Izzatullah Khan

Assistant Professor (LCPS)

Pharm D (LCPS), M.Sc. (UK)

ONCOLOGY UNIT
Introduction
 Cancer is a disease characterized by a shift in the control mechanisms that
govern cell survival, proliferation, and differentiation.

 Cells that have undergone neoplastic transformation usually express cell surface
antigens that may be of normal fetal type, may display other signs of apparent
immaturity, and may exhibit qualitative or quantitative chromosomal
abnormalities, including various translocations and the appearance of amplified
gene sequences.

 Such cells proliferate excessively and form local tumors that can compress or
invade adjacent normal structures.

 A small subpopulation of cells within the tumor can be described as tumor stem
cells.

 They retain the ability to undergo repeated cycles of proliferation as well as to

migrate to distant sites in the body to colonize various organs in the process
called metastasis
 Such tumor stem cells thus can express clonogenic or colony-
forming capability.

 Tumor stem cells are characterized by chromosome

abnormalities reflecting their genetic instability, which leads to
progressive selection of subclones that can survive more readily
in the multicellular environment of the host.

 Quantitative abnormalities in various metabolic pathways and

cellular components accompany this neoplastic progression.

 The invasive and metastatic processes as well as a series of

metabolic abnormalities resulting from the cancer cause illness
and eventual death of the patient unless the neoplasm can be
eradicated with treatment.
 THE GENESIS OF A CANCER CELL
 A normal cell turns into a cancer cell because of one or more mutations
in its DNA, which can be inherited or acquired.

 The development of cancer is a complex multistage process, involving

not only more than one genetic change but usually also other, epigenetic
factors (hormonal action, co-carcinogen and tumour promoter effects,
etc.

 There are two main categories of genetic change that lead to cancer:
 the activation of proto-oncogenes to oncogenes
 the inactivation of tumour suppressor genes.

 These changes are a result of point mutations, gene amplification or

chromosomal translocation, often due to the action of certain viruses or
chemical carcinogens
 Activation of proto-oncogenes to oncogenes
 Proto-oncogenes are genes that normally control cell division,
apoptosis and differentiation but which can be converted to
oncogenes by viral or carcinogen action.

 Inactivation of tumour suppressor genes

 Normal cells contain genes that have the ability to suppress
malignant change-termed tumour suppressor genes (anti-
oncogenes)-and there is now good evidence that mutations of
these genes are involved in many different cancers.

 The loss of function of tumour suppressor genes can be the

critical event in carcinogenesis. About 30 tumour suppressor
genes and 100 dominant oncogenes have been identified.
THE SPECIAL
CHARACTERISTICS OF CANCER
CELLS
 UNCONTROLLED PROLIFERATION
 The proliferation of cancer cells is not controlled by the processes
that normally regulate cell division and tissue growth.
 It is this, rather than their rate of proliferation, that distinguishes them
from normal cells.
 Some normal cells (such as neurons) have little or no capacity to
divide and proliferate, but others, for example in the bone marrow and
the epithelium of the gastrointestinal tract, have the property of
continuous rapid division.
 Some cancer cells multiply slowly (e.g. those in plasma cell tumours)
and some fast (e.g. the cells of Burkitt's lymphoma).
 DEDIFFERENTIATION AND LOSS OF FUNCTION
 The multiplication of normal cells involves division of the stem cells in
a particular tissue to give rise to daughter cells.
 These daughter cells eventually differentiate to become the mature
cells of the relevant tissue and carry out their programmed functions.
 For example, fibroblasts become capable of secreting and organising
extracellular matrix, muscle cells become capable of contraction, and so on.

 One of the main characteristics of cancer cells is that they dedifferentiate-to

a varying degree in different tumors. In general, poorly differentiated cancers
multiply faster and have a poorer prognosis than well-differentiated cancers.

 INVASIVENESS
 Normal cells are not found outside their 'designated' tissue of origin; for
example, liver cells are not found in the bladder, and pancreatic cells are not
found in the testis.

 This is because during differentiation and during the growth of tissues and
organs, normal cells develop certain spatial relationships with respect to
each other. These relationships are maintained by various tissue-specific
survival factors-anti-apoptotic factors. Any cells that escape accidentally
lose these survival signals and undergo apoptosis
 Consequently, although the cells of the normal mucosal epithelium of
the rectum proliferate continuously as the lining is shed, they remain
as a lining epithelium.

 A cancer of the rectal mucosa, by comparison, invades the tissues in

the other layers of the rectum and may invade the tissues of other
pelvic organs.

 METASTASES
 Metastases are secondary tumours formed by cells that have been
released from the initial or primary tumour and have reached other
sites through blood vessels or lymphatics, or as a result of being
shed into body cavities.

 Metastases are the principal cause of mortality and morbidity in most

cancers and constitute a major problem for cancer therapy
 Types of tumours
 Tumours are groups of abnormal cells that form lumps or growths. They can
start in any one of the trillions of cells in our bodies. Tumours grow and
behave differently, depending on whether they are cancerous (malignant),
non-cancerous (benign) or precancerous.

 Cancerous tumours
 Cancer can start in any part of the body. When cancer cells form a lump or
growth, it is called a cancerous tumour. A tumour is cancerous when it:

 grows into nearby tissues

 has cells that can break away and travel through the blood or lymphatic
system and spread to lymph nodes and distant parts of the body
 Cancer that spreads from the first place it started (called the primary
tumour) to a new part of the body is called metastatic cancer. When cancer
cells spread and develop into new tumours, the new tumours are called
metastases.
 Non-cancerous tumours
 Tumours that aren’t cancerous are called non-cancerous tumours. Non-
cancerous tumours:
 stay in one place and don’t spread to other parts of the body
 don’t usually come back after they are removed
 tend to have a regular and smooth shape and have a covering called a
capsule
 may be moved easily in the tissue

 Precancerous conditions
 Precancerous cells are abnormal cells that may develop into cancer if they
aren’t treated. Some of these cells have mild changes that may disappear
without any treatment.
 But some precancerous cells pass on genetic changes and gradually
become more and more abnormal as they divide until they turn into cancer.
It can take a long time for a precancerous condition to develop into cancer.
 Precancerous changes can be mild to severe. There are different ways
of describing precancerous changes based on how mild or severe the
changes are.

 Hyperplasia means that abnormal cells are dividing and increasing in

number faster than normal. The cells look normal under the microscope
but there are more cells than normal. Some types of hyperplasia are
precancerous but most aren’t.

 Atypia means that cells are slightly abnormal (atypical). Sometimes

atypia may be caused by healing and inflammation but some types of
atypia are precancerous.

 Metaplasia means that there has been a change to the types of cells
that are normally found in this area of the body. The cells look normal
but they aren’t the type of cells that are normally found in that tissue or
area. Most types of metaplasia aren’t precancerous but some are.