Cancer – Evidence of malignancy – B. Pharma 2nd Semester Pathophysiology notes pdf

Cancer – Evidence of malignancy

Content

Cancer

       Evidence of malignancy

       Carcinogenesis

       Pathogenesis of cancer

Objectives
 

At the end of this lecture, student will be able to

         Categorize the  evidence of malignancy

         List various tumor markers

         Discuss the etio-pathogenesis of cancer

         Describe 
various types of carcinogen

Evidence of malignancy

A. Clinical evidence

q  Age
of patient – cancer, a disease of adults

q  Rate
of growth – rapid growth of tumor indicates malignancy

q  Evidence
of infiltration  – sign of malignancy

q  Presence
of metastasis –  distant metastasis
indicates cancer that is not operable

B. Macroscopic evidence

       Tumor
makes its appearance either as a mass or as an ulcer

       Size
& shape of different tumor are different

       Benign
tumor
– Sharply marked from surrounding tissues, shows fibrous capsule all
around

       Malignant
tumor
– poorly defied, capsule is missing

       Different
tumor may have different color

       Malignant
melanoma – jet black

       Renal
cell carcinoma – yellow

       Most
of the cancers are greyish white in color

C. Microscopic evidence

q  Cytological
diagnosis :

       Discharges,
secretion, excretion and effusion in body cavities examined for the presence of
cancer cells

       Thin
smear of the materials are fixed, wet with ethyl alcohol and stained by special
techniques

       Aspiration
biopsy

       Tumor
mass is aspirated with a needle or syringe

       Cylinder
portion of tumor tissue is obtained

       Histological
sections are prepared

       If
fluid obtained – Smears are made for cytological diagnosis 

        Incisional biopsy

       Portion
of tumor tissue removed surgically, examined histologically

        Excisional biopsy

       Whole
of small lesion excised along with a safe margin of healthy tissue

q  Tumor
Marker

       Biochemical assays of products
elaborated by the tumour cells in blood or other body fluids

       Tumour markers include: cell surface
antigens (or oncofoetal antigens), cytoplasmic proteins, enzymes, hormones and
cancer antigens

Tumor
markers

Etio-pathogenesis
of cancer

CARCINOGENS

Carcinogens are categorized into 4 groups

       Chemical
carcinogens – includes chemicals and drugs

       Physical
carcinogens – includes radiations

       Hormonal
carcinogens

       Biological
carcinogens – Viruses

Chemical
carcinogenesis

Process of cellular transformation of chemical carcinogen
occurs in

2 stages Initiation
of carcinogenesis

         – Promotion
of carcinogenesis

q  Initiation
of carcinogenesis

2 types of chemical carcinogens – directly acting &
indirectly acting

       Directly
acting
(alkylating agents) – Does not require conversion to become
carcinogenic; Can induce cellular transformation

       Indirectly
acting/ Procarcinogens 
(aromatic
amines, azodyes)– require metabolic conversion to become active

Promotion
of carcinogenesis

       In
this stage, cells are selectively stimulated to proliferate by activation of growth
factor

       Promoters
of carcinogens – Phenols, Hormones, artificial sweeteners, drugs like
phenobarbitone

       Pro
carcinogenesis
– when 2 carcinogens acting simultaneously to enhance the
effect

Physical
carcinogenesis

Radiation carcinogenesis

       Ionising
radiations & UV rays can cause cancer

       UV
rays – immune suppression &DNA damage

     Eg. Squamous cell
carcinoma, basal cell carcinoma, malignant melanoma

       Ionising
radiations – X- rays, α
rays, β– rays, radioactive
isotope, protons, neutrons

     Eg. Blood cancer,
cancer of thyroid, skin, lungs, breast & salivary glands 

Non radiation carcinogens

       Mechanical
injury as a result of gall bladder stones, 
kidney stones, scars of bones & trauma

       Other
examples include glass and plastics

Hormonal
carcinogenesis

Organs or tissues which undergo proliferation under the
influence of hormones are likely to develop cancer

Examples:

       Estrogen
induced cancer
– breast cancer, squamous cell carcinoma, carcinoma of
cervix, tumor of myometrium

       Contraceptive
steroids
– oral contraceptives for long time can cause breast and liver
cancer

       Anabolic
steroids
– increases risk of developing cancer

Biological
carcinogenesis

       Viruses
cause different type of cancer (oncogenic viruses)

       Parasites
cause cancer of urinary bladder

       Bacteria
– gastric lymphoma and carcinoma

Examples of viruses causing cancer

       Human
papilloma virus

       Epstein
barr virus

       Hepatitis
B virus

Pathogenesis
of cancer

       Basis
for tumor formation – change in genetic factors leading to non-lethal damage to
cells

       2
genes involved during the development of cancer

      Growth
promoter proto oncogene

      Growth
supressor anti oncogene

       Most
well studied tumor suppressor gene – P53 gene

       P53,
critical gate keeper, prevent formation of cancer

       Localized
in nucleus, transcribe several gene when required

When DNA damage by irradiation, mutagenic chemical –
increase in

P53 gene – it binds to DNA – simulates its repair

2 major effects of P53 gene

       Cell
cycle arrest

       Apoptosis

ü  Cell
cycle arrest in late G1 phase – prevent cell from entering into next cell cycle

ü  Allows
time for DNA repair

ü  If
damaged repaired
– stimulates MDM2 gene, down regulates P53 gene
, relieve cell block

ü  If
damaged not repaired
– cell apoptosis

ü  Inhibition
of P53 gene by its mutation may leads to cancer

Summary

       Malignancy
can be determined by evidences obtained by clinical, microscopical examination
of tumor

       Carcinogens
are the agents that causes cancer

       Cancinogens
can be physical, chemical, hormonal or biological

        Basis for tumor formation is change in genetic
factors leading to non-lethal damage to cells

       2
genes involved during the development of cancer growth promoter proto oncogene
and growth suppressor anti oncogene

       P53
gene is mainly involved in the development of cancer

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