|
Treatments > Chemo agents & mechanisms
Last update: 03/03/2014
|
TYPES
DNA-Altering | Anti-tumor Antibiotics | Antimetabolites | DNA Repair Enzyme Inhibitors | Block Cell Duplication
Proteasome inhibition | Rituxan | Steroidal
Recommended Reading:
ncbi.nlm.nih.gov
Cancer Multidrug Resistance (MDR) nature.com
How Chemotherapy Works Cancer.org
Chemotherapy Overview oralcancerfoundation.org
 "The ability of chemotherapy to kill cancer cells depends on its ability to halt cell division. Usually, the drugs work by damaging the RNA or DNA that tells the cell how to copy itself in division. If the cells are unable to divide, they die. The faster the cells are dividing, the more likely it is that chemotherapy will kill the cells, causing the tumor to shrink. They also induce cell suicide (self-death or apoptosis)." chemocare.com
|
DNA-Altering Drugs
Alkylating agents:
DNA cross linking is a primary role of agents
Replicating cells are most susceptible to agents
Alkylating agents are not cell cycle specific
fpnotebook.com
Also see Consequences and Targets of Alkylating Agents
PDF
Return to top
|
DNA-Altering Drugs
These drugs change DNA, the building block of cells, to prevent cell growth.
.gif) |
Bendamustine - micromedex.com > Treatment abstracts
|
|
Carboplatin (Paraplatin®) - BCCancer | Cancerbacup
|
|
Carmustine (BCNU®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Chlorambucil (Leukeran®) - BCCancer | Cancerbacup > Treatment abstracts
|
|
Cisplatin (Platinol®) - BCCancer | Cancerbacup | MedlinePlus
|
Evaluation of long-term toxicity in patients after cisplatin-based chemotherapy for non-seminomatous testicular cancer - PubMed
|
|
|
Cyclophosphamide injection (Cytoxan®) - BCCancer | Cancerbacup
|
|
Cyclophosphamide oral (Cytoxan®) - BCCancer
|
|
Dacarbazine (DTIC®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Ifosfamide (ifex®)Lomustine (CCNU®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Mechlorethamine (nitrogen mustard, Mustargen®) - BCCancer | MedlinePlus
|
|
Melphalan (Alkeran®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Procarbazine (Matulane®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Anti-tumor Antibiotics
Interact with DNA and decrease cell survival
Return to top
|
Anti-tumor Antibiotics
These drugs interact with DNA and decrease cell survival. Drugs that come from natural sources, such as plants or yeast, include the following. Click link to read details.
|
Bleomycin (Blenoxane®) - BBCancer | Cancerbacup | MedlinePlus
|
|
Doxorubicin (Adriamycin®, Rubex®) anthracyline drug- BCCancer | Cancerbacup | MedlinePlus
|
|
Doxorubicin, Liposomal (Doxil) - BBCancer | MedlinePlus | Project Inform
Full prescribing info from Doxil.com - PDF | PDF-Help | Cancerbacup
|
|
Epirubicin, anthracyline drug http://www.cancerbacup | nlm.nih.gov
|
|
Idarubicin (Idamycin®) - BBCancer | Cancerbacup | MedlinePlus
|
|
Mitoxantrone (Novantrone®) - BBCancer | Cancerbacup | MedlinePlus
|
|
Antimetabolites -
About Antimetabolites - pharmacology.unmc.edu
"Antimetabolites are very similar to normal substances within the cell. When the cells incorporate these substances into the cellular metabolism, they are unable to divide. Antimetabolites are cell-cycle specific. They attack cells at very specific phases in the cycle. Antimetabolites are classified according to the substances with which they interfere." chemocare.com
|
Antimetabolites
These drugs interfere with normal cell growth.
|
Chlorodeoxyadenosine (Cladribine®) - BBCancer | MedlinePlus
Other names: 2-chlorodeoxyadenosine; 2-CdA
|
|
Cytarabine IV (cvtosine arabinoside, Ara-C, Cytosar - BBCancer | MedlinePlus
|
|
Fludarabine IV (Fludara®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Fludarabine oral (Fludara®) - BCCancer | Cancerbacup | MedlinePlus
|
|
Gemcitabine (Gemzar®) - BBCancer | Treatment abstracts
|
|
Mercaptopurine oral (Purinethol®) - BBCancer | MedlinePlus | Cancerbacup
|
|
Methotrexate oral (Rheumatrex®) - BBCancer| MedlinePlus | Cancerbacup
Other name: amethopterin
|
|
Pentostatin IV (Nipent®) - BBCancer | MedlinePlus
|
|
Thioguanine oral (Lanvis®) - BBCancer | MedlinePlus | Cancerbacup
|
|
DNA Repair Enzyme Inhibitors
Return to top
|
DNA Repair Enzyme Inhibitors
These drugs act on certain proteins (enzymes) that normally work to repair faulty DNA and therefore make cells more likely to die when they are injured.
-
Etoposide oral (VP-16, VePesid®, Etopophos) - BBCancer
-
Etoposide IV (VP-16, VePesid®, Etopophos) - BBCancer | MedlinePlus
|
Block Cell Duplication --
Damage cell structures that are required for a cell to divide
Microtubule inhibitors
About mechanism of action
|
Block Cell Duplication
These drugs damage cell structures required for cells to divide.
|
Vinblastine (Velban®) - BBCancer | Cancerbacup | MedlinePlus
|
|
Vincristine (Oncovin®) - BBCancer | Cancerbacup | MedlinePlus
|
Vinorelbine is a vinca alkaloid that interferes with microtubule assembly.
-
Vinorelbine (Navelbine®) - FDA | BBCancer | Treatment abstracts
|
Targets Proteasome
inhibits proteasomal degradation
"The proteasomal degradation pathway is essential for many cellular processes, including the cell cycle, the regulation of gene expression, and responses to oxidative stress."
wikipedia
Velcade is classified as a targeted therapy because it inhibits proteasomal
degradation within the cell. I'll try to explain what that means:
A cancer cell is like an unruly engine that races fast, burns lots of gas, and runs unevenly ... and so it expels more byproducts than an engine that runs
normally. The way velcade works is to close down the waste disposal (exhaust) system of the cell (the proteasome) so that the engine is less able expel the large amount of cellular waste (proteins), causing the
abnormally running cells to choke and stall out. Normal cells are less effected by the inhibition of the cellular garbage disposal system because they run more efficiently.
Return to top
|
Targets Proteasome
|
Velcade (bortezomib) Approved for Mantle Cell lymphoma (MCL)
|
FDA full prescribing information PDF
|
|
Highlights of prescribing information
|
|
Mantle Cell: Multicenter phase II study of bortezomib in patients with relapsed or refractory mantle cell lymphoma. J Clin Oncol. 2006 Oct 20;24(30):4867-74. Epub 2006 Sep 25. PMID: 17001068
RESULTS: In total, 155 patients were treated. Median number of prior therapies was one (range, one to three).
Response rate in 141 assessable patients was 33% including 8% complete response (CR)/unconfirmed CR. Median DOR was 9.2 months. Median TTP was 6.2 months.
Results by investigator assessments were similar. Median OS has not been reached after a median follow-up of 13.4 months. The safety profile of bortezomib was similar to previous experience in relapsed multiple myeloma.
The most common adverse events grade 3 or higher were peripheral neuropathy (13%), fatigue (12%), and thrombocytopenia (11%). Death from causes that were considered to be treatment related was reported for 3% of patients.
CONCLUSION: These results confirm the activity of bortezomib in relapsed or refractory MCL, with predictable and manageable toxicities. Bortezomib provides significant clinical activity in terms of durable and complete responses, and may therefore represent a new treatment option for this population with usually very poor outcome. Studies of bortezomib-based combinations in MCL are ongoing.
|
|
Other lymphomas: Phase II clinical experience with the novel proteasome inhibitor bortezomib in patients with indolent non-Hodgkin's lymphoma and mantle cell lymphoma. Abstract
|
|
|
Steroidal
(Corticosteroids)
steroidal: anti-inflammatory, Immunosuppressant
|
Steroidal (Corticosteroids)
Corticosteroids, including Prednisone, Prednisolone, Methylprednisolone and Dexamethasoneare are a group of synthetic hormones closely related to cortisol (a glucocorticoid), a natural hormone produced in the adrenal cortex.
"Prednisone decreases inflammation by preventing white blood cells from functioning properly. More specifically, the drug interferes with lymphocytes (one of several types of white blood cells). The presence of white blood cells result in inflammation (for many reasons, damage to tissue, fungus, virus, bacteria, allergens and almost any foreign invader) - they go to a site and their presence inflames the area. Prednisone causes lymphocytes to break apart and die." Source: members.cox.net
|
Recent insights into the mechanism of glucocorticosteroid-induced apoptosis.
Cell Death Differ. 2002 Jan;9(1):6-19. Review. PMID: 11803370
Glucocorticosteroid hormones induce apoptosis (cell death) in lymphocytes.
|
|
ncbi.nlm.nih.gov
|
|
Dexamethasone (Decadron®) BBCancer | MedlinePlus
|
|
Methylprednisolone (Medrol®) MedlinePlus
|
|
Prednisone (Deltasone®) BBCancer | MedlinePlus
|
Background:
|
Glucocorticoids Disease Mechanism II: Inflammation - Powerful Anti-inflammatory Compounds stanford.edu
|
|
Pretreatment with glucocorticoids enhances T-cell effector function: possible implication for immune rebound accompanying glucocorticoid withdrawal.
Cell Transplant. 1999 Nov-Dec;8(6):637-47. PMID: 10701493 | Related abstracts
|
|
Mechanisms of anti-inflammatory action Related abstracts
|
|
Mechanisms of killing lymphoid cells Related abstracts
|
|
Overview & side effects About.com
|
|
