Biochemistry of cancer

1. Biochemistry of
CANCER
Dr. Azad Alam Siddiqui
Assistant Professor
Department of B.Voc (MMDT)
Km. Mayawati Govt.Girls PG College
Badalpur, G.B. Nagar (U.P.)

2. Normal Cell
• Normal cells have certain characteristics that are important for the
proper functioning of tissues, organs, and body systems.
➢ability to reproduce correctly,
➢stop reproducing when necessary,
➢remain in a specific location,
➢specialized for specific functions,
➢and self destruct when necessary.
• Cell Reproduction: Cell reproduction is needed to replenish the cell
population that ages or becomes damaged or destroyed. Normal cells
reproduce properly. Except for sex cells, all cells of the body reproduce by
mitosis. Sex cells reproduce through a process called meiosis.
• Cell Communication: Cells communicate with other cells through
chemical signals. These signals help normal cells to know when to
reproduce and when to stop reproducing.

3. • Cell Adhesion: Cells have adhesion molecules on their surface that allow
them to stick to the cell membranes of other cells. This adhesion helps
cells to stay in their proper location and also aids in the passage of signals
between cells.
• Cell Specialization: Normal cells have the ability to differentiate or
develop into specialised cells. For example, cells can develop into heart
cells, brain cells, lung cells or any other cell of a specific type.
• Cell Death: Normal cells have the ability to self destruct when they
become damaged or diseased. They undergo a process called
apoptosis in which cells break down and are disposed of by white blood
cells.

4. Cancer Cells
• Growth- cancer cells don’t stop growing when there are enough cells
present. This continued growth often results in a tumor (a cluster of
cancer cells).
• Communication- Normal cells respond to signals sent from other
nearby cells that say, essentially, “you’ve reached your boundary.”
When normal cells “hear” these signals they stop growing. Cancer cells
do not respond to these signals.
• Cell repair and cell death- Normal cells are either repaired or die
(undergo apoptosis) when they are damaged or get old. Cancer cells are
either not repaired or do not undergo apoptosis.
• Stickiness—Cancer cells fail to stick to membrane and “float away” to
locations nearby, or through the bloodstream or system of lymph
channels to distant regions in the body (Metastasis).

5. • Appearance—Under a microscope, normal cells and cancer cells may
look quite different. some are larger than normal and some are smaller
than normal. In addition, cancer cells often have an abnormal shape,
both of the cell, and of the nucleus.
• The rate of growth—Normal cells reproduce themselves and then stop
when enough cells are present. Cancer cells reproduce rapidly before the
cells have had a chance to mature.
• Maturation—Normal cells mature. Cancer cells, because they grow
rapidly and divide before cells are fully mature, remain immature.
Doctors use the term undifferentiated to describe immature cells.
• Evading the immune system—When normal cells become damaged, the
immune system (via cells called lymphocytes) identifies and removes
them. Cancer cells are able to evade (trick) the immune system long
enough to grow into a tumor by either by escaping detection or by
secreting chemicals that inactivate immune cells that come to the scene.

6. • Functioning—Normal cells perform the function they are meant to
perform, whereas cancer cells may not be functional. For example,
normal white blood cells help fight off infections.
• Blood supply— Angiogenesis is the process by which cells attract blood
vessels to grow and feed the tissue. Cancer cells undergo angiogenesis
even when growth is not necessary.
• Invasiveness—Normal cells listen to signals from neighbouring cells and
stop growing when they encroach on nearby tissues (something called
contact inhibition.) Cancer cells ignore these cells and invade nearby
tissues.

7. • The term cancer applies to a group of diseases
in which cells grow abnormally and form a
malignant tumor.
• Malignant cells can invade nearby tissues and
metastasize (establish secondary areas of
growth).
• This aberrant growth pattern results from
mutations in genes that regulate proliferation,
differentiation, and survival of cells in a
multicellular organism.
• Because of these genetic changes, cancer cells
no longer respond to the signals that govern
growth of normal cells.

9. • Every sixth death in the world is due to cancer, making it the second leading
cause of death (second only to cardiovascular diseases).
• In 2016, 8.9 million people are estimated to have died from the various forms
of cancer.
• According to the National Cancer Registry Programme of the India Council of
Medical Research (ICMR), more than 1300 Indians die every day due to
cancer.
• Between 2012 and 2014, the mortality rate due to cancer increased by
approximately 6% in India.
• Breast cancer and Lung cancer kill the most women and men respectively.
• One woman dies of cervical cancer every 8 minutes in India.
• For every 2 women newly diagnosed with breast cancer, one woman dies of it
in India.
• As many as 2,500 persons die every day due to tobacco-related diseases in
India.
• Smoking accounts for 1 in 5 deaths among men and 1 in 20 deaths among
women, accounting for an estimated 9,30,000 deaths in 2010.

10. The 10 Most Common Causes of Cancer Death: 2012 Estimates

13. • Neoplasm is an abnormal growth of tissue which, if it forms a mass,
is commonly referred to as a tumor.
• The tumors are of two types.
➢ Benign tumors : They usually grow by expansion and remain
encapsulated in a layer of connective tissue. Normally benign tumors
are not life-threatening. eg. moles, warts. These types of benign
tumors are not considered as cancers.
➢ Malignant tumors or cancers : They are characterized by
uncontrolled proliferation and spread of cells to various parts of the
body, a process referred to as metastasis. Malignant tumors are
invariably life-threatening. eg . Lung cancer/ leukaemia
• Cancers arising from epithelial cells are referred to as carcinomas
while that from connective tissues are known as sarcoma.

14. Etiology
• Cancers are multifactorial in origin. The causative agents include
physical, chemical, genetic and environmental factor.
• 90% of all cancer deaths are due to avoidable factors such as
tobacco, pollution, occupation, alcohol and diet.
• Most of the cancers are caused by chemical carcinogens, radiation
energy and viruses. These agents may damage DNA or interfere
with its replication or repair.
• One mutation occurs out of 106 cell divisions. By the time a person
reaches adulthood, about 1026 cell divisions have occurred. Thanks
to the surveillance by the immune system, these aberrant cells are
usually destroyed.

15. Mutagens
• Substance that increases the rate of mutation also enhance the rate
of incidence of cancer. Therefore, all carcinogens are mutagens.
• Some human cancers are caused by chemicals. (a) occupation (aniline,
asbestos), (b) diet (aflatoxins) or (c) lifestyle (smoking).
• Tobacco, food additives, colouring agents, and aflatoxins are common
carcinogens in our environment.
• Chemical carcinogens:
• Almost 80% of the human cancers are caused by chemical
carcinogens:
1. Occupation. eg. Asbestos, benzene
2. Diet. eg. Aflatoxin B produced by fungus (AspergiIIus fIavus)
contamination of foodstuffs, particularly peanuts.
3. Drugs- certain therapeutic drugs can be carcinogenic. eg.
diethylstibesterol.
4. Life style. eg. Cigarette smoking.

16. ➢ It is estimated that one cigarette reduces 10 minutes from the
lifespan of the individual. The incidence of lung cancer is increased to
15 times more in persons smoking 10 cigarettes per day and 40 times
more when smoking 20 cigarettes per day.
➢ non-smoking spouse of a heavy smoker will have 5 times more
probability to get lung cancer than a non-smoker.

17. Mechanism of action
• Although a few of the chemicals are directly carcinogenic majority
of them require prior metabolism to become carcinogenic.
• A chemically non-reactive pro-carcinogen is converted to an
ultimate carcinogen by a series of reactions.
• Most carcinogens require promoters for the production of a
cancer. Benzo(a)pyrene applied on skin does not produce cancer.
Croton oil application also does not lead to skin cancer. But when
benzo(a)pyrene application is followed by croton oil, tumor is
developed. In this case, croton oil is termed as the promoter.
• 2-acetyl amino fluorene (AAF) when ingested, is metabolized to
produce the ultimate carcinogen, N-hydroxy-AAF. The enzymes
responsible for the activation of procarcinogens are cytochrome P-
450 system.

18. • Mechanisms of action of chemical carcinogens are:
a) Carcinogens are generally electrophiles they readily attack
nucleophilic groups of DNA.
b) Carcinogens may bind covalently to cellular DNA. N2, N3, and N7
atoms of guanine are highly prone to addition of carcinogen
groups.
c) These changes will lead to DNA alterations, in spite of DNA
repair, with increased probability of mutations.
• Chemical carcinogens may produce the cancer:
a) At the sit of exposure, e.g. buccal cancer in tobacco chewers,
skin cancer in tar workers.
b) At the site of metabolism, e.g. liver cancer produced by aflatoxin.
c) At the site of elimination, e.g. bladder cancer in persons working
with aromatic dyes.

19. Radiation energy
• X-ray, gamma-ray and UV-ray have been proved to be mutagenic
in nature and causing cancer by:
1) formation of pyrimidine dimers,
2) apurinic sites with consequent break in DNA,
3) formation of free radicals and superoxides which cause DNA
break, leading to somatic mutations.
Exposure of X-ray in foetal life will increase the risk of leukaemia in
childhood. In population studies, 1 radiation per year will increase
the cancer incidence by 40/million people per year.

20. Ames assay:
• A test to check the carcinogenicity of chemicals.
• Ames assay employs the use of a special mutant strain of
bacterium, namely Salmonella typhimurium (His-).
• This organism can not synthesize histidine; hence the same should
be supplied in the medium for its growth.
• Addition of chemical carcinogens causes mutations (reverse
mutation) restoring the ability of the bacteria to synthesize
histidine (His+).
• By detecting the strain of Salmonella (His+) in the colonies of agar
plates, the chemical mutagens can be identified.
• The Ames assay can detect about 90% of the chemical
carcinogens. This test is regarded as a preliminary screening
procedure. Animal experiments are conducted for the final
assessment of carcinogenicity.

21. These are substances which will interfere with tumor promotion.
1) Vitamin A and carotenoids are shown to reverse precancerous
conditions.
2) Vitamin E acts as an antioxidant, preventing the damage made by free
radicals and superoxides.
3) Vitamin C regularly given to persons working with aniline prevented
the production of new cancer cases.
4) Tubers, beans and leafy vegetables are shown to interrupt tumor
promotion.
5) Curcumin, the yellow substance in Turmeric is known to prevent
mutations.
6) Low protein, low fat, diet decreases the risk of cancer in animal
studies.
7) Phenolic compounds found in fruits like grapes, strawberries, walnuts,
etc. are found to be antimutagenic. Green tea is shown to be effective
against smoke induced mutations.
Antimutagens

22. Carcinogenic viruses
• The involvement of viruses in cancer was first reported by Rous in
1911.
• cell-free filtrates from certain chicken sarcomas (tumors of
connective tissues) promote new sarcomas in chickens.
• But this important discovery of Rous was ignored for several years.
• Rous was awarded the Nobel Prize in 1966 at the age of 85 for his
discovery in 1911.
• DNA of Malignant cells shows presence of viral particles and the
enzyme reverse transcriptase besides the occurrence of base
sequence.
• The viruses involved in the development of cancer, commonly
known as oncogenic viruses.
• Oncogenic viruses may be either DNA viruses or RNA viruses.

23. ➢ Burkitt in 1964 reported a type of lymphoma seen mainly in
African children.
➢ In 1969, Epstein reported that all the biopsies of BL when placed
in tissue culture for some time, generated the viral particles
which could be seen under electron microscope (Barr was the
technician who first perfected this technique). The new virus was
named as Epstein-Barr (EB) virus.

24. ▪Oncogenes– The genes capable of causing cancer are known as
oncogenes. Oncogenes were originally discovered in tumor
causing viruses.
▪Proto-oncogenes– Proto-oncogenes are a group of genes that
cause normal cells to become cancerous when they are mutated.
Mutations in proto-oncogenes are typically dominant in nature,
and the mutated version of a proto-oncogene is called an
oncogene.
▪Tumor suppressor genes- (normal growth suppressor
genes) -- encode proteins that inhibit proliferation, promote cell
death, or repair DNA
Activation of oncogenes or absence /inactivation
of tumor suppressor genes can lead to cancer.

25. DNA VIRUSES
• Three DNA viruses have been established as causing human
cancers, viz. EBV, HBV and HPV:
a) Burkitt’s Lymphoma:
• Belongs to herpes family and produces Burkitt’s lymphoma.
• It is a tumor of B lymphocytes that is consistently associated with a
[t 8:14] translocation.
• It is endemic in Africa and patient’s tumor cells carry EBV genome.
• EBV alone cannot cause the tumor. EBV causes sustained B-cells
proliferation; they acquire additional mutations and sometimes
translocation [t 8:14] and becomes tumorigenic.
b) Hepatitis B Virus (HBV):
• Hepatitis B virus infection is found to be closely associated with
formation of liver cancer.

26. c) Nasopharyngeal Carcinoma :
• Is endemic in southern China.
• EBV genome is found in all such tumour cells.
d) Human Papillomavirus (HPV):
• is the most common sexually transmitted infection in adults.
• HPV types 16 and 18 are associated with human uterine cervical
cancer; they cause 70% of all cervical cancers.
• HPV infects epithelial cells in the cervical mucosa; the virus
multiplies and lyses the host cells, causing a lesion.
• In 99% of such cases healing occurs within 6 months to 2 years. But
in about 1% cases, the HPV DNA is integrated into some of the host
cells and develop invasive cancer.
• Vaccines against high risk HPV 16 and 18 types are now developed
that provide 95% protection from infection of HPV, thereby
reducing the chances of developing cervical cancer.

27. RNA VIRUSES
• All oncogenic RNA viruses are retroviruses
Human T-Cell Leukaemia Virus (HTLV):
• HTLV-1, found associated with human leukaemia/ lymphoma.
• It is endemic in parts of Japan. Sporadic cases seen in other parts.
• HTLV-1 contains a segment in its genome called “tat”. The proteins
encoded by ‘tat’ gene are believed to be responsible for
transformation.
• They affect the transcription of certain growth factors and
receptors like IL-2 and IL-2R.

28. • In chronic myeloid leukaemia,
deletion of short arm of
chromosome 22, called
Philadelphia (Ph’) chromosome is
seen in 80% cases. In the rest,
there is translocation of 9 to 22
leading to activation of c-abl
present in chromosome 9.
• In non-Hodgkin’s lymphoma,
translocation of chromosome 14 to 18
is very common, involving the bcl- 2
oncogene. The bcl-2 product
suppresses programed cell death
leading to tumor formation.

29. Activation of proto-oncogenes to oncogenes
1. Viral insertion into chromosome:

30. 2. Chromosomal translocation: Some of the tumors exhibit
chromosomal abnormalities. This is due to the rearrangement of
genetic material (DNA) by chromosomal translocation i.e. splitting
off a small fragment of chromosome which is joined to another
chromosome. Chromosomal translocation usually results in
overexpression of proto-oncogenes.
Burkitt's lymphoma, a
cancer of human B-
lymphocytes, is a good
example of chromosomal
translocation. In this case, a
fragment from chromosome
8 is split off and joined to
chromosome 14.

31. 3. Gene amplification: Several fold amplifications of certain DNA
sequences are observed in some cancers. Administration of
anticancer drugs methotrexate (an inhibitor of the enzyme
Dihydrofolate reductase) is associated with gene amplification. The
drug becomes inactive due to gene amplification resulting in a
several fold (about 400) increase in the activity of dihydrofolate
reductase.

32. 4. Point mutation: The ras proto-oncogene is the best example of
activation by point mutation (change in a single base in the DNA).
The mutated ras oncogene produces a protein (GTPase) which
differs in structure by a single amino acid. This alteration diminishes
the activity of GTPase, a key enzyme involved in the control of cell
growth.
• The presence of ras mutations is
detected in several human
tumors- 90% of pancreatic, 50%
of colon and 30% of lung.

33. Some cellular oncogenes

34. Mechanism of action of oncogenes
• Oncogenes encode for certain proteins, namely oncoproteins.
• These proteins are the altered versions of their normal
counterparts and are involved in the transformation and
multiplication of cells.
• Growth factors :
• Several growth factors stimulating the proliferation of normal cells
are known. They regulate cell division by transmitting the message
across the plasma membrane to the interior of the cell
(transmembrane signal transduction). lt is believed that growth
factors play a key role in carcinogenesis.

35. • The cell proliferation is stimulated by growth factors.
• A growth factor binds to a protein receptor on the plasma
membrane.
• This binding activates cytoplasmic protein kinases leading to the
phosphorylation of intracellular target proteins.
• The phosphorylated proteins, in turn, act as intracellular
messengers to stimulate cell division.
• eg. Transforming growth factor (TGF-α) is a protein synthesized
and required for the growth of epithelial cells. TGF-α is produced
in high concentration in individuals suffering from psoriasis, a
disease characterized by excessive proliferation of epidermal cells.
How Growth Factors Work

37. Differences between Normal and Tumor
cells Tumor Kinetics
• The cell cycle is divided into G1, S, G2 and M phases and
completes within 18–24 hours. The cell cycle time is more or less
same for normal cells and cancer cells.
• In a normal tissue, only 1% cells are in the dividing state. In
cancer tissues, about 2–5% of cells are in the cell cycle and this
number demarcates a mildly growing tumor (2%) from an
aggressive one (5%).
• This difference is used for the treatment. Cytotoxic drugs and
radiation will kill the cells in the cell cycle, while sparing the
resting cells. Cyclin dependent kinase inhibitors (p16 and p27)
have been shown to be lost in various cancers.

38. Doubling Time
• The doubling time is the time taken by a tumor to exactly
double its mass, and is a constant for a particular growth over a
long period.
• The tumor doubling time in human cancers varies widely
between 10 days to 450 days, with a mean of about 100 days.
• Very rapidly growing tumors will need lesser days to double the
volume.
• In the case of tumor with a doubling time of 100 days, the time
taken for this growth to reach 1cm size from the initial mutated
cell is about 8–10 years.
• Thus, the tumor was present in the body for a considerable
period before the clinical detection.
• The same fact explains the development of the secondaries
several years after the treatment of the primary growth.

39. • GTP-binding proteins :
• These are a group of signal transducing proteins. Guanosine
triphosphate (GTP)-binding proteins are found in about 30% of
human cancers.
• The mutation of ras proto-oncogene is the single-most dominant
cause of many human tumors.
• The inactive ras is in a bound state with GDP. When the cells are
stimulated by growth factors, ras P21 gets activated by exchanging
GDP for GTP.
• This exchange process is catalysed by guanine nucleotide releasing
factor (GRF).
• The active ras P21 stimulates regulators such as cytoplasmic
kinases, ultimately causing DNA replication and cell division.
• In normal cells, the activity of ras P21 is short lived. The GTPase
activity, which is an integral part (intrinsic) of ras P21, hydrolyses
GTP to GDP, reverting ras 21 to the original state.

40. Anti-oncogenes or cancer-suppressor Genes
• The genes, which normally
protect the individual from
getting the cancer.
• RB gene encodes a protein
(p105) that suppress cell
proliferation, and prevent
the activity of various
oncogenes.
• Retinoblastoma occurs
only when both alleles of
the RB gene are deleted.

41. Role of p53
• A part of short arm of chromosome 17 was shown to be deleted in
various human cancers. This region is now known to contain an
onco-suppressor gene, called p53.
• This gene encodes a phosphoprotein with molecular weight
53kDa.
• It blocks the cells that have damaged DNA by triggering the
production of another protein p21, which blocks cell division until
the damage is repaired.
• If the DNA damage is severe, p53 directs the cell to commit suicide
by apoptosis.
• Most tumors have a complete absence of p53, whereas others
show mutant non-functional p53.
• It is also seen that p53 activates the expression of genes that
suppress cell proliferation.

42. Tumor Immunology
• All forms of treatment of cancer (surgery, radiotherapy and
chemotherapy) leave some residual cancer cells in the body.
These are annihilated by the body’s immune mechanism.
• (a) T cells, (b) NK cells, (c) antibody dependent complement
mediated lysis, (d) antibody dependent cell mediated cytolysis
(ADCC), and (e) macrophages play role in removal of these cancer
cells.
• In the tumor bearing host, appreciable level of immunological
reaction against the cancer is detected. This is because of the
presence of tumor associated antigens (TAA) on the surface of
cancer cells.

43. TUMOR MARKERS
• The biochemical indicators that detect the presence of cancers
are collectively referred to as tumor markers.
• These are the abnormally produced molecules of tumor cells
such as surface antigens, cytoplasmic proteins, enzymes and
hormones.
• They are useful for the following purposes:
1. For follow-up of cancer and to monitor the effectiveness of the
therapy and also to detect the recurrence of the tumor .
2. To facilitate detection of cancer. The presence of tumor marker
suggests the diagnosis.
3. For prognosis. Serum level of the marker may indicate roughly
the tumor load, which in turn indicates whether the disease is
curable or not.

44. Clinically Important Tumor Markers
•Alpha Fetoprotein (AFP):
• It is fetal albumin and has similarities with adult albumin.
• It is increased in the circulation of patients with hepatocellular
carcinoma, germ cell tumors, teratocarcinoma of ovary and in
pregnancy with fetal malformations of neural tube.
• In adult males and non-pregnant females, normal value is less than
15 ng/L. A value of AFP above 300 ng/L is often associated with
cancer (although levels in this range may be seen in non-malignant
liver diseases).
• Levels above 1000 ng/L are almost always associated with cancer
(except in pregnancy).
• The fucosylated fraction of AFP (AFP-L3) has been reported to be a
more specific marker for hepatocellular carcinoma.

45. •Carcinoembryonic Antigen (CEA):
• This is a complex glycoprotein, normally produced by the
embryonic tissue of liver, gut and pancreas.
• The CEA level is markedly increased in colorectal cancers.
• Over 50% of persons with breast, colon, lung, gastric, ovarian,
pancreatic, and uterine cancer have elevated levels of CEA.
• CEA levels may also be elevated in inflammatory bowel disease
(IBD), pancreatitis, and liver disease. Heavy smokers and about
5% of healthy persons have elevated plasma levels of CEA.
• Due to this, CEA lacks specificity for cancer detection.

46. Beta Chain of Chorionic Gonadotropin:
• Beta-hCG is synthesized by normal syncytiotrophoblasts (cells
of placental villi).
• hCG is a glycoprotein; it has alpha and beta subunits. The alpha
subunit is identical with those of FSH, TSH and LH.
• The beta subunit is specific for hCG. It is increased in
hydatidiform mole, choriocarcinoma and germ cell tumors.
About 60% of testicular cancers secrete hCG.
• Normal value is less than 20 IU/L for males and non-pregnant
females. Greater than 100,00 IU/L indicates trophoblastic
tumor.

47. Cancer Antigen 125
• CA-125 is a tumor marker for ovarian cancers. It is a glycoprotein
with a molecular weight of 10 million.
• Approximately 75% of persons with ovarian cancer will have
elevated serum levels.
• Elevated levels of CA-125 are also found in approximately 20% of
persons with pancreatic and digestive tract cancers.
• This test is used to determine whether recurrence of the cancer
has occurred following chemotherapy.
• Normal blood level of CA-125 is less than 35 U/mL.

48. Common tumor markers

49. Cancer therapy
• Chemotherapy, employing certain anticancer drugs, is widely used
in the treatment of cancer.
• The effectiveness of cytotoxic drugs is directly proportional to the
doubling time of the tumors.
• The effectiveness of anticancer drugs is inversely proportional to
the size of the tumor.
• The major limitation of cancer chemotherapy is that the rapidly
dividing normal cells (of hematopoietic system, gastrointestinal
tract, hair follicles) are also affected.
• Cell destruction by cytotoxic drug follows the first order kinetics,
that is, it reduces a constant percentage and not a constant
number of cancer cells.

50. Common Anti-Cancer Drugs

51. ➢Methotrexate:
• It inhibits dihydrofolate reductase.
• In presence of methotrexate, tetrahydrofolic acid is not
produced, which is necessary for incorporation of C2 and C8 of
purines and C5 methyl group in thymidine.
➢6-Mercaptopurine:
• It prevents amination of IMP to AMP, so that the availability of
AMP is reduced. This leads to inhibition of synthesis of DNA,
and in turn cell division.
➢5-Fluorouracil:
• Fluorouracil will inhibit thymidylate synthase, thereby reducing
the conversion of dUMP to dTMP.
• Thereby thymine incorporation in the DNA, and consequent
DNA synthesis are prevented.

52. ➢ Cyclophosphamide:
• It is extensively used in different cancers, especially lymphomas and
myeloid leukaemia.
• It is an alkylating agent, causing cross linkage between adjacent bases of
the double helix.
• DNA strands cannot separate, and new DNA synthesis is blocked.
➢ Mitomycin C:
• It is derived from Streptomyces. The drug causes cross bridge between
DNA strands, preventing separation of strands, and inhibiting new DNA
synthesis.
➢ Vincristine and Vinblastine:
• They are alkaloids isolated from the leaves of periwinkle or vinca rosea.
• In 1958, Irving Johnson first established the clinical usefulness of the drug
in human leukaemia's.
• The drugs are now widely used in leukaemia's, lymphomas as well as in
solid tumors.
• cells are arrested in metaphase and cell division is inhibited.

53. Monoclonal Antibody
• These drugs are a relatively new innovation in cancer treatment.
1. The antibody marks the cancer cell and makes it easier for the
immune system to attack.
• The drug rituximab attaches to CD20 found only on B cells;
makes the cells more visible to the immune system, which can
then attack.
2. Block growth factors:
• Certain cancer cells make extra copies of the growth factor
receptor. This makes them grow faster than the normal cells.
Monoclonal antibodies can block these receptors and prevent
the growth signal.
3. Stop new blood vessels from forming:
• Monoclonal antibodies blocks growth Signals from cancer cells
that may help prevent a tumor from developing a blood supply.

54. Prevention of Cancer
• certain precautionary measures are advocated to prevent or
reduce the occurrence of cancer.
• Most important among them, from the biochemical perspective,
are the antioxidants namely vitamin E, β-carotene, vitamin C and
selenium.
• The antioxidants prevent the formation or detoxify the existing free
radicals. In addition, antioxidants stimulate body's immune system,
and promote detoxification of various carcinogens.
• most of the vegetables and fruits are rich in antioxidants. Their
increased consumption is advocated to prevent cancer.