anticancer drugs, classification of anticancer drug , types of cancer ,mechanism action of anticancer drugs

1. anticancer drugs
Presented by
Rasika.R.Walunj
M.pharm (QAT)
Modern College Of Pharmacy (For Ladies),
Moshi, Pune. 412105

2. What is cancer..???
• Cancer: An abnormal growth of cells which tend
to proliferate in an uncontrolled way and, in some
cases, to metastasize (spread).
• There are more than 100 types of cancer,
including breast cancer, skin cancer, lung cancer,
colon cancer, prostate cancer, and lymphoma.
Symptoms vary depending on the type.
• Cancer treatment may include chemotherapy,
radiation, and/or surgery.

3. How to cancer arise…
• Genetic changes that cause cancer can be inherited from
our parents.
• They can also arise during a person’s lifetime as a result of
errors that occur as cells divide or because of damage to
DNA caused by certain environmental exposures.
• Cancer-causing environmental exposures include
substances, such as the chemicals in tobacco smoke, and
radiation, such as ultraviolet rays from the sun.
• In general, cancer cells have more genetic changes, such as
mutations in DNA, than normal cells. Some of these
changes may have nothing to do with the cancer; they may
be the result of the cancer, rather than its cause.

4. "Drivers" of Cancer
• The genetic changes that contribute to cancer tend to affect
three main types of genes—proto-oncogenes, tumor
suppressor genes, and DNA repair genes. These changes are
sometimes called “drivers” of cancer.
• Proto-oncogenes are involved in normal cell growth and
division. However, when these genes are altered in certain
ways or are more active than normal, they may become
cancer-causing genes (or oncogenes), allowing cells to grow
and survive when they should not.
• Tumor suppressor genes are also involved in controlling cell
growth and division. Cells with certain alterations in tumor
suppressor genes may divide in an uncontrolled manner.

5. Conti..
• DNA repair genes are involved in fixing damaged
DNA. Cells with mutations in these genes tend to
develop additional mutations in other genes. Together,
these mutations may cause the cells to become
cancerous.
• As scientists have learned more about the molecular
changes that lead to cancer, they have found that certain
mutations commonly occur in many types of cancer.
Because of this, cancers are sometimes characterized by
the types of genetic alterations that are believed to be
driving them, not just by where they develop in the
body and how the cancer cells look under the
microscope.

6. When Cancer Spreads
• A cancer that has spread from the place where it first started to another
place in the body is called metastatic cancer. The process by which
cancer cells spread to other parts of the body is called metastasis.
For example, breast cancer that spreads to and forms metastatic
tumor in the lung is metastatic breast cancer, not lung cancer.
Under a microscope, metastatic cancer cells generally look the same as
cells of the original cancer. Moreover, metastatic cancer cells and cells of
the original cancer usually have some molecular features in common,
such as the presence of specific chromosome changes.

7. Types of Cancer
• Carcinoma: Cancer that begins in the skin or
in tissues that line or cover internal organs
• Sarcoma: Cancer that begins in bone,
cartilage, fat, muscle, blood vessels, or other
connective or supportive tissue.
• Leukemia: Cancer that starts in blood-forming
tissue such as the bone marrow and causes
large numbers of abnormal blood cells to be
produced and enter the blood

8. Conti..
• Lymphoma and myeloma: Cancers that begin in the cells of the
immune system
• Central nervous system cancers: Cancers that begin in the tissues
of the brain and spinal cord
• Other Types of Tumors
• Germ Cell Tumors begins in the cells that give rise to sperm or
eggs. These tumors can occur almost anywhere in the body and can
be either benign or malignant
• . Neuroendocrine Tumors Neuroendocrine tumors form from
cells that release hormones into the blood in response to a
signal from the nervous system.
• These tumors, which may make higher-than-normal amounts
of hormones, can cause many different symptoms.
• Neuroendocrine tumors may be benign or malignant.

9. Anticancer drugs
• The anticancer drug either kill cancer cells or
modify their growth.
• Discovery of anticancer agents started after
1940’s (when nitrogen mustard was used)
• Most of the agents were discovered in 1950-1970.
• Cancer treatment:
• Chemotherapy
• Radiotherapy
• Immunotherapy
• Surgery

10. Classification Anticancer Drugs
• Alkylating Agents
– Nitrogen mustards: Melphalan,
Cyclophosphamide, Ifosfamide
– Nitrosoureas
– Alkylsulfonates
– Ethyleneimines
– Triazene
– Methyl Hydrazines
– Platinum Coordination complexes: Cisplatin,
Carboplatin, Oxaliplatin

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• Antimetabolites
– Folate Antagonists: Methotrexate
– Purine antagonists
– Pyrimidine antagonists: 5-Fluorouracil, Cytarabibe
• Natural Products
– Plant Products
• Vinca Alkaloids: Vincristine, Vinblastine
• Taxanes: Paclitaxel, Docetaxel
• Epipodophyllotoxins: Etoposide
• Camptothecins: Irinotecan
– Microorganism Products
• Antibiotics: Doxorubicin, Bleomycin
• Enzymes: L-Asparaginase

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• Miscellaneous
– Hydroxyurea
– Imatinib Mesylate
– Rituximab
– Epirubicin
– Bortezomib
– Zoledronic Acid
– Geftinib
– Leucovorin
– Pamidronate
– Gemcitabine

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• Hormones and Antagonists
– Corticosteroids: Prednisone, Dexamethasone
– Estrogens: Ethinyloestradiol
– Antiestrogens: Tamoxifen
– Progesteron derivative: Megestrol Acetate
– Androgen: Testosterone propionate
– Antiandrogen: Flutamide , Bicalutamide
– Aromatase inhibitor: Letrozole , Anastrazole
– 5-alpha reductase inhibitor: Finasteride
– GnRH Analogue: Leuprolide, Buserelin
– Growth Hormone, glucagon and insulin inhibitor:
Octreotide

14. Mechanism action of anticancer
drugs
• The available anticancer drugs have distinctly different mechanisms
of action which may vary at different drug concentrations and in
their effects on different types of normal and neoplastic cells. While
not selectively lethal to cancer cells, as such, in many instances
• These drugs produce more extensive injury and death to certain
neoplastic cells than to the normal tissues, presumably because of
quantitatively altered metabolic processes in the cancer cell.
• In the great majority of cases, also initially responsive cancers recur
in a form resistant to the previously effective agent. Despite the
many unsolved problems, there is a great deal of information on
how anticancer drugs act at the cellular level to inhibit the growth of
or to destroy, susceptible cells.

15. Molecular biology is deoxyribonucleic acid (DNA) to
ribonucleic acid (RNA) to protein synthesis. DNA, the genetic
material of the cell, acts as the selective template for the
production of the specific forms of transfer, ribosomal and
messenger ribonucleic acid (RNA).
DNA, in directing the formation of specific sequences of
messenger RNA, determines which proteins (enzymes) will be
synthesized on the RNA templates.
The enzymes in turn are responsible for the structure, metabolic
activity, proliferative rate, and function of the cell. Interference
with the structure of DNA (alkylating agents, procarbazine) or its
function(dactinomycin) disorganizes and disrupts the cell.
Compounds with this mechanism of action have been useful
anticancer drug
DNA Function

17. Antimetabolite's
• Antimetabolites which are incorporated into RNA or act to
inhibit protein synthesis have not proved to be clinically
useful in the treatment of cancer.
• Certain antimetabolites inhibit the biosynthesis of the
nucleic acids. Interruption in the formation of these essential
components of DNA and RNA, which each cell produces in
order to function and multiply, results in cell death.
• Antimetabolites with this mechanism of action are useful in
some forms of cancer. 6-Mercaptopurifle and 6-thioguanine
are prevent purine ring biosynthesis and inter conversion of
the purine bases.

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• Methotrexate are inhibits folic acid reductaseto block
the reduction of folic acid totetrahydrofolic acid which
transports single carbon fragments for the synthesis of
the purine ring and for themethylation of deoxyuridylic
acid tothymidylic acid, an essential component of DNA.
5-Fluorouracil is metabolized to its deoxynucleotide
form to inhibit the enzyme, thymidylate
• Synthetase, which also is involved in the methylation of
deoxyuridylic acid to thymidylic acid;
arabinosylcytosine blocks the reduction of cytidylic to
deoxycytidylic acid, and by preventing the formation of
another essential component of DNA, DNA replication

19. Vinca alkaloids
• All vinca alkaloids are administered intravenously
(IV). They are eventually metabolized by the liver
and excreted.
• The vinca alkaloids are cytotoxics – they halt the
division of cells and cause cell death. During cell
division, vinca alkaloid molecules bind to the
building blocks of a protein called tubulin, inhibiting
its formation. Tubulin protein normally works in
cells to create “spindle fibers,” (also called
microtubules).

20. Continue…
• These microtubules provide cells with both the
structure and flexibility they need to divide
and replicate. Without microtubules, cells
cannot divide.
• The vinca alkaloid’s mechanism in a nutshell:
by occupying tubulin’s building block
structure, vinca alkaloids prevent cancer cells
from successfully dividing cells.

22. Steroid Hormones
• Un Physiological doses of exogenously
administered steroid hormones alter hormonal
balance in the patient and modify the growth
of some cancers arising from tissues
particularly susceptible to hormonal
influences.
• The mechanism whereby the steroid hormones
stimulate or inhibit cellular growth and
function is not clear, but it is believed to be at
the level of processes concerned with RNA to
protein synthesis.

23. L-asparaginase
• L-asparaginase acts in a unique manner to
hydrolyse asparagine to aspartic acid, and
neoplastic cells unable to make this amino acid,
die if the supply of L-asparagine in the
circulating blood, on which they are dependent,
is destroyed by the enzyme.
• Normal cells synthesize L-asparagine for their
needs, and thus appear to be unaffected by
the L-asparagine deficiency in the body.