Neoplasia

Neoplasm means new growth

Neoplasms are irreversible growths
Neoplasm may be benign or malignant
Benign neoplasms :Tumours which do not invade adjacent tissues nor do they spread to
other areas
Simple surgical removal is curable
Malignant neoplasms :It is called as cancer
It infiltrates, grows rapidly and spreads to other areas
General characteristics of neoplasm
Differentiation and anaplasia
Differentiation means the extent to which a neoplasm resembles both histologically and
functionally the normal cells
Based on the differentiation it is classified into 3 types
i) Well differentiated : This maximally resembles normal cells. Seen in benign neoplasms.
ii) Moderately differentiated: This shows intermediate resemblance to normal cells
iii) Undifferentiated : This show hardly any resemblance to normal cells. Seen in malignant
neoplasms.
Lack of differentiation is called anaplasia

Differentiation is shown by the following morphological changes

1. Pleomorphism : It is defined as variation in size and shape of the cells or nucleus.
2.Alteration of nuclear cytoplasm ratio:
Normally nuclear- cytoplasm ratio is 1:4
3.Staining of nucleus: Abundant DNA in nucleus results dark staining called hyperchromasia
4.Mitosis: The rate of mitosis increases in malignancy
5.Loss of polarity: This means loss of normal arrangement of the tumour cells
6.Tumour giant cells: Tumour cells often form bizarre, giant cells

Classification and nomenclature of tumours

The tissue of origin and behaviour pattern forms the basis of tumour classification
Main characteristics of the classification are:
Suffix ‘oma’ is used to denote a neoplasm
Benign tumours of surface epithelium is called papilloma e.g

i) Squamous cell papilloma

ii) Transitional cell papilloma
iii) Columnar cell papilloma
 Classification and nomenclature of tumours
Benign tumours of epithelium are called adenomas e.g cystadenoma of ovary
When they produce mucin, they are called mucinous cystadenoma
When they produce serous fluid they are called as serous cystadenoma
Malignant tumours of epithelium are called as carcinomas e.g
Squamous cell carcinoma
Transitional cell carcinoma - urinary bladder
Adenocarcinoma

Classification and nomenclature of tumours

Benign tumours of connective tissue is named as:
Fibroma from fibrous tissue origin
Osteoma from osteoid of bone
Leiomyoma from smooth muscle
Malignant tumours of connective tissue is named as sarcoma e.g
Fibrosarcoma - fibrous tissue origin
Osteosarcoma - Malignant bone tumour
Chondrosarcoma - Malignant tumour of cartilage
Leiomyosarcoma –Malignancy of smooth muscle
Rhabdomyosarcoma- Malign of striated muscle

Etiology of Cancer
1.Racial factors

2.Environmental factors

3.Occupational factors

4.Lifestyle habits

5.Genetic factors

6.Alcohol and smoking

Alcohol abuse causes the following cancers:
Oropharyngeal carcinoma
Laryngeal carcinoma
Oesophageal carcinoma
Hepatocellular carcinoma

Smoking causes carcinoma of mouth, pharynx,

lung-90% , oesophagus and urinary bladder.
Genetic predisposition
Multiple genetic abnormalities predispose to cancer formation. There are 3 types:
1. Autosomal dominant e.g Retinoblastoma
2. Autosomal recessive e.g Xerodrema Pigmentosum
3. Familial : Some families may have higher frequency of cancer.
They are characterised by:
Early age of cancer onset
Two or more members having tumour
Multiple or bilateral tumours
Relatives have risk of two or three times more than non-relatives e.g Breast cancer,
Familial melanoma, Ovarian tumours
10 – 20 % breast cancer patients have familial origin

Non-genetic predisposition
Chronic diseases predispose to cancer
Certain diseases that cause cell proliferation may lead to neoplastic transformation
Chronic inflammatory conditions:
Marjolin’s ulcers: Skin ulcers following burns, varicose veins or chronic osteomyelitis
forming a sinus
They may give rise to squamous cell carcinoma
Gastric ulcers: 4% of gastric ulcers may become malignant

Chronic inflammatory conditions:

Ulcerative colitis: Colon shows ulceration and pseudopolyps which may turn malignant
Crohn’s disease:
Ulceration of small intestine, which may turn to become adenocarcinoma
Cholelithiasis (Gall stone) : A costant irritation by stone may cause development of cancer
Viral hepatitis: Particularly due to Hepatitis B and C virus may lead cirrhosis, which in turn
progress to carcinoma

Genesis of malignancy
Multiple factors may be involved.
Chronic inflammation cause cytokine production which stimulate proliferation of
transformed cells
Chronic inflammation cause increase in stem cells which are transformed by carcinogens
Genomic instability causing malignant transformation
 Premalignant conditions
Premalignant conditions are the signs that have high risk of cancer formation.
The important ones are:
Leukoplakia of oral cavity, penis and vulva
Villous and tubulovillus adenoma of colon
Ulcerative colitis
Chronic atrophic gastritis

Spread of Tumours

Types of spread:

1.Direct spread

2. Spread by metastasis

Direct spread:
1. Local spread - Breast carcinoma, Basal cell carcinoma

2. Lymphatic invasion- Most of carcinomas

3. Perineural invasion – Prostate carcinoma, Pancreatic carcinoma

4. Venous invasion- Most of sarcomas

5. Arterial invasion- sarcomas

Spread by Metastasis is mainly by:

1. Lymphatic spread
2. Vascular spread
3. Transcoelomic spread

Sentinal lymph node

The first lymph node in a regional lymphatic drainage that gets involved by tumour
metastasis is called Sentinal lymph node.
 Differentiation
Well differentiated neoplasm
Resembles mature cells of tissue of origin

Poorly differentiated neoplasm

Composed of primitive cells with little differentiation

Undifferentiated or “Anaplastic” tumor

Correlation with biologic behavior

Benign tumors are well differentiated
Poorly differentiated malignant tumors usually have worse prognosis

LAB DIAGNOSIS
1. BIOPSY
2. CYTOLOGY: (exfoliative)
3. CYTOLOGY: FNAC – (Fine Needle Aspirate Cytology)
4. IMMUNOHISTOCHEMISTRY
5. Categorization of undifferentiated tumors
Leukemias/Lymphomas
6. Site of origin
7. Receptors, e.g., ERA, PRA

TUMOR MARKERS
HORMONES: (Paraneoplastic Syndromes)
“ONCO”FETAL: AFP, CEA
ISOENZYMES: PAP, NSE
PROTEINS: PSA, PSMA (“M” = “membrane”)
GLYCOPROTEINS: CA-125, CA-19-5, CA-15-3
MOLECULAR: p53, RAS
MICRO-ARRAYS
THOUSANDS of genes identified from tumors give the cells their own identity and
FINGERPRINT and may give important prognostic information as well as guidelines for
therapy. Some say this may replace standard histopathologic identifications of tumors.