You are on page 1of 5

Angelyne E.

De Paz BSN IV-A01 Assignment in NCM 106 Some chemotherapy agents are able to kill a cell during any phase of the cycle (these are called cell-cycle nonspecific), others are only able to kill during a specific phase and are unable to work in the resting phase (called cell-cycle specific). By giving cell-cycle specific agents at multiple time points, they are able to reach the maximum number of cells in the particular phase they affect. Therefore, these are most effective when given in divided doses (over multiple days or time points, for example: once a day for 5 days or every three hours for 4 doses) or by continuous infusion. Cell-cycle nonspecific drugs act against cancer cells at any phase of the cell cycle, including the resting phase. Cell-cycle nonspecific drugs are most effective when given in bolus doses (for example, over 20 minutes once). Cell death may not take place at the exact time the chemotherapy is given. Often a cell must undergo several divisions before it ultimately dies. Because not all the cancer cells die after a chemotherapy treatment, repeated doses are used to continue to reduce the number of cells. Drug Cell-CycleClass Specific (ccs)/ Cell-CycleNonspecific (ccnS) Cell-CycleANTIMETABOLIT Specific (CCS) E Action

Methotrexate (mexate)

Methotrexate is used to treat choriocarcinoma, leukemia in the spinal fluid, osteosarcoma, breast cancer, lung cancer, non-Hodgkin lymphoma, and head and neck cancers. It is also used to treat other cancers and non-cancerous conditions. Methotrexate is part of a general group of chemotherapy drugs known as antimetabolites. It prevents cells from

using folate to make DNA and RNA. Because cancer cells need these substances to make new cells, methotrexate helps to stop the growth of cancer cells. 5 Fuorouracil (5 FU) Cell-CycleSpecific (CCS) ANTIMETABOLIT E As a pyrimidine analogue, it is transformed inside the cell into different cytotoxic metabolites which are then incorporated into DNA and RNA, finally inducing cell cycle arrest and apoptosis by inhibiting the cell's ability to synthesize DNA. It is an Sphase specific drug and only active during certain cell cycles. In addition to being incorporated in DNA and RNA, the drug has been shown to inhibit the activity of the exosome complex, anexoribonuclease co mplex of which the activity is essential for cell survival. Capecitabine is a prodrug that is converted into 5-FU in the tissues. It can be administered orally. ANTINEOPLASTIC Vincristine's ; CYTOTOXIC; (Oncovin, Vincasar PLANT ALKALOID PFS, Vincrex) anticancer properties

Vincristine (Oncovin)

Cell-CycleSpecific (CCS)

Paclitaxel (Taxol)

Cell-CycleNonspecific (CCNS)

MITOTIC INHIBITOR (spindle poison)

Mithramycin (Mithracin)

Cell-CycleSpecific (CCS)

ANTIBIOTIC (isolated from Streptomyces plicatus)

Cyclophospham Cell-Cycleide (Cytoxan) Nonspecific


result from its ability to inhibit cell division during earlymitosis. Vincristine binds to the tubulin monomers preventing the formation of spindle microtubules. By binding to the building blocks of microtubules, vincristine disables the cell's mechanism for aligning and moving the chromosomes. Vincristine stops the separation of the duplicated chromosomes and prevents cell division. While vincristine works to keep the cancer cells from dividing, it does not selectively inhibit cancer cell division. It can also halt the division of some healthy cells, leading to some of the common side effects. Promotes early microtubule assembly; prevents depolymerization, bringing about cell arrest. In the presence of magnesium ions, the drug binds with guanine bases of DNA and inhibits DNAdirected RNA synthesis. Cell cyclespecific for S-phase. Cyclophosphamide is a drug that is used


Cisplatin (platinol)

Cell-CycleNonspecific (CCNS)


Bleomycin (Blenoxane)

Cell-CycleNonspecific (CCNS)


primarily for treating several types of cancer. In order to work, cyclophosphamide first is converted by the liver into two chemicals, acrolein and phosphoramide. Acrolein and phosphoramide are the active compounds, and they slow the growth of cancer cells by interfering with the actions of deoxyribonucleic acid (DNA) within the cancerous cells. Unfortunately, normal cells also are affected, and this results in serious side effects. In addition to slowing the growth of cancerous cells, cyclophosphamide also suppresses the immune system and is referred to as immunosuppressive. Cisplatin selectively inhibits the synthesis of DNA, and thus slows or stops the growth of cancer cells in the body. Although the exact mechanism of action of BLENOXANE is unknown, available evidence indicates that the main mode of action is the inhibition of DNA synthesis with some evidence of

lesser inhibition of RNA and protein synthesis. Bleomycin is known to cause single, and to a lesser extent, doublestranded breaks in DNA. In in vitro and in vivo experiments, bleomycin has been shown to cause cell cycle arrest in G2 and in mitosis. When administered into the pleural cavity in the treatment of malignant pleural effusion, BLENOXANE acts as a sclerosing agent.