Download MBBS Surgery Presentations 48 Principles of Oncology Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Surgery 48 Principles of Oncology PPT-Powerpoint Presentations and lecture notes


PRINCIPLES OF ONCOLOGY

Dept. of Surgery

ETIOLOGY OF CANCER

A cancer, is thought to develop from a cell in which the

normal mechanisms for control of growth and proliferation

are altered.

Current evidence supports the concept of carcinogenesis as

a multistage process that is genetically regulated
The first step in this process is initiation, which requires

exposure of normal cells to carcinogenic substances.

Substances that may act as carcinogens or initiators include

chemical, physical, and biologic agents

Two major classes of genes are involved in carcinogenesis:

oncogenes and tumor suppressor genes

PATHOLOGY OF CANCER

Tumors may arise from any of four basic

tissue types
? Epithelial tissue
? Connective tissue (Muscle, bone, and cartilage)
? Lymphoid tissue
? Nerve tissue
Malignant cells are divided into those of epithelial

origin or the other tissue types.

? Carcinomas are malignant growths arising from epithelial

cel s.

? Sarcomas are malignant growths of muscle or connective

tissue.

? Adenocarcinoma is a malignant tumor arising from

glandular tissue.

TUMOR CHARACTERISTICS

? Invade and destroy the surrounding tissue.

? The cel s are genetical y unstable

? Loss of normal cel architecture results in cel s that are

atypical of their origin.

? Lose the ability to perform their usual functions.

? Metastasize, and consequently, recurrences are common

after removal or destruction of the primary tumor.
THE THREE AXES OF CANCER CLASSIFICATION

? Topographic site

Topographic

Histologic type

? Histology

site

(disease site)

? Anatomic extent

(Staging)

Patient'sAnatomic extent

Disease (TNM)

Staging: Why?

? To aid the clinician in planning treatment

? To give some indication of prognosis

? To assist in evaluating the results of treatment

? To facilitate the exchange of information between treatment

centers

? To contribute to continuing investigations of human

malignancies


ANATOMIC STAGING

Based on three components

T

The extent of the primary tumor

N

The absence or presence and extent of regional

lymph node metastasis

M

The absence or presence of distant metastasis

TUMOR (T): COLORECTAL CANCER








TUMOR (T): LUNG CANCER

T1 T2

T3

T4

CLINICAL, PATHOLOGIC, COLLABORATIVE STAGING

Clinical (cT, cN, cM)

Beforeinitiationofprimarytreatment

Importantindecidngprimarytreatment

Pathologic (pT, pN, pM)

Fromresctedtisues

Collaborative (CS)

Clinical,pathologicstaging&nonanatomic(site-specifc)factors
LIMITATIONS OF STAGING

Not used in hematologic malignancies
Ann Arbor Staging System
Not used in pediatric cancer

Not useful in rare diseases
Not enough cases to stratify T, N, M (Merkel Cel Cancer)
Lumping different histopathologic subtypes (Soft tissue

sarcoma: multiple histologies)

Dominated by anatomic pathology and histology (size,

nodes, histopathology, grade)
Gradual y incorporating other prognostic variables

DESCRIPTORS

Suffix

m

Presence of multiple primary T

pT(m)NM

Prefix

y

Post initial treatment (staging

ycTNM or

after preop treatment)

ypTNM

r

Recurrent tumor after a disease rTNM

free interval

a

Autopsy

aTNM
OTHER FACTORS

Histopathologic subtype
Adenocarcinoma, SCCA

Histology/Grade
Poor, mod, wel differentiated, Undifferentiated

Lymphovascular invasion
Residual tumor
RX, R0 ? 2 resections

Site-specific factors

? Breast: ER, PR, Her2-neu
? Thyroid: Age
? CRC: Microsatel ite instability, MMR, K-ras status
? Prostate: PSA, Gleason's Score

STAGING IN THE FUTURE?

Essential

TNM categories Histologic grade

Factors

Extramural venous invasion Obstruction
Quality of surgery

Additional

Grade Tumor perforation

Factors

Perineural invasion Invasion pattern
Medul ary type CEA serum level
Number of lymph nodes resected
Peritumoral lymphoid reaction

New and

Microsatel ite instability LOH 18q status

Promising

Factors

P53 DNA ploidy
VEGF, K-ras expression 20q copy number

Greene, CA Cancer J Clin

2008; 58:180-90


MANAGEMENT

? Prevention
? Screening
? Diagnosis
? Treatment
? Rehabilitation
? Follow-up care
? Palliative care
? Terminal Care

MULTIDISCIPLINARY APPROACH

FOR MANAGEMENT
Surgery

Nutrition

Radiation

Cancer

Management

Radiology

Chemotherapy

Pathology

GOALS OF CANCER TREATMENT

1- Primary goal

Cure the patient

Render him clinically and pathologically free of

disease and return their life expectancy to that of

healthy individuals of the same age and sex.
GOALS OF CANCER TREATMENT

2- The best alternative goal

To prolong survival while maintaining the

patient's functional status and quality of life.

3- The 3rd goal

Relieve symptoms such as pain for patients

in whom the likelihood of cure or prolonged

survival is very low

SURGERY

Long considered the most important aspect of cancer

treatment for solid tumours

Controls the disease local y

May be curative for many tumours especial y if caught

early
RADIATION THERAPY

? Local therapy

? Causes DNA damage to cancer cells and

leads to their death

? May be curative on its own

CHEMOTHERAPY

? Multitude of drugs developed to kil cancer cel s

? DNA damage, RNA damage, inhibit cell growth and

division, antimetabolites

? Can be used as sole modality for cure (hematologic

malignancies) or as adjunct to either surgery or radiation to
cure

? May also be given to incurable individuals to palliate
NEW PARADIGM OF TREATMENT

? Target unique proteins/genes/structures in cancer cells with novel

agents

? Differential toxicity between the tumour cell and normal tissues

? More specificity for tumours makes cancer kill greater

? Combine newer treatments with traditional strategies

? Molecular profiling
Oncogenes, protooncogenes, apoptotic markers, cytogenetics

This post was last modified on 08 April 2022