Week 12 Introduction to Cancer

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Introduction to Cancer

Biomedical Science and Nursing 2Week 12



10 facts about Cancer (WHO, 2006)

1. There are more than 100 types of cancers; any part of thebody can be affected.

2. In 2005, 7.6 million people died of cancer - 13% of the 58million deaths worldwide.

3. More than 70% of all cancer deaths occur in low and

middle income countries.4. Worldwide, the 5 most common types of cancer that kill

men are (in order of frequency): lung, stomach, liver,colorectal and oesophagus.

5. Worldwide, the 5 most common types of cancer that killwomen are (in the order of frequency): breast, lung,stomach, colorectal and cervical.



10 facts about Cancer (WHO, 2006)

6. Tobacco use is the single largest preventable cause ofcancer in the world.7. One fifth of all cancers worldwide are caused by a chronic

infection, for example human papillomavirus (HPV) causescervical cancer and hepatitis B virus (HBV) causes livercancer.

8. A third of cancers could be cured if detected early andtreated adequately.

9. All patients in need of pain relief could be helped if currentknowledge about pain control and palliative care wereapplied.

10.40% of cancer could be prevented, mainly by not usingtobacco, having a healthy diet, being physically active andpreventing infections that may cause cancer.



What is Cancer?

A definition• Cancer is " a general term for a large group of diseaseswhich all display uncontrolled growth and spread ofabnormal cells. The process of cell division, by whichtissues normally grow and renew themselves, gets out ofcontrol. These cancer cells multiply in an uncoordinatedway, usually to form a tumour. Cells from the original, orprimary, cancer site may infiltrate surrounding tissue tocause damage. They may also travel by means of thebloodstream or lymph system to form secondary cancerselsewhere in the body.”

(The Cancer Word Book, C.C.V., 2001)• Cancer is defined as the loss of cell division control



US Mortality, 2003

Source: US Mortality Public Use Data Tape 2003, National Center for Health Statistics, Centers for Disease Controland Prevention, 2006.

1. Heart Diseases 685,089 28.0

2. Cancer 556,902 22.7

3. Cerebrovascular diseases 157,689 6.4

4. Chronic lower respiratory diseases 126,382 5.2

5. Accidents (Unintentional injuries) 109,277 4.5

6. Diabetes mellitus 74,219 3.0

7. Influenza and pneumonia 65,163 2.7

8. Alzheimer disease 63,457 2.6

9. Nephritis 42,453 1.7

10. Septicemia 34,069 1.4

Rank Cause of Death

No. of

deaths

% of all

deaths



Trends in the Number of Cancer DeathsAmong Men and Women, US, 1930-2003

0

50,000

100,000

150,000

200,000

250,000

300,000

1930 1940 1950 1960 1970 1980 1990 2000

Women

Men

N u m b e r o f C a n c

e r D e a t h s

265,000

270,000

275,000

280,000

285,000

290,000

2000 2001 2002 2003

Men

Women

Source: US Mortality Public Use Data Tape, 2003, National Center for Health Statistics, Centers for Disease

Control and Prevention, 2006.



Normal Cell Biology

• The basic unit of structure & function in all livingthings is the cell.

• Most cells have the ability to reproduce

• Control mechanisms govern cell replication

• The normal healthy cell perfectly copies itself overand over.



Cell Biology

• Conditional RenewalCells which have the ability to regenerate or reproduce butonly do so under special circumstances Eg. Osteocytes ofbone, parenchymal cells of the liver

• Continuous Renewal

Cells which regenerate frequently & have a life spanmeasured in hours or days Eg. White blood cells, epithelialcells

• Essentially non- renewing

Cells which live for the entire life of the organism Eg. Nervecell bodies, myocardial muscle cells



Cancer Cell Biology

• If something goes wrong and the usual restrictionsplaced by the host on cell replication do not occur,abnormal cellular growth results

• Hyperplasia – increase in number of cells

• Metaplasia – transformation of a cell• Dysplasia – abnormal tissue development

• Anaplasia – loss of differentiation

• Neoplasia – the process resulting in the formationor growth of a neoplasm (abnormal tissue, fastergrowth)



Cancer Cell Biology

• Tumor - abnormal swelling – may be malignant or benign

• Neoplasm - new growth of cells and often refers to a tumoror a cancerous growth

• Benign neoplasm - is a growth which is not malignant

– slow growing

– encapsulated and looks like cell of origin

• Malignant neoplasm - immature cells

– grows rapidly

– invades and spreads

– does not look like cell of origin



Classification

• Benign & malignant tumours are named accordingto tissue of origin

• Tumours are classified according to their behaviour& their cell type

• Malignant tumours are divided into 3 subgroups: – Carcinomas

– Sarcomas

– Leukaemias & lymphomas



Examples of Malignant Neoplasms

• Carcinoma - cancer arising from epithelial tissuee.g. skin - squamous cell carcinoma or from asolid/hollow organ e.g. rectum/liver

• Sarcoma - cancer arising from connective tissuee.g. bone – osteosarcoma

• Glioma - cancer arising from connective tissue inthe CNS

• Lymphoma - cancer arising from the lymph-reticularsystem

• Myeloma - cancer arising from myeloid cells or cellforming tissue



Characteristic Malignant BenignEncapsulated Rarely Usually

Differentiated Poorly Partially

Metastases Frequently present Rarely

Recurrence Frequent Rare

Vascularity Moderate to marked Slight

Mode of growth Infiltrative & expansive Expansive

Cell characteristics Cells abnormal &become moreunlike parent cells

Fairly normal;similar to parentcells



Cancer Cell Properties

• Immortal• Limited contact inhibition

• Diminished growth requirements

• Grow without anchorage support• Loss of restriction point in cell cycle

• Disorderly and multi-layered patterns of growth



Carcinogenesis

• Process in which cancer develops• Transformation of normal cells to cancer cells

involves the steps of:

– Initiation

– Promotion

– Progression

– Carcinogens



Cancer - A Disease of the Genes

• Carcinogens - agents that have the capacity to permanentlyalter the molecular structure of the genetic component of acell (DNA)

– elimination of 1 of the components of the DNA chain

– errors in DNA repair• This is different to a “hereditary” cancer where the mutated

gene is passed down to children



Protoncogenes Oncogenes

• Normal cell gene

• Function to tightly regulate& control normal cellproliferation &differentiation

• Can be damaged by avirus, mutation/ carcinogenetc to become anoncogene

• Genes that may cause

cancer if mutated/ regulatory mechanismdamaged

• Mutated forms of

protoncogenes (normalgenes)

• Regulation of these genesusually well controlled bythe body

Tumor suppressor genes – normal - inhibit cell proliferation and growththerefore, if inactivated, cancer may develop



Risk factors

• Chemical Carcinogens – Polycyclic aromatic hydrocarbons (smoke, exhaustfumes, products of combustion)

– Aromatic amines & azo dyes (coal tar, insecticides,food dyes)

– Alkylating agents (mustard gas, cyclophosphamide)

– Nitrosamines (nicotine, food additives)

– Industrial compounds, asbestos

• Radiation Carcinogens

– Ionizing radiation

– Atomic bomb detonation

– Ultraviolet radiation



Risk factors

• Viruses – Herpes Simplex –type II

– Epstein Barr

– Human Papilloma Virus

• Genetic Factors

– Down’s Syndrome

– Familial Cancers

• Genetic Factors – Deficient immune system (HIV, organ

transplant)



Risk Factors for Developing Cancer

• Risk Factor - element of personal behaviour or geneticmakeup, or exposure to a known cancer causing agent thatincreases a person’s chance of developing a particular formof cancer

• Non controllable

– Hereditary, age, gender, socio-economic status, geneticpredisposition

• Controllable

– Stress, diet, occupation, tobacco, alcohol, obesity, sun

exposure, geographical location, environmental factors,sexual practices



Risk Factors for Selected Cancers

CANCER SITE HIGH RISK FACTORS

Lung Heavy smoking over age 50Asbestos exposure

Breast Family history

Diet high in fatNulliparous

Colo-rectal Obesity Increasing ageFamilial adeno-polyposis

Skin Excessive exposure to UV radiationFair skinFamily history

SEVEN WARNING SIGNS OF CANCER



SEVEN WARNING SIGNS OF CANCER

“CAUTION”

• Perubahan pd kebiasanBAB & BAK

• Adanya luka yg sulitsembuh

• Perdarahan/sekresi yg takbiasa

• Benjolan pd dada ataubagian tubuh lain

• G3 mencerna makananatau sulit menelan

• Perubahan pada tahi lalat

• Batuk atau suara serak ygtidak mau hilang

•C…

Change in bowel &bladder habits

• A…A sore that doesn’t heal

• U…Unusual bleeding or

discharge• T…Thickening or a lump in

the breast or elsewhere

• I…Indigestion or difficulty in

swelling• O…Obvious charge in a

wart

• N…Nagging cough or

hoarseness



Metastases

• Invasion/ direct spread• Lymphatic dissemination

• Gravitational dissemination

• Blood stream dissemination

– Vascularisation – Cell detachment

– Aggregation

– Arrest

– Establishment – Proliferation



Copyright © 2006 by the American Roentgen Ray Society

Ibukuro, K. et al. Am. J. Roentgenol. 2001;176:1059-1065

Diagrams of vertebral venous system in thoracic inlet

Anterior view:

• Az = azygos vein,

• EDV = epidural venous plexus,

• DCV = deep cervical vein,

• IVV = intervertebral vein,

• LBCV = left brachiocephalic vein,

• LPV = longitudinal prevertebral vein,

• RSICV = right superior intercostalvein,

• VV = vertebral vein,

• ICV = intercostal vein. Asterisk

indicates esophageal veins, dottedline indicates peripheral branches ofdeep cervical vein in back neck.



Metastatic spread

• Is not just a “random process”• Main sites of metastases are to:

– liver

– lung – bone

– lymph nodes

• Undifferentiated tumors more likely to metastasizethan well differentiated tumor



Characteristics of malignant tumours

• Progressive, uncontrolled growth at secondary site• Metastatic cells more poorly differentiated than the

primary tumour - can make them more difficult totreat

• Able to penetrate basement membrane• Anchorage-independent growth

• Secondary tumours can develop and maintain theirown blood supply



Usual sites of Metastasis

Breast Cancer Lymph nodes, Bone marrow, lung,liver, brain

Colo-rectal Cancer Lymph nodes, liver, bone marrow

Lung Cancer Liver, brain, adjacent structures

Prostate Cancer Bone, Pelvic structures

Leukemia CNS, Visceral organs

Cervical Cancer Adjacent pelvic structures, lymphnodes



Manifestations of Cancer

• Tumour involvement• Invasion

• Infiltration

• Compression

• Metastases

• Systemic effects

• Associated with treatment

• Related to chronic / debilitating disease



Principles of Treatment

The goals in the treatment of cancer are:• Cure

• Control

• Palliation



Treatment decision

• Age• Size and site of tumour

• Staging

• Aggressiveness of thecancer

• Prognosis

• Quality of life

• Predictability ofspread

• Expected cure rate

• Risks associated withtreatment

• Host resistance

• Patient’s wishes



Surgery

• Oldest form of cancer treatment• Diagnosis & staging

• Cure

• Palliation• Reconstruction

• Prevention



Surgery & Nursing Implications

• Pre operative care

• Education

• Post operative care• Assessment

• Preventing post operative complications

• Rehabilitation



Chemotherapy

• Use of chemicals to treat cancer• Target rapidly dividing cells

• Over 50 chemotherapeutic agents in use

• Cure• Control

• Palliation



Chemotherapy & Nursing Implications

• Assessment

• Education

• Cytotoxic precautions• Management of side effects of therapy



Radiotherapy

• Use of high energy x-rays to treat cancer• 60% of cancer patients will receive radiotherapy

• Alters the biological material in the atom of the cell

• Cure• Control

• Palliation



Biotherapy

• Use of agents from biological sources to affect thebody’s biological responses

• Manipulate the immune system

• Cytokines

• Interferon

• Antibodies

• Growth factors



5 year survival by cancer type

• 60% ALL CANCERS• 91% MELANOMA

• 12% LUNG

• 85% PROSTATE• 84% BREAST

• 58% BOWEL



Colorectal cancer – an overview

• Highest incidence of all cancers• 2nd leading cause of cancer related death

• Risk increases from age 40 & onwards

Risk factors are:

• Familial adeno polyposis (FAP)

• Hereditary nonpolyposis colorectal cancer(HNPCC)

• Diet• Inflammatory bowel disease

Ri k F



Risk Factors

•Familial adeno polyposis (FAP) – genetic disorder causing cancer in 100% pts

by age 50 – Accounts for 1 % of colorectal cancer

• Hereditary nonpolyposis colorectal cancer – genetic disorder causing cancer in 70% ptsby age 65

– accounts for 4% of colorectal cancer

• Inflammatory bowel disease – ulcerative colitis• Diet

FAMILIAL ADENOPOLYPOSIS



FAMILIAL ADENOPOLYPOSIS

• an inherited disorder characterized by thedevelopment of myriad polyps in the colon,beginning in late adolescence or early adulthood.

Untreated, the condition nearly always leads tocolon cancer

Ri k f t



Risk factors

• Diet- attributed to 50% of colorectal cancer• Strong correlation between diet and colorectal

cancer• Incidence greatest in industrialised western

countries – diet high in refined carbohydates – diet high in saturated fats – diet high in animal fats - red meat

– diet low in fibre – diet low in vegetables esp green leafyvegetables

– diet high in alcohol/low in folate

Wh t l t l ?



What causes colorectal cancer?

• Diet – 50%• Genetics – 15%

• Unknown Factors – 22%

• Inactivity – 13%

Cli i l



Clinical course

• Most colorectal cancers develop from a benign

precursor lesion or adenoma (polyp)• Dysplastic changes occur in the original

lesion/polyp - becomes malignant, grow and invadeinto surrounding tissue

• Eventual penetration through the bowel wall & localspread into surrounding tissues/organs/lymphnodes

• Spread widely through the lymphatic system andblood stream

• Most common sites of spread are to the liverfollowed by peritoneal cavity, lung, adrenals,

ovaries & bone

S i f C l t l C



Screening for Colorectal Cancer

• Screening is usually done for people who have astrong family history of colorectal cancer -recommended for people over 50

• For those people with a genetic predisposition/risk

factors - screening needs to be done on a morefrequent basis

• Screening involves the following:

– early FOB to check for bleeding/PR examination – Sigmoidoscopy/colonoscopy every 3 to 5 years

T t t f l t l



Treatment for colorectal cancer

• Surgery – Curative – palliative

• Chemotherapy – Used post operatively for patients with stage II/III disease

– Advanced disease• Radiotherapy

– Pre & Post operatively – Used for patients with high risk of local recurrence

– Positive lymph nodes – Painful metastases

L i



Lung cancer – an overview

• Is the 4th site of new cancers• Leading cause of cancer deaths• Incidence & mortality rates are declining in males

but increasing in females

Risk Factors are:• Smoking – Active & passive

• Exposure to asbestos

– Malignant Mesothelioma• ? Exposure to radiation & other chemicals

– Heavy metals

T pes of l ng cancer



Types of lung cancer

• Non Small Cell Lung cancer (NSCLC)(approx 80%)

– Squamous cell (approx 30%)

– Adenocarcinoma (approx 30-50%) – Large cell (approx 10-15%)

• Small Cell Lung Cancer (approx 20%)

SQUAMOUS CELL LUNG CANCER



SQUAMOUS CELL LUNG CANCER

• Cancer that begins in squamous cells, which arethin, flat cells that look like fish scales.

• Squamous cells are found in the tissue that formsthe surface of the skin, the lining of the hollow

organs of the body, and the passages of therespiratory and digestive tracts.

• Also called epidermoid carcinoma.

ADENOCARCINOMA



ADENOCARCINOMA

• "Adeno-" is a prefix that means "gland"• “Carcinoma” is a malignant tumor that starts in

epithelial tissue.

• "adenocarcinoma," which means a malignant tumor

in epithelial tissue, specifically in a gland.

• Cancer that begins in the cells that line the alveoliand make substances such as mucus.

LARGE CELL CARCINOMA



LARGE CELL CARCINOMA

• Cancer that may begin in several types of largecells

• Lung cancer in which the cells are large and lookabnormal when viewed under a microscope.

SMALL CELL LUNG CANCER



SMALL CELL LUNG CANCER

• An aggressive (fast-growing) cancer that formsin tissues of the lung and can spread to otherparts of the body. The cancer cells look smalland oval-shaped when looked at under a

microscope• It is sometimes called "oat cell carcinoma" due

to the flat cell shape and scanty cytoplasm.

• This type of cancer is usually always caused bysmoking.

Staging & prognostic indicators



Staging & prognostic indicators

• Non Small Cell Lung Cancer

– TNM system

– Stage of disease

– ECOG (performance) status

– Weight loss• Small Cell Cancer

– Limited disease

– Extensive disease – ECOG status

– Site of metastatic spread



ECOG PERFORMANCE STATUS*

Grade ECOG

0Fully active, able to carry on all pre-disease performance without restriction

1

Restricted in physically strenuous activity but ambulatory and able to carry out work of alight or sedentary nature, e.g., light house work, office work

2 Ambulatory and capable of all self-care but unable to carry out any work activities. Up and

about more than 50% of waking hours

3Capable of only limited self-care, confined to bed or chair more than 50% of waking hours

4Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair

5Dead

* As published in Am. J. Clin. Oncol.:

Staging (TNM)



Staging (TNM)

• Tumour size (T):

– Tx: Primary tumour not able to be assessed

– T0: No evidence of primary tumour, ie. cancer cells seen on sputumsampling or bronchial washing only

– Tis: Carcinoma in situ

– T1: Tumour 3 cm or less, surrounded by pleura, without evidence ofinvasion more proximal than the lobar bronchus.

– T2: Tumour with any of the following features:

– >3cm in greatest dimension

– Invades visceral pleura

– Associated with atelectasis or obstructive pneumonitis,extending to the hilar region but not involving the entire lung.

Staging (TNM)



Staging (TNM)

• Tumour size (T):

• T3: Tumour of any size, – directly invading the chest wall, diaphragm,

mediastinal pleura or parietal pericardium; ortumour in the main bronchus; or

– in the main bronchus, less than 2cm distal to thecarina, but without involvement of the carina; or

– with associated atelectasis or obstructivepneumonitis of the entire lung

• T4: Tumour of any size, invading the mediastinum,heart, great vessels, trachea, oesophagus, vertebralbody, carina; or with separate tumour nodules in onelobe, or with malignant pleural effusion

Staging (TNM)



Staging (TNM)

• Regional lymph nodes (N):

– NX: Regional lymph nodes not able to be assessed

– N0: No regional lymph node metastasis

– N1: Metastasis in ipsilateral peribronchial and/or

ipsilateral hilar lymph nodes and intrapulmonary nodes,including involvement by direct extension

– N2: Metastasis in ipsilateral mediastinal and/orsubcarinal lymph nodes

– N3: Metastasis in contralateral mediastinal, contralateralhilar, ipsilateral or contralateral scalene, orsupraclavicular lymph nodes

Staging (TNM)



Staging (TNM)

• Distant Metastasis (M) – MX: Distant metastasis not able to be assessed

– M0: No distant metastasis

– M1: Distant metastasis, including separatetumour nodule(s) in a different lobe (ipsi- orcontralateral).

Staging



Staging

• Non-small cell lung cancers are grouped into stages asfollows:

• Stage 0: TIS N0 M0

• Stage Ia: T1 N0 M0

• Stage Ib: T2 N0 M0• Stage IIa: T1 N1 M0

• Stage IIb: T2 N1 M0, T3 N0 M0

• Stage IIIa: T1 N2 M0, T2 N2 M0, T3 N1 M0, T3 N2 M0

• Stage IIIb: any T N3 MO, T4 any N M0• Stage IV: any T any N M1

Clinical course



Clinical course

• NSCLC – Usually arise in the periphery of the lung – Often remain localised or have minimal spread to

surrounding lymph nodes – Spread via blood stream to the brain, bone, liver &

kidney – Spread directly to chest wall• SCLC

– Usually arise in the central region of the lung – Very aggressive & patients often have widespread

disease at diagnosis – often bilateral chest wallinvolvement

– Spread via blood stream & lymphatics to lymphnodes, liver, adrenal glands, bones & CNS

Clinical manifestations



Clinical manifestations

• Specific:

– Cough

– Shortness of breath

– Haemoptysis

– Recurrent pneumonia

• Non specific:

– Anorexia

– Malaise – Weight loss

• Metastatic Symptoms

– Spinal Cord

• Compression

– Cerebral symptoms

– Bone pain

– SVC obstruction

Treatment of lung cancer



Treatment of lung cancer

• NSCLC

– Stage I/II – surgery or radiotherapy/chemotherapy if unfitfor surgery

– Stage III – surgery (if fit) chemotherapy & radiotherapy

– Stage IV – palliative treatment with chemo/radiotherapy

• SCLC

– Chemotherapy for limited & extensive disease + thoracicradiotherapy

– Prophylactic radiotherapy to the brain

Survival rates (nsclc)



Survival rates (nsclc)

• For each stage, the prognoses, or estimated 5-year

• survival rates, in Europe are as follows:

– Stage IA - 60%

– Stage IB - 38%

– Stage IIA - 34%

– Stage IIB - 24%

– Stage IIIA - 13% (Stage IIIA lesions have a poor

• prognosis, but they are technically resectable)

• • Stage IIIB - 5% (Stage IIIB lesions are non resectable)

• • Stage IV - Less than 1%

Documents

Week 12 Introduction to Cancer