Rate of Growth
Benign tumors
-it is generally true that most benign tumors increase in size
slowly over the span of months to years
- may come to standstill or regress
Malignant tumors
- erratic & may be slow to rapid
most grow much faster, spreading locally & to distant site
( metastasizing) & causing death
- The rate of growth of malignant tumors correlates in
general with their level of differentiation.
- the notion that they emerge out of the blue is not true
C. Local Invasion
Benign Tumors
- remains localized at its site of origin
- does not have the capacity to infiltrate, invade, or
metastasize to
distant sites
- most develop an enclosing capsule
that separates them from host
tissue
- not all benign neoplasms are
encapsulated
Malignant Tumors
- grow by progressive infiltration,
invasion, destruction, and penetration
of the surrounding tissue
- do not develop well- defined capsule
- microscopic examination reveals tiny,
crablike feet penetrating the
margin &
infiltrating adjacent structures
- next to the development of
metastases, local invasiveness is the most
reliable feature that distinguishes
malignant from benign tumors
D. Metastasis
- connotes the development of secondary
implants(metastases) discontinuous with
the primary tumor possibly in remote
tissues
- unequivocally identify a neoplasm as malignant
- not all cancers have equivalent ability to metastasize
Examples are basal carcinoma of the skin & most primar
tumors of the
CNS(highly invasive in their primary sites of origin
but rarely metastasize.)
- generally the more anaplastic & the larger the primary neoplasm,
the more likely is metastatic spread but exceptions abound

CHARACTERISTICS OF BENIGN & MALIGNANT NEOPLASMS


A. Differentiation and Anaplasia

refer only to the parenchymal cells that constitute the


transformed elements of neoplasms.

The differentiation of parenchymal cells refers to the extent


to which they resemble their normal forebears
morphologically and functionally.

The stroma carrying the blood supply is crucial to the growth


of tumors but does not aid in the separation of benign from
malignant ones.

The amount of stromal connective tissue does determine,


however, the consistency of a neoplasm
** Anaplasia refers to a reversion of differentiation in cells and is
characteristic of malignant neoplasms(tumors). Sometimes, the term
also includes an increased capacity for multiplication. [1]Lack of
differentiation is considered a hallmark of aggressive malignancies.
The term anaplasia literally means "to form backward
Benign neoplasms

composed of well-differentiated cells closely resembling


their normal counterparts

mitoses are extremely scant in number and are of normal


configuration.
Malignant neoplasms

are characterized by a wide range of cell differentiation,


from well differentiated to completely undifferentiated..

Anaplasia (lack of differentiation) is a hallmark of


malignancy. The cells:

display pleomorphism (marked variation in size & shape)

nuclei are hyperchromatic & large, variable & bizarre in size


& shape

nuclear-cytoplasmic ratio may approach 1:1 ( normal is 1:4


or 1:6)

MODES OF SPREAD OF MALIGNANT NEOPLASMS

Seeding within body cavities

occurs when neoplasms invade a natural body


cavity

is particularly characteristic of cancers of the


ovary, which often cover the peritoneal surfaces
widely.

Here is an instance of the ability to reimplant


elsewhere that seems to be separable from the
capacity to invade.

Lymphatic spread

More typical of carcinomas

pattern of lymph node involvement depends


principally on the site of the primary neoplasm and
the natural pathways of lymphatic drainage of the
site

Neoplastic cells are conducted to lymph nodes


where they become trapped & set up secondary
tumors

e.g.
* breast cancer spreading to lymph nodes in the axilla
* carcinoma of the tongue spreading to lymph nodes in the
neck

A "sentinal lymph node" is defined as the first


lymph node in a regional lymphatic basin that
receives lymph flow from a primary tumor

It can be delineated by injection of blue dyes or


radiolabelled tracers. Biopsy of sentinal lymph
nodes allows determination of the extent of spread
of tumor, and can be used to plan treatment.

Hematogenous spread or vascular spread

Most feared consequence of a cancer

Favored pathway for sarcomas but carcinomas


use it as well

arteries are penetrated less readily than are veins

With venous invasion, the blood-borne cells follow


the venous flow draining the site of the neoplasm,
with tumor cells often stopping in the first capillary
bed they encounter

All portal area drainage flows to the liver, All caval


blood flows to the lungs(the most frequently
involved secondary sites)
EPIDEMIOLOGY
o
Cancer Incidence

Overall, it is estimated that about 1.4 million new cancer


cases will occur in 2006, and 565,000 people will die of
cancer in the United States

Geographic and Environmental Factors

65% of common cancers are due to


environmental causes

26% to 42% - heritable factors

Geography Death rates

breast cancer fourfold to fivefold higher


in the USA & Europe compared with
Japan

stomach carcinoma 7 times higher in


Japan than in USA

Liver carcinoma is infrequent in the US


but is the most lethal in Africa (natives)

Environmental influences

workplace

food

personal practices like cigarette


smoking, chronic alcohol consumption,
age at first intercourse and number of
sex partners

Age

Frequency of cancer increases with age

due to the accumulation of somatic


mutations associated with the
emergence of cancer

decline in immune competence that


accompanies aging

Most cancer mortality occurs between ages 55 &


75 years

Rate declines after age 75

Cancer causes more than 10% of all deaths


among children younger than 15 years

major lethal cancers in children are


leukemia, tumors of the CNS,
lymphomas, soft tissue sarcomas and
bone sarcomas

Heredity

Mortality rate of lung cancer has been shown to


be
4 times greater among non-smoking relatives (parents & siblings) of
lung cancer patients than among nonsmoking relatives of controls
T H R E E C AT E G O R I E S O F H E R E D I TA RY F O R M S O F
CANCER
1.
Inherited Cancer Syndromes - inheritance of a
single mutant gene greatly increases the risk of a
persons developing a tumor.
e.g. Retinoblastoma - (Rb) is a rapidly
developing cancer that develops in the cells
of retina, the light-detecting tissue of the eye

40% are familial

carriers of the gene have a 10,000 fold


increased risk of developing
retinoblastoma (bilateral)

Increased risk of developing second cancer


particularly osteogenic sarcoma

Cancer suppressor gene implicated in


thepathogenesis of this tumor e.g. Familial
Adenomatous polyposis of the colon

individuals who inherit the gene will have


innumerable polypoid adenomas of the
colon at birth or soon thereafter

100% of patients develop carcinoma of the


colon by age 50

Associated with specific marker phenotype

e.g. presence of multiple benign tumors in familial


& multiple endocrine

polyposis
neoplasia
2.

Familial Cancers
e.g. carcinomas of colon, breast,
ovary & brain

Features that characterize familial


cancers

early age at onset

tumors arising in two or more


close relatives

sometimes multiple or
bilateral tumors

Familial cancers are not associated with


specific marker phenotypes
e.g. familial colonic cancers
do not arise in preexisting benign polyps

Transmission pattern is not clear

Certain familial cancers can be linked


to the inheritance of mutant genes
3.
Autosomal Recessive Syndromes of
Defective DNA Repair

Autosomal recessive disorder is


characterized by DNA or chromosomal
instability
e.g. xeroderma
pigmentosum DNA repair is defective
5% to 10% of all human cancers fall into
one ofthe three categories

ACQUIRED PRENEOPLASTIC DISORDERS


- clinical conditions which are predisposed to develop
malignant neoplasia
o
Persistent regenerative cell replication ( e.g. squamous
cell carcinoma in the margins of a chronic skin fistula or
in a long-unhealed skin wound; hepatocellular
carcinoma in cirrhosis of the liver)
o
Hyperplastic & dysplastic proliferations ( e.g.
Endometrialcarcinoma in atypical endometrial
hyperplasia; bronchogenic carcinoma in the dysplastic
bronchial mucosa of habitual cigarette smokers)
o
Chronic atrophic gastritis ( e.g. gastric carcinoma in
pernicious anemia)
o
Chronic ulcerative colitis ( e.g. an increased incidence
of colorectal carcinoma in long-standing disease)
o
Leukoplakia of the oral cavity, vulva, or penis (e.g.,
increased risk of squamous cell carcinoma)
o
Villous adenomas of the colon (e.g., high risk of
transformation to colorectal carcinoma)
ETIOLOGY
OF
CANCER:
CARCINOGENIC
AGENTS

Chemicals

Radiant energy

Microbial agents
Chemical Carcinogens

DIRECT ACTING AGENTS

require no metabolic conversion to become


carcinogenic
e.g. Alkylating agents

Anticancer drugs (cyclophosphamide, chlorambucil)

for leukemia, lymphoma, Hodgkin disease & ovarian

carcinoma later form a second cancer usually

leukemia
INDIRECT-ACTING AGENTS
- refers to chemicals that require metabolic conversion before
they become active
Radiation Carcinogenesis

Radiation is an established carcinogen

Sources: UV rays of sunlight, x-rays, nuclear fission,


radionuclides

Examples

Pioneers of roentgen x-rays developed skin


cancers

Miners of radioactive elements have suffered


increased incidence of lung cancer

Increased incidence of leukemia after a latent


period of 7 years in survivors of atomic bombs
dropped in Hiroshima & Nagasaki

High cancer incidence in the surrounding areas of


Chernobyl in Russia as a result of nuclear power
accident

Therapeutic irradiation like the development of


papillary thyroid cancers in 9% of individuals
exposed during infancy & childhood to head &
neck irradiation

Radiation is oncogenic
The effect of ionizing radiation is related to its mutagenic
effects: it causes chromosome breakage, translocations less
frequently point mutations
Natural UV radiation derived from the sun can cause skin
cancers (melanomas, squamos cell carcinomas & basal cell
carcinomas)

Cancers of the exposed skin are common in


Australia & New Zealand

Nonmelanoma skin cancers are associated with


total cumulative exposure to UV radiation,
whereas melanomas are associated with intense
intermittent exposure as with sunbathing

UV light has biologic effects on the cells like the


ability to damage DNA by forming pyrimidine
dimers

DNA damage is repaired by a complex set of


proteins
that effect nucleotide excision repair

UV light causes mutations in the TP53 gene

Three other disorders of DNA repair & genomic


instability that are characterized by an increased
risk of cancer:
1) ataxiatelangiectasia
2) Fanconi anemia
3) Bloom syndrome
Viral and Microbial Oncogenesis

RNA ONCOGENIC VIRUSES

Human T-Cell Leukemia Virus Type 1 (HTLV-1)

associated with a form of T-cell leukemia/lymphoma


that is endemic in certain parts of Japan & the
Carribean basin

human infection requires transmission of infected T


cells via sexual intercourse, blood products or breast
feeding

Leukemia develops in only 1% of infected individuals


after a latent period of 20-30 years

DNA ONCOGENIC VIRUSES

Human Papilloma Virus (HPV)

Types 1, 2, 4 & 7 cause benign squamos


papillomas
(warts) in humans

Has been implicated in the genesis of squamos


cell carcinoma of the cervix, anal, perianal,
vulvar and penile
cancer

20% of oropharyngeal cancers are HPVassociated

Types 16 & 18 are found in 75% to 100%


invasive
squamos cell cancers

Genital warts with low malignant potential are


associated with HPV-6 and HPV-11

Infection with high-risk HPV simulates the loss of


tumor
suppressor genes, activates cyclins, inhibits
apoptosis &
combats cellular senescence

Infection with HPV itself is not sufficient for


carcinogenesis

Epstein-Barr Virus (EBV)

Has been implicated in the


pathogenesis of :

Burkitt lymphoma which is


endemic in certain part of
Africa

Post-transplant
lymphoproliferative disease

primary CNS lymphoma in


AIDS patients

a subset of Hodgkin
lymphoma

nasopharyngeal carcinoma
which is endemic inSouthern
China

Hepatitis B Virus (HBV)

Strongly linked to hepatocellular


carcinoma likeHepatitis C virus (HCV)
which is not a DNA virus

Mechanism of HBV-related cancer

chronic liver cell injury and


regeneration predisposes cells
to mutation

disruption of normal growth


of liver cells

secondary arrangement of
chromosomes

HELICOBACTER PYLORI

causes peptic ulcer, gastric lymphoma


and gastric carcinoma

Gastric lymphomas
o
B-cell in origin
o
called MALTomas (marginal
zone associated lymphomas)
o
Pathogenesis- initial chronic
gastritis that causes lymphoid
follicles to develop in the
gastric mucosa

Gastric carcinoma
o
Pathogenesis initial
development of chroni
gastritis, followed by gastric
atrophy, intestinal metaplasia
of the lining cells, dysplasia &
cancer
Takes decades to complete &
occurs in only 3% of infected
patients

Patients with duodenal ulcers almost


never develop gastric carcinoma
ASPECTS
OF
NEOPLASIA

CLINICAL

Effects of Tumor on Host

Location & impingement on adjacent structures

A small (1-cm) pituitary adenoma can compress


& destroy the surrounding normal gland & give
rise to hypopituitarism

A 0.5-cm leiomyoma in the wall of renal artery


may lead to renal ischemia & hypertension

Small carcinoma within a common bile duct may


induce fatal biliary tract obstruction

Functional activity ( Hormone Synthesis)

seen in benign & malignant neoplasms arising in


endocrine glands

adenomas & carcinomas arising in the cells of


the islets of the pancreas often produce
hyperinsulinism, sometimes fatal

Production of bleeding & secondary infections when the


lesion ulcerates through adjacent surfaces tumor that
protrudes into the gut lumen may lead to ulceration &
obstruction
CANCER CACHEXIA

A wasting syndrome where there is progressive loss of body


fat and lean body mass accompanied by profound weakness
anorexia and anemia

There is in general some correlation between the size &


extent of spread of the cancer & the severity of the cachexia
Small, localized cancers are generally silent & produce no
cachexia
PARANEOPLASTIC SYNDROMES

These are symptom complexes that occur in patients with


cancer & that can not be readily explained by local or distant
spread of the tumor or by the elaboration of hormones
indigenous to the tissue of origin of the tumor

Appear in 10% to 15% of patients with cancer

Example- Clinical Syndrome


Underlying Cancer
hypercalcemia
breast carcinoma

renal carcinoma
Three classes of normal regulatory genes are the
principa targets of genetic damage:

1) growth- promoting protooncogenes


2) growth-inhibiting cancer suppressor genes
(antioncogenes)
3) genes that regulate programmed cell death

Oncogenes which are the mutant


alleles of protooncogenes are dominant
because they transform cells despite the
presence of their normal counterpart

4th category - genes that regulate repair of damaged DNA


which are pertinent in carcinogenesis

DNA repair genes affect cell proliferation


or survival indirectly by influencing the
ability of the organism to repair
nonlethal damage in other genes

A disability in the DNA repair genes can


predispose to widespread mutations

Carcinogenesis is a multistep process at both the phenotypic


and the genetic levels

The phenotypic attributes of a malignant


neoplasm which are acquired in a stepwise fashion
are: excessive growth, local invasiveness & the
ability to form distant metastases. This
phenomenon is called tumor progression.

At the molecular level progression results from


the accumulation of genetic lesions which are
favored by defects in DNA repair.

Cancer cells bypass the normal process of aging


which limits cell division.
Examples of cancer associated genes
1.
P53 tumor suppressor gene

one of the most commonly mutated


genes in human cancers

guardian of the genome- assists in DNA


repair

regulates apoptosis
2.
RB gene

loss of this gene is a common event in


breast cancer, small cell cancer of the
lung & bladder cancer
3.
ADENOMATOUS POLYPOSIS COLI (APC) gene

exerts antiproliferative effects

loss of this is common in colon cancer


Grading and Staging of Cancer

Grading attempts to establish some of cancers estimate


aggressiveness or level of malignancy based on the:

cytologic differentiation of tumor cells

number of mitoses within the tumor

degree of variability in cellular shape & size

The cancer may be classified as grade I, II, III or IV in order


of increasing anaplasia
Broders Classification- one of
of CA
Differentiaated Cells
Grade I
100 75%
Grade II
75 - 50%
Grade III
50 25%
Grade IV
25 0%

Cytologic (Papanicolaou) smears

Used widely for the discovery of carcinoma of the


cervix

Used also with other forms of suspected malignancy


like endometrial carcinoma, bronchogenic carcinoma
bladder & prostate tumors & gastric carcinomas

For identification of tumor cells in abnominal,


pleural, joint & cerebrospinal fluids

Immunocytochemistry

Powerful adjunct to routine histology

Prostate-specifc antigen (PSA) in metastatic deposits indicate


definitive diagnosis of a primary tumor in the prostate

Estrogen receptors & HER-2 (neu) indicate breast cancers

Flow cytometry

Used routinely in the classification of leukemias and


lymphomas

Useful in assessing DNA content of the tumor cells


BIOCHEMICAL ASSAYS

For tumor- associated enzymes, hormones and


other tumor markers in the blood

Prostatic carcinoma can be suspected when


elevated levels of PSA are found in the blood

Benign prostatic hyperplasia may have an


elevated PSA levels

Elevations in PSA are not diagnostic of cancer

the most widely used grading system


Undifferentiated Cells
0 25% well differentiated
25- 50% medium differentiation
50-75% poorly differentiated
75-100%

Staging of cancers is based on the

size of the primary lesion

its extent of spread to regional lymph nodes

the presence or absence of metastases

Staging is usually based on clinical and radiographic


examination (computed tomography and magnetic
resonance imaging) & in some cases surgical exploration.

Compared with grading, staging has proved to be of greater


clinical value
Two Methods of Staging
1.
TNM system (T, primary tumor; N, regional lymph node
involvement; M, metastases)
1.
AJC (American Joint Committee)
Cancers are divided into stages 0 to IV, incorporating the size of
primary lesions & the presence of nodal spread & of distant metastases
TNM
System
T1, T2, T3 and T4 describe the increasing size of the primary
lesion
N0, N1, N2 and N3 indicate progressively advancing node
involvement
M0 and M1 reflect the absence and presence of distant
metastases
Example of TNM method of breast cancer staging:
T0= breast free of tumor
N0= no axillary nodes involved
T1= local lesion <2 cm in size
N1= mobile nodes involved
T2= lesion 2-5 cm in diameter
N2=fixed nodes involved
T3= lesion >5 cm in diameter
N3=ipsilateral internal
T4= skin &/or chest wall
mammary node involved

involved
M0 = no metastases
M1 = demonstrable metastases
MX = suspected metastases

Cancers Seven Warning Signals


1.
2.
3.
4.
5.
6.
7.
8.
9.

Change in bowel or bladder habits


A sore throat that does not heal
Unusual bleeding or discharge
Thickening or lump in the breast or elsewhere
Indigestion or difficulty in swallowing
Obvious change in wart or mole
Nagging cough or hoarseness of voice
Unexplained anemia or paleness
Sudden unexplained weight loss

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