UNIVERSITY OF ABUJA

FACULTY OF NURSING AND ALLIED HEALTH SCIENCES

DEPARTMENT OF MEDICAL SURGICAL NURSING

TOPIC: MANAGEMENT OF PATIENTS WITH ONCOLOGICAL DISORDERS

LEARNING OBJECTIVES

At the end of this chapter, the student will be able to:

1. Define Oncology
2. Understand the epidemiology of cancer
3. Discuss the genetic and molecular basis of cancer:
4. Understand cancer screening guidelines and early detection:
5. Identify clinical signs and symptoms of common cancers
6. Describe diagnostic procedures and tools in oncology
7. Discuss the principles of cancer staging
8. Review the principles of cancer treatment
9. Discuss the management of specific cancers
10. Evaluate the role of multidisciplinary teams in cancer management
11. Recognize the need for palliative care in oncology
12. Understand the management of cancer-related complications
13. Understand the principles of survivorship care
14. Discuss the psychological and social aspects of oncology care
15. Discuss the ethical dilemmas in oncology
16. Evaluate the role of patient-centered care
17. Stay informed about advances in oncology research
18. Identify the challenges in global cancer care

Module one:
1.0 Introduction to Oncology

Oncology refers to the branch of medicine focused on the prevention, diagnosis, and treatment of
cancer. Cancer involves uncontrolled cell growth and spread to other parts of the body.

1.1 Epidemiology of Cancer

Epidemiology involves the study of the distribution and determinants of cancer in populations.
Key statistics provide insight into the burden of cancer worldwide.

Although significant progress has been made in the fight against cancer, it remains a major
public health challenge both in the United States and globally. In the United States, an estimated
2,001,140 new cases of cancer were diagnosed in 2024, and 611,720 people died from the
disease.

Global Cancer Statistics

According to the World Health Organization (WHO), cancer is a leading cause of death
worldwide.

Incidence: 19.3 million new cancer cases were diagnosed globally in 2020.

Mortality: 10 million people died from cancer in 2020.

Risk Factors

Cancer risk factors include:

Genetic: Family history of cancer, inherited mutations (e.g., BRCA1, BRCA2).

Environmental: Exposure to carcinogens (tobacco, radiation, etc.).

Lifestyle: Diet, physical inactivity, alcohol consumption.

Age: Cancer risk increases with age.

Infections: Human papillomavirus (HPV) leading to cervical cancer, Hepatitis B and C leading
to liver cancer.

Top 5 Most Common Cancers (Incidence):

a. Breast cancer: The most commonly diagnosed cancer worldwide, with approximately 2.3
million cases.
b. Lung cancer: The second most common, with about 2.2 million cases.
c. Colorectal cancer: Approximately 1.9 million cases.
d. Prostate cancer: Around 1.4 million cases.
 e. Stomach cancer: Roughly 1 million cases.

Top 5 Leading Causes of Cancer Mortality:

a. Lung cancer: Over 1.8 million deaths.

b. Colorectal cancer: About 935,000 deaths.
c. Stomach cancer: Around 769,000 deaths.
d. Liver cancer: Approximately 830,000 deaths.
e. Breast cancer: Around 685,000 deaths.

Regional Cancer Burden

High-Income Countries

North America and Europe have a high incidence of cancers due to both better healthcare
infrastructure (leading to earlier diagnosis) and lifestyle factors.

Breast cancer and prostate cancer have the highest incidence rates.

Lung cancer is also a significant cause of death, particularly due to smoking habits.

The overall 5-year survival rate for cancers is higher due to access to advanced treatment
options.

Low- and Middle-Income Countries

Cancer incidence rates are rising in low- and middle-income countries, driven by lifestyle
changes, aging populations, and the increasing burden of tobacco use, alcohol consumption, and
obesity.

Lung cancer is also common, especially in regions with high rates of tobacco use.

Cervical cancer remains one of the leading causes of cancer in women, particularly in low-
resource settings where screening and vaccination programs are limited.

Illustration 1:
In 2024, a little over 2 million new cancer cases are expected to be diagnosed in the United
States. Prostate cancer is the most common cancer among males (29%), followed by lung (11%)
and colorectal (8%) cancers. Among females, breast (32%), lung (12%), and colorectal (7%)
cancers are the most common.

Common Oncological Disorders

Carcinomas (e.g., lung, breast, prostate, colorectal cancer)

Sarcomas (e.g., soft tissue sarcomas, bone cancers)

Leukemias

Lymphomas

Central Nervous System Tumors

Common Risk Factors for Cancer

Cancer incidence is influenced by a range of modifiable and non-modifiable risk factors.

Non-Modifiable Risk Factors

Age: The risk of cancer increases with age. The majority of cancers are diagnosed in people over
50 years old.

Genetic factors: Family history and inherited mutations (e.g., BRCA1/2, TP53 mutations)
increase the risk for certain cancers (e.g., breast, ovarian, colorectal cancers).

Gender: Certain cancers are more prevalent in one gender, such as breast cancer in women and
prostate cancer in men.

Modifiable Risk Factors

Tobacco use: The leading cause of lung cancer and associated with several other cancers (e.g.,
oral, esophageal, pancreatic).

Alcohol consumption: Increased risk of cancers such as liver, colorectal, and head and neck
cancers.

Obesity: Associated with an increased risk of several cancers, including breast (post-
menopausal), colorectal, and endometrial cancers.

Diet: Diets high in red meat, processed foods, and low in fiber are linked to certain cancers.

Physical inactivity: Sedentary lifestyle increases the risk of cancers like colorectal and breast
cancer.

Sun exposure: Increases the risk of skin cancers, including melanoma.

Infections: Certain viruses and bacteria increase cancer risk:

Human papillomavirus (HPV): Cervical, anal, and oropharyngeal cancers.

Hepatitis B and C: Liver cancer.

Helicobacter pylori: Stomach cancer.

Trends in Cancer Incidence and Mortality

Rising Incidence

Global cancer rates are increasing, particularly in low- and middle-income countries, driven by
urbanization and lifestyle changes.

Aging populations worldwide will also contribute to higher cancer rates in the coming decades.
Declining Mortality in Some Regions

In high-income countries, advancements in cancer detection, treatment, and prevention (e.g.,

screening programs) have led to declining cancer mortality.

For example, in the United States, mortality rates from breast cancer have significantly dropped
due to better early detection and targeted therapies.

Emerging Cancers

Certain cancers are on the rise, including those related to lifestyle factors and environmental
exposures.

Lung cancer in women (especially non-smokers).

Colorectal cancer in younger individuals, possibly due to dietary and lifestyle changes.

Skin cancers, particularly in regions with intense sun exposure.

1.2 Pathophysiology of Cancer

Cancer is fundamentally a disease of uncontrolled cell growth and division. It arises from
mutations in the genetic material of normal cells that disrupt the processes regulating cell cycle,
apoptosis (programmed cell death), and cellular differentiation. These genetic alterations result
in the formation of a tumor, which can invade surrounding tissues and metastasize to distant
organs.

1. Normal Cell Cycle Regulation vs. Cancerous Cell Growth

Normal Cell Cycle

The cell cycle is a series of stages through which a cell passes in order to divide and create two
daughter cells. The major phases of the cell cycle are:

Interphase: The cell grows and replicates its DNA.

G1 phase (Gap 1): The cell grows and prepares for DNA replication.

S phase (Synthesis): DNA is replicated.

G2 phase (Gap 2): The cell prepares for mitosis.

Mitosis (M phase): The cell divides into two daughter cells, through processes like

prophase, metaphase, anaphase, and telophase, followed by cytokinesis.

Checkpoints in the Cell Cycle:

Cell cycle progression is controlled by checkpoints, which are points where the cell assesses
whether it is ready to move on to the next phase. These checkpoints prevent the cell from
progressing to the next stage if something is wrong, like DNA damage or incomplete replication.
The major checkpoints are:

1. G1 checkpoint: This is the "restriction point." It checks if the cell is ready to enter the S
phase, ensuring that the environment is favorable and there is no DNA damage.
2. G2 checkpoint: Before entering mitosis, the cell checks whether DNA replication was
completed without errors.
3. M checkpoint: During mitosis, it checks whether all chromosomes are properly aligned
and attached to the spindle fibers before proceeding with cell division.

Tumor Suppressor Genes:

Tumor suppressor genes produce proteins that regulate the cell cycle and prevent uncontrolled
cell division, acting as a brake on the cell cycle. When these genes are working properly, they
can stop a cell from dividing if something is wrong (such as DNA damage). A famous example
is the p53 protein, which can halt the cell cycle at the G1 checkpoint if DNA is damaged. It also
activates DNA repair mechanisms or can trigger apoptosis (programmed cell death) if the
damage is too severe.

If tumor suppressor genes are mutated or inactivated, the cell may bypass checkpoints, leading
to uncontrolled cell division, which can contribute to cancer.

Oncogenes:

Oncogenes are mutated forms of normal genes (called proto-oncogenes) that promote cell
growth and division. When these genes are mutated, they can cause excessive cell division and
growth. Oncogenes often act like a "gas pedal" for the cell cycle, speeding up cell division.

If oncogenes are activated or overexpressed, they can push the cell through the checkpoints too
quickly or force it to continue dividing inappropriately, increasing the risk of cancer.

In Summary:

Tumor suppressor genes act like brakes on the cell cycle, ensuring that cells only divide when
everything is in order.

Oncogenes act like accelerators, promoting cell division, and if overactive, they can
lead to uncontrolled growth and contribute to cancer.

The cell cycle is tightly regulated by these genes, and any malfunction in these regulatory
systems can lead to cancer or other diseases related to abnormal cell division.
Cancer Cell Cycle Dysregulation

In cancerous cells, mutations in genes that regulate the cell cycle can lead to uncontrolled cell
division. This occurs when:

Oncogenes (mutated or overexpressed forms of normal genes) drive the cell to divide
uncontrollably.

Tumor suppressor genes (e.g., TP53, Rb) lose their ability to suppress cell division or
induce apoptosis.

2. Key Genetic Alterations in Cancer

Mutations in Oncogenes

Oncogenes are mutated forms of proto-oncogenes, which are normal genes involved in cell
growth and differentiation. When mutated, they can lead to excessive cell proliferation.

Common oncogenes include:

Ras family: Mutations in the RAS gene are common in cancers like colorectal and lung cancers,
leading to continuous activation of signaling pathways that promote cell growth.

HER2/neu: Amplified in breast cancer, leading to increased cell proliferation and resistance to
cell death.

Myc: Overexpression of c-Myc promotes cell cycle progression and inhibits differentiation.

Loss of Function in Tumor Suppressor Genes

Tumor suppressor genes encode proteins that inhibit cell division or promote apoptosis.
In cancer, these genes often undergo loss-of-function mutations, allowing abnormal cell
growth.

p53 (TP53 gene): The most frequently mutated gene in human cancers, which regulates cell
cycle arrest and apoptosis. Loss of p53 function allows cells with DNA damage to continue
dividing.

Rb (Retinoblastoma protein): Loss of Rb function leads to unchecked progression through the

cell cycle.
BRCA1/BRCA2: Mutations in these genes, involved in DNA repair, increase susceptibility to
breast and ovarian cancers.

DNA Repair Defects

Mismatch repair genes: Mutations in genes like MLH1, MSH2 (involved in DNA mismatch
repair) are associated with hereditary nonpolyposis colorectal cancer (HNPCC).

Nucleotide excision repair: Defects in the XP genes can lead to conditions like xeroderma
pigmentosum, increasing skin cancer risk.

3. Hallmarks of Cancer

In 2000, researchers Hanahan and Weinberg proposed "Hallmarks of Cancer" that describe
key biological capabilities acquired by cancer cells, allowing them to survive and proliferate.

1. Sustaining proliferative signaling

Cancer cells continuously signal themselves or surrounding cells to keep proliferating. This
occurs through mutations in growth factor receptors (e.g., HER2), signaling molecules (e.g.,
RAS), or downstream effectors.

2. Evading growth suppressors

Cancer cells overcome normal regulatory signals that would typically prevent excessive cell
growth. This occurs through mutations in tumor suppressor genes like p53 and Rb, which
normally restrain cell cycle progression.

3. Resisting cell death (apoptosis)

Cancer cells evade apoptosis by disabling the apoptotic machinery, which normally acts as a
protective mechanism.

4. Enabling replicative immortality

Cancer cells acquire the ability to maintain or lengthen their telomeres (the protective caps at the
ends of chromosomes) to prevent normal cellular aging and continue to divide indefinitely. This
is often facilitated by the activation of telomerase.

5. Inducing angiogenesis

To grow beyond a small size, tumors require a blood supply. Cancer cells stimulate the
formation of new blood vessels known as angiogenesis.

6. Activating invasion and metastasis

Cancer cells acquire the ability to invade surrounding tissues and spread to distant organs. This
involves:

1. Invasion of the extracellular matrix (ECM)

2. Metastasis through blood and lymphatic vessels to distant organs

4. Tumor Microenvironment

The tumor microenvironment plays a crucial role in cancer progression and metastasis. It
consists of:

Cancer-associated fibroblasts (CAFs) that secrete growth factors and extracellular

matrix proteins.

Immune cells: Cancer cells often evade immune surveillance by suppressing immune
responses or recruiting immunosuppressive cells like T-regulatory cells.

Endothelial cells involved in the formation of new blood vessels (angiogenesis).

Exosomes and cytokines that enable communication between tumor cells and
surrounding stromal cells, promoting cancer progression and resistance to therapy.

5. Metastasis: Mechanisms of Cancer Spread

Metastasis of involves the spread of cancer cells from the primary tumor to distant organs. The
steps metastasis include:

1. Invasion: Cancer cells break through the basement membrane and invade surrounding
tissues by secreting enzymes like matrix metalloproteinases.
2. Intravasation: Cancer cells enter the bloodstream or lymphatic vessels.
3. Circulation: Tumor cells travel through the bloodstream or lymphatics to distant organs.
4. Extravasation: Cancer cells exit the bloodstream or lymphatic vessels and invade distant
tissues.
5. Colonization: Cancer cells establish a secondary tumor at a distant site, often facilitated
by the new microenvironment.

Metastasis can lead to the formation of secondary tumors in organs like the lungs, liver, bones,
and brain, which is a major contributor to cancer-related morbidity and mortality.

Molecular Mechanisms in Cancer Pathogenesis

Cancer is driven by a combination of genetic mutations, epigenetic changes, and alterations in

the tumor microenvironment that collectively enable uncontrolled cell growth, resistance to cell
death, and the ability to invade and metastasize. Understanding the molecular pathophysiology of
cancer has led to the development of targeted therapies, immunotherapies, and other treatment
modalities that aim to specifically address these molecular alterations and improve patient
outcomes.

1.3 Characteristics of malignant cells:

1. Uncontrolled Proliferation

Loss of growth regulation: Malignant cells have the ability to proliferate uncontrollably.

Escape from cell cycle checkpoints: Mutations in genes that control the cell cycle, such
as p53 and Rb, allow malignant cells to bypass checkpoints and continue dividing even
when DNA is damaged.

Autocrine signaling: Some malignant cells produce growth factors that stimulate their
own growth (autocrine signaling) or activate nearby cells (paracrine signaling),
enhancing their proliferative capacity.

2. Resistance to Growth Suppressors

Inactivation of tumor suppressor genes: Tumor suppressor genes such as p53, Rb, and
BRCA1/2 normally act as breaks on cell division. Malignant cells often have mutations
that inactivate these genes, allowing them to continue proliferating.

Increased expression of cyclins: Cyclins and cyclin-dependent kinases (CDKs) regulate

the progression through the cell cycle. Malignant cells often have overexpression of
cyclins, leading to unchecked cell division.

3. Evading Apoptosis (Programmed Cell Death)

Resistance to cell death signals: Malignant cells evade apoptosis by mutating or

downregulating genes that induce cell death, such as p53, and upregulating genes that
inhibit apoptosis, like Bcl-2.

Alterations in apoptotic pathways: Malignant cells may activate alternative survival

pathways, such as PI3K-Akt, that promote cell survival in the presence of damage or
stress.

4. Sustained Angiogenesis

Formation of new blood vessels: For tumors to grow beyond a small size, they need a
blood supply. Malignant cells secrete pro-angiogenic factors, particularly vascular
endothelial growth factor (VEGF), to stimulate the growth of new blood vessels.
 Tumor vascularization: The newly formed blood vessels are often abnormal and leaky,
providing a pathway for the tumor to receive nutrients and oxygen while facilitating the
spread of cancer cells.

5. Tissue Invasion and Metastasis

Invasive properties: Malignant cells can invade surrounding tissues and penetrate the
basement membrane, a key characteristic of cancer. This process is facilitated by the
secretion of enzymes like matrix metalloproteinases (MMPs), which break down
extracellular matrix components.

Metastatic potential: Malignant cells can spread through the bloodstream or lymphatic
system to distant organs, a process known as metastasis. This spread allows secondary
tumors to form in distant tissues such as the lungs, liver, bones, and brain.

6. Limitless Replicative Potential

Telomerase activation: Most normal cells have a limited number of divisions due to the
shortening of telomeres (protective caps on chromosomes). Malignant cells often express
the enzyme telomerase, which maintains or elongates telomeres, allowing the cells to
divide indefinitely and avoiding cellular senescence.

7. Deregulated Metabolism

Altered energy production: Malignant cells often exhibit altered metabolism, such as
the Warburg effect, where they rely on aerobic glycolysis (the conversion of glucose to
lactate) rather than oxidative phosphorylation, even in the presence of oxygen. This
metabolic shift supports rapid growth by providing intermediate metabolites for
biosynthesis.

Increased nutrient uptake: Malignant cells may upregulate receptors and transporters
for nutrients such as glucose and amino acids to fuel their increased metabolic demands.

8. Immune Evasion

Immune checkpoint inhibition: Malignant cells can evade immune surveillance.

Immunosuppressive microenvironment: Malignant cells can promote the recruitment

of immunosuppressive cells, like T-regulatory cells and myeloid-derived suppressor
cells (MDSCs), which inhibit the function of cytotoxic T cells and other immune
responses.

9. Genetic Instability

Increased mutation rate: Malignant cells often have a higher rate of genetic mutations,
which can result from defects in DNA repair mechanisms, such as those seen in
 BRCA1/2 mutations or defects in mismatch repair. This genetic instability accelerates
tumor progression by generating a pool of variations that can confer a growth advantage.

Chromosomal instability: Malignant cells frequently exhibit chromosomal

abnormalities, such as aneuploidy (an abnormal number of chromosomes) and
translocations, which further contribute to cancer progression.

10. Evading the "Normal" Tissue Architecture

Loss of cellular differentiation: Malignant cells often lose the specialized functions they
would normally perform in healthy tissues, a process called dedifferentiation. This loss
of differentiation allows them to divide rapidly but often results in the formation of
poorly organized tissue.

Altered cell-cell adhesion: Malignant cells often express altered cell adhesion molecules
(e.g., E-cadherin downregulation), which allows them to detach from the primary tumor
and invade surrounding tissues or enter the bloodstream and lymphatics.

11. Ability to Survive in Harsh Environments

Malignant cells can adapt to low-oxygen environments (hypoxia) often present within
the tumor mass due to rapid growth. They do this by activating hypoxia-inducible factors
(HIFs), which trigger the expression of genes involved in angiogenesis, glycolysis, and
survival.

Increased ability to survive metabolic stress: Cancer cells can also adapt to other forms
of stress (e.g., nutrient deprivation, oxidative stress) through various survival pathways
that maintain cell viability.

These characteristics contribute to the aggressive nature of cancer and its ability to cause
significant morbidity and mortality.

1. 4 Carcinogenesis is the process by which normal cells transform into cancer cells through a
series of genetic and epigenetic changes. This process occurs over time, often involving multiple
stages, including initiation, promotion, and progression. Carcinogenesis can be caused by various
internal and external factors, such as genetic mutations, environmental exposures, lifestyle
choices, and infections. Below is an explanation of the steps and mechanisms involved in
carcinogenesis.

Carcinogenesis: Overview

Carcinogenesis is typically divided into three stages:

1. Initiation
 2. Promotion
3. Progression

These stages reflect the cumulative genetic and epigenetic changes that accumulate in cells,
ultimately leading to uncontrolled growth and malignancy.

1. Initiation: The First Step in Carcinogenesis

Initiation refers to the initial genetic alteration in a cell that makes it susceptible to further
changes. This stage is often caused by mutations in the DNA, which may occur due to exposure
to carcinogens, genetic predispositions, or random errors during DNA replication.

Key Features:

DNA damage: Initiation begins with a genetic mutation that disrupts the normal
function of genes controlling the cell cycle, apoptosis, or DNA repair. The mutation may
be in an oncogene (promoting cell growth) or a tumor suppressor gene (which normally
inhibits cell growth).

Irreversible: The mutation is usually irreversible and passed on to subsequent cell

generations.

Carcinogenic agents: These mutations are often induced by external carcinogens such as
chemicals, radiation, or viruses. For example:

Chemical carcinogens: Tobacco smoke, asbestos, or industrial chemicals (e.g.,

benzene).

Radiation: UV radiation (skin cancer), ionizing radiation (leukemias, thyroid

cancer).

Viruses: Human papillomavirus (HPV) causing cervical cancer, hepatitis B/C

causing liver cancer.

Example:

A mutation in the TP53 gene, a tumor suppressor gene, could lead to a loss of its ability
to induce apoptosis in cells with damaged DNA, setting the stage for further tumorigenic
changes.

2. Promotion: Expansion of the Mutated Cell Population

Promotion involves the selective growth and proliferation of initiated cells (those with
mutations). During this stage, mutations are not necessarily the cause of cancer, but the mutated
cells are stimulated to grow uncontrollably due to various promoting factors.

Key Features:

Reversible process: Unlike initiation, the promotion phase is often reversible if the
promoting agents are removed or inhibited.

Exogenous promoting agents: Promoters may include hormones (estrogen, insulin-like

growth factors), inflammatory cytokines, or other external agents that stimulate cell
proliferation.

Clonal expansion: The initiated cell undergoes clonal expansion, meaning that more and
more cells with the same genetic mutation proliferate and accumulate further genetic
alterations.

Inflammation: Chronic inflammation can act as a promoter by producing growth factors,

cytokines, and reactive oxygen species (ROS), all of which contribute to cell proliferation
and genomic instability.

Example:

In liver cancer (hepatocellular carcinoma), chronic infection with hepatitis B or C virus

can promote the expansion of mutated liver cells, with repeated cycles of liver cell death
and regeneration, increasing the likelihood of further mutations.

3. Progression: Transformation into Malignant Cancer

Progression is the final stage in carcinogenesis, in which the genetically altered cells evolve into
invasive, malignant cancer cells capable of metastasis. This stage involves the accumulation of
further mutations that result in increasingly aggressive behavior, such as resistance to apoptosis,
tissue invasion, and metastasis.

Key Features:

Genetic instability: Progression is marked by genetic instability, in which mutations

accumulate rapidly. These genetic changes can lead to the activation of oncogenes and
the loss of function of tumor suppressor genes (e.g., p53).

Invasiveness and metastasis: The cancer cells acquire the ability to invade surrounding
tissues and enter the bloodstream or lymphatics to spread to distant organs (metastasis).
 Angiogenesis: Tumors begin to induce angiogenesis, the formation of new blood vessels
to supply the growing tumor with nutrients and oxygen.

Evasion of immune surveillance: Cancer cells acquire mechanisms to evade detection

and destruction by the immune system, often by expressing immune checkpoint proteins
like PD-L1.

Example:

In colorectal cancer, progression involves the sequential accumulation of mutations in

tumor suppressor genes (APC, TP53) and oncogenes (K-ras), leading to the
development of invasive carcinoma that can metastasize to distant organs such as the
liver and lungs.

4. Genetic and Epigenetic Mechanisms of Carcinogenesis

The pathogenesis of cancer involves a combination of genetic mutations and epigenetic

alterations that disrupt the normal functioning of the cell.

Genetic Mutations

Point mutations: A change in a single nucleotide in the DNA sequence, which can lead
to altered protein function (e.g., activating an oncogene or inactivating a tumor
suppressor gene).

Chromosomal translocations: Rearrangements of chromosomes that can create fusion

genes or dysregulate the expression of oncogenes (e.g., BCR-ABL in chronic
myelogenous leukemia).

Gene amplification: Increased copies of an oncogene (e.g., HER2 in breast cancer) can
lead to excessive signaling for cell growth.

Loss of heterozygosity: The loss of one allele of a tumor suppressor gene can result in
the loss of its protective function.

Epigenetic Changes

DNA methylation: Addition of methyl groups to DNA, typically at CpG islands, can
silence tumor suppressor genes (e.g., MLH1 in Lynch syndrome).

Histone modification: Changes in the packaging of DNA by histones can alter gene
expression. For example, acetylation can promote gene expression, whereas methylation
can silence genes.
 MicroRNAs: Small non-coding RNAs that regulate gene expression can also be
dysregulated in cancer, leading to the overexpression of oncogenes or silencing of tumor
suppressors.

5. External and Internal Factors in Carcinogenesis

External Factors (Carcinogens)

Chemical carcinogens: Exposure to chemicals such as tobacco smoke, pesticides, and

industrial chemicals increases the risk of cancer. For example, benzene is linked to
leukemia, and asbestos exposure increases the risk of mesothelioma.

Radiation: Ionizing radiation (e.g., X-rays, nuclear fallout) can cause DNA breaks and
mutations. UV radiation leads to skin cancer by inducing DNA damage and impairing
DNA repair mechanisms.

Infections: Certain viruses, bacteria, and parasites can increase the risk of cancer. For
example, HPV is linked to cervical cancer, and helicobacter pylori can lead to gastric
cancer.

Internal Factors

Genetic predisposition: Some individuals inherit mutations in cancer-related genes, such

as BRCA1/2 mutations in breast and ovarian cancers.

Hormones: Hormonal influences can promote carcinogenesis. For example, estrogen has
been linked to an increased risk of breast and endometrial cancers.

Chronic inflammation: Persistent inflammation, often due to infections or autoimmune

diseases, can promote cancer by increasing cellular turnover, oxidative stress, and
genomic instability.

NOTE: Carcinogenesis is a complex and multi-step process in which normal cells accumulate
genetic and epigenetic alterations, leading to the development of malignant tumors. These
alterations allow cancer cells to acquire characteristics such as uncontrolled growth, resistance to
apoptosis, and the ability to invade and metastasize. Understanding the mechanisms of
carcinogenesis is essential for developing effective cancer prevention, early detection, and
treatment strategies.