Biological overview of Cancer

1. PATHOPHYSIOLOGICA
L OVERVIEW OF
CANCER

3. CONTENT
INTRODUCTION
CATEGORIZATION OF TUMOURS.
BASIC COMPARISION OF BENIGN AND MALIGNANT TUMOURS.
NOMENCLATURE OF TUMOUR.
CARCINOGENESIS.
STEPS OF CARCINOGENESIS.
METASTASIS.
CASCADE OF METASTASIS.
PATTERNS OF SPREAD CANCER.
STAGING OF CANCERS.
EFFECTS OF TUMOUR ON HOST.
CAUSE OF DEATH FROM CANCER.
CONCLUSION.

4. INTRODUCTION
ONCOLOGY :
ONCOLOGY IS THE SPECIALIZED BRANCH OF MEDICINE THAT
DEALS WITH PREVENTION, DIAGNOSIS AND TREATMENT OF CANCER.
TUMOUR :
TUMOURS ARE NEOPLASTIC MASSES THAT MAY CAUSE SWELLING AT
THE SITE OF THEIR OCCURANCE.
CANCER :
CANCER IS NOT A DISEASE IN ITSELF RATHER IT IS A GROUP OF MORE
THAN 100 DISEASES CAUSED BY UNCONTROLLED DIVISION OF THE CELLS.

5. CATEGORIZATION OF TUMOURS
ON THE BASIS OF THEIR BIOLOGICAL BEHAVIOUR THE TUMOURS
MAINLY CAN BE CATEGORIZED INTO TWO MAJOR GROUPS –
 BENIGN TUMOURS
 MALIGNANT TUMOURS
 BENIGN TUMOURS : THEY ARE MASS OF CELLS WHICH DO NOT HAVE
CAPABILITY TO INVADE NEARBY TISSUE OR SPREAD TO OTHER REMOTE
SITES IN THE BODY OF HOST.
 MALIGNANT TUMOURS : THEY ARE OPPOSITE OF BENIGN TUMOURS SINCE
THEY HAVE ABILITY TO INVADE THE NEARBY TISSUE OR SPREAD
(METASTASIS ) TO THE DISTANT SITES OF THE BODY AWAY FROM THEIR
SITES OF ORIGIN.

6. BASIC COMPARISION OF BENIGN AND MALIGNANT TUMOURS
FEATURE BENIGN MALIGNANT
GROWTH RATE SLOW VARIABLE, MAY BE
RAPID
MARGIN ENCAPSULATED INVASIVE
LOCAL EFFECT LITTLE DESTRUCTIVE
DIFFENRENTIATION GOOD VARIABLE, MAY BE
POOR
METASTASIS NO FREQUENTLY
USUAL OUTCOME GOOD FATAL

7. COMPARISION BETWEEN A BENIGN AND MALIGNANT
TUMOUR OF MYOMETRIUM

8. NOMENCLATURE OF TUMOUR
NOMENLATURES OF TUMOUR CAN MAINLY BE DONE ON THE BASIS OF
THEIR TISSUE OF ORIGIN, MACROSCOPIC AND MICROSCOPIC PATTERN.
A. NOMENCLATURE OF BENIGN TUMOURS :
IN GENERAL THE BENIGN TUMOURS ARE DESIGNATED BY ATTACHING THE
SUFFIX “ –OMA ’’, TO THE CELL TYPE FROM WHICH THE TUMOUR ARISES.
EXAMPLE :
1. CHONDRO ( RELATED TO CARTILAGES ) + OMA = CHONDROMA.
2. OSTEO ( RELATED TO BONE ) + OMA = OSTEOMA.
3. ADENO ( RELATED TO GLAND ) + OMA = ADENOMA.

9. B. NOMENCLATURE OF MALIGNANT TUMOURS :
THE NOMENCLATURE OF MALIGNANT TUMOURS ARE SAME AS THE BENIGN
TUMOURS WITH SOME EXCEPTIONS AND ADDITIONS –
a) SARCOMA – THEY ARE MALIGNANT TUMOURS WHICH ARISES FROM THE
MESENCHYMAL TISSUE OR IT’S DERIVATIVES. HERE THE SUFFIX “ SARCOMA
’’ WOULD BE ATTACHED IN FRONT OF THEIR CELLS OF ORIGIN.
EXAMPLE :
1. FIBRO ( REALTED TO FIBROUS TISSUE ) + SARCOMA = FIBROSARCOMA.
2. CHONDRO ( RELATED TO CARTILAGES ) + SARCOMA = CHONDROSARCOMA.

10. b) CARCINOMA – TUMOURS OF EPITHELIAL CELLS ARE KNOWN AS
CARCINOMA.
EXAMPLE :
1) RENAL CELL CARCINOMA (RCC).
2) BASAL CELL CARCINOMA (BCC) OF SKIN.
3) SQUAMOUS CELL CARCINOMA (SCC) OF SKIN.
c) LYMPHOMA – GENERALLY THE LYMPHOMAS ARE MALIGNANT
TUMOURS OF IMMUNE SYSTEM WHICH USES SUFFIX “OMA”
EXCEPTIONALLY (AS THE SUFFIX “OMA” IS USED FOR BENIGN
TUMOURS.
EXAMPLE :
1) HODGKIN’S LYMPHOMA.
2) NON HODGKIN’S LYMPHOMA (NHL).
3) MULTIPLE MYELOMA.

11. CARCINOGENESIS
CARCINOGENESIS / ONCOGENESIS ARE TERMS WHICH ARE USED TO
DESCRIBE THE PROCESS OF CHANGING OF A NORMAL CELL INTO
CANCER CELL.
THE CARCINOGENESIS IS A COMPLEX AND MULTISTEP PROCESS
STEPS OF CARCINOGENESIS :
 INITIATION : INITIATION IS THE DIRECT EXPOSURE OF DNA TO A
CARCINOGEN, RESULTING IN IRREVERSIBLE CHANGES THAT WILL
PERMIT MALIGNANT TRANSFORMATION. INITIATION IS THE FIRST
STEP OF CARCINOGENESIS.
 PROMOTION : ENHANCEMENT OF GROWTH OF THE INITIATED
CANCER CELL IS KNOWN AS PROMOTION AND THE AGENTS THAT
PROMOTE TUMOUR GROWTH ARE KNOWN AS PROMOTERS,
EXAMPLE :- CHEMICALS, DRUGS, HORMONES,ETC.
 PROGRESSION : IN THIS STEP OF CARCINOGENESIS THE TUMOUR
DEVELOPS NEW BLOOD SUPPLY (ANGIOGENESIS) TO FULFILL THEIR
NUTRITIONAL DEMANDS.

12. STEPS OF CARCINOGENESIS.
 CLINICAL CANCER: FINALLY, THE NEOPLASM BECOMES MANIFEST AS A
CLINICALLY SIGNIFICANT TUMOUR. UNLESS REMOVED, IT WILL
CONTINUE TO PROGRESS.

13. METASTASIS
METASTASIS IS THE MOVEMENT OF CANCER CELLS FROM THE
PRIMARY SITE LOCATION AND THE ESTABLISHMENT OF
SECONDARY TUMOURS AT REMOTE SITE. ALTHOUGH THE
METASTASIZED TUMOUR CELLS ARE NOW IN A DIFFERENT
ORGAN, THEY ARE STILL KNOWN BY THE PRIMARY CANCER
TYPE.

14. CASCADE OF METASTASIS
 METASTASIS INVOLVES SEVERAL DISTINCT STEPS OR PROCESSES KNOWN
AS THE METASTATIC CASCADE.
1) VASCULARIZATION OR ANGEOGENESIS : INCREASED TUMOUR SIZE
STIMULATES FORMATION OF NEW BLOOD VESSELS FOR THE
NUTRITIONAL SUPPLY, THIS PROCESS IS KNOWN AS VASCULARIZATION
OR ANGEOGENESIS.
2) INVASION : THE MALIGNANCY EXTENDS INTO SURROUNDING TISSUE
BY PRODUCING ENZYMES THAT DISSOLVE SUBSTANCES THAT HOLD
NORMAL CELLS TOGETHER. THE TUMOUR ALSO PRODUCES AGENTS
THAT HELP MOVE TUMOUR CELLS INTO NORMAL TISSUE.
3) INTRAVASION : IN THIS PROCESS THE TUMOUR PENETRATES INTO
BODY CAVITIES AND BLOOD VESSELS.
4) EMBOLIZATION AND TRANSPORT : TUMOUR CELLS ARE CARRIED TO
OTHER BODY SITES, WHILE DOING THIS MOST OF THE TUMOUR CELLS
ARE KILLED BY THE HOST IMMUNE SYSTEM AND ONLY 1% TUMOUR
CELLS RECHING THIS STAGE.

15. 5) ARREST : EVENTUALLY THE TUMOUR CELLS ARE TRAPPED IN THE
CAPILLARY BED OF THE TARGET ORGAN, AND THE CLOT OF BLOOD
SURROUND THE TUMOUR CELLS AND THIS WAY THE TUMOUR CELLS
ESCAPE THE DETECTION OF HOST’S IMMUNE SYSTEM.
6) EXTRAVASATION : THE TUMOUR CELL RELEASES ENZYMES THAT
DISSOLVE THE BLOOD VESSEL MEMBRANES AND ALLOW THE CELLS TO
INVADE THE SURROUNDING TISSUES.
7) ESTABLISHMENT : THE MALIGNANT CELLS MANIPULATE THE NEW
ENVIRONMENT TO PROMOTE GROWTH AND DEVELOPMENT OF THE
METASTATIC COLONY. IF IT IS UNABLE TO ESTABLISH ITS OWN
VASCULAR SUPPLY IN THIS NEW LOCATION, THE COLONY WILL DIE.

16. PATTERNS OF SPREAD OF CANCER
SPREAD OF THE CANCER MAY OCCUR IN SEVERAL WAYS –
1) BY LOCAL INVASION - AS THE TUMOUR INVADES, ADJACENT TISSUES ARE
DISPLACED AND DESTROYED TO BE REPLACED BY TUMOUR. BECAUSE OF
IRREGULAR MARGIN OF THE TUMOUR COMPLETE SURGICAL REMOVAL OF
THE TUMOUR IS NOT POSSIBLE AND DUE TO THIS SOME TUMOUR BEING
LEFT BEHIND, WHICH PROLIFERATES AND GIVE RISE TO LOCAL
RECCURANCE.
2) BY LYMPHATIC VESSELS – INVASIVE TUMOURS CAN PENETRATE THE THIN
WALL OF LYMPHATICS. THEN FRAGMENTS OF TUMOUR ARE CARRIED
DOWNSTREAM TO LODGE IN ONE OR MORE LOCAL LYMPH NODES. IF THE
TUMOUR CELLS SURVIVE THIS JOURNEY AND PROLIFERATE IN THE NODE
THEY FORM A METASTASIS, OR SECONDARY TUMOUR.

17. 3) BY BLOOD VESSELS – THIN WALLED BLOOD VESSELS ARE SIMILARLY AT
RISK OF TUMOUR INVASION. THE FRAGMENTS OF TUMOUR CAN LODGE IN
THE CAPILLARY BED, WHERE THEY MAY DEVELOP INTO SECONDARY
METASTASIS.
4) ACROSS CAVITIES – ACCESS TO THE PLEURA ENABLES TUMOUR CELLS TO
SEED THEMSELVES ARROUND THE PLEURAL CAVITY, FORMING NUMEROUS
FURTHER DEPOSITS OR SEEDLINGS.
5) IMPLANTATION – OCCASIONLLY THE TUMOUR CELLS MAY BE IMPLANTED
IN THE SCAR BY THE SURGEON’S KNIFE WHILE REMOVING A TUMOUR.

18. STAGING OF CANCERS
 TO ESTIMATE THE EXTENT OF SPREAD OF A TUMOUR AT THE TIME OF
INITIAL DIAGNOSIS IS CALLED STAGING. A NUMBER OF STAGING
CLASSIFICATIONS ARE IN USE –
a) THE SIMPLEST AND OLDEST CLASSIFICATION IS AS FOLLOWS –
STAGE 1 – TUMOUR CONFINED TO THE ORGAN OF ORIGIN.
STAGE 2 – LOCAL LYMPH NODES INVADED.
STAGE 3 – INVASION OF DISTANT NODES, OR LOCAL SPREAD BEYOND THE
ORGAN OF ORIGIN.
STAGE 4 – BLOOD-BORNE METASTASIS PRESENT.

19. b) TNM CLASSIFICATION – IT IS THE INTERNATIONALLY RECOGNISED
STAGING SYSTEM.
T-EXTENT OF PRIMARY TUMOUR
N- EXTENT OF REGIONAL LYMPH NODE INVOLVEMENT
M-PRESENCE OR ABSENCE OF METASTASIS
EXTENT OF DISEASE – T0 EXCISED TUMOUR
T1
T2
T3
EXTENT OF NODAL INVOLVEMENT – N1
N2
N3
PRESENCE OF METASTASIS –
M0 – NOT PRESENT
M1 – PRESENT
INCREASING PRIMARY TUMOUR SIZE.
INCREASING INVOLVEMENT.

20. EFFECTS OF TUMOUR ON HOST.
 THE EFFECT OF TUMOUR IS MAINLY DEPENDS ON THE SITE OF ITS
OCCURANCE.
 LOCATION – IT IS CRITICAL BECAUSE A SMALL (1cm) PITUTARY ADENOMA
CAN COMPRESS AND DESTROY THE SURROUNDING NORMAL GLAND WHICH
MAY CAUSE HYPOPITUTARISM.
 TUMOURS ARISING IN ENDOCRINE GLANDS CAN AFFECT THE HORMONE
PRODUCTION ABILITY.
 CANCER ARISING IN THE BETA CELLS OF ISLETS OF PANCREAS OFTEN
PRODUCE HYPERINSULINISM.
 TUMOUR ON THE SURFACE OF THE ORGANS OR SKIN CAN CAUSE
ULCERATION AND BLEEDING OR SECONDARY INFECTION.
 CANCER OF THE LUMEN OF THE GUT CAN CAUSE OBSTRUCTION.
 CANCER RELATED CACHEXIA (WEIGHT LOSS & MUSCLE WASTING) AND
PARANEOPLASTIC SYNDROMES ARE THE MAJOR CAUSES OF CANCER
RELATED HEALTH ISSUES.

21. CAUSE OF DEATH FROM CANCER
 CAUSES OF DEATH FROM CANCER ARE SITE SPECIFIC.
 MAINLY PATIENTS WITH LOCALLY ADVANCED OR METASTATIC CANCER
BECOME BEDRIDDEN AND DIE FROM BRONCHOPNEUMONIA OR
METABOLIC DISTURBANCES.
 SOMETIMES THERE MAY BE LIVER FAILURE DUE TO NUMEROUS LIVER
SECONDARIES.
 PATIENTS WITH THE CANCER ARE STILL AT RISK OF NON-NEOPLASTIC
CONDITIONS SUCH AS CORONARY ARTERY DISEASE (CAD).
 OFTEN ACTUAL CAUSE OF DEATH FROM CANCER IS UNCLEAR AND IT IS
IMPORTANT TO CARRYING OUT A POST-MORTEM EXAMINATION TO
KNOW THE REASONABLE CAUSE OF DEATH.

22. CONCLUSION
APPART FROM CARDIOVASCULAR DISEASES (CVDs) CANCER IS THE
SECOND MOST LETHAL DISEASE WHICH IS THE CAUSE OF MILLIONS
OF DEATH ANNUALLY. FOR THE PREVENTION DIAGNOSIS,
TREATMENT AND BETTER POSSIBLE CLINICAL RESULTS. IT IS
IMPORTANT TO UNDERSTAND THE BIOLOGICAL BEHAVIOUR OF THE
CANCER, APPART FROM THIS THE UNDERSTANDING OF
PATHOPHYSIOLOGICAL ASPECT OF CANCER IS ESSENTIAL AS WELL AS
INTEGRAL PART TO PLANT THE TREATMENT STRATEGY FOR
SATISFACTORY OUTCOME.

23. THANK YOU