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Treatments
> Chemo agents & mechanisms
Last update:
04/23/2010
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TOPICS
DNA-Altering
| Anti-tumor Antibiotics |
Antimetabolites
| DNA Repair Enzyme Inhibitors |Block Cell Duplication |
Proteasome inhibition
| Rituxan | Steroidal
Recommended Reading:
Cancer Multidrug Resistance (MDR)
nature.com
| How Chemotherapy Works
Cancer.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
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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
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DNA-Altering Drugs
These drugs change DNA, the building block of cells, to prevent cell growth.
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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
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Mechlorethamine (nitrogen mustard, Mustargen®) - BCCancer
| MedlinePlus
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Anti-tumor Antibiotics
Interact with DNA and decrease
cell survival
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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.
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Antimetabolites -
"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
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Antimetabolites
These drugs interfere with normal cell growth.
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DNA Repair Enzyme Inhibitors
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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.
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Block Cell Duplication
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Damage cell
structures that are required for a cell to divide
Microtubule inhibitors
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Block Cell Duplication
These drugs damage cell structures required for cells to divide.
Vinorelbine is a vinca alkaloid that interferes with microtubule
assembly.
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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.
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Targets
Proteasome
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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
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Steroidal
(Corticosteroids)
steroidal: anti-inflammatory, Immunosuppressant
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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
NEW: 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.
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Methylprednisolone (Medrol®) MedlinePlus
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Background:
Glucocorticoids Disease Mechanism II: Inflammation - Powerful Anti-inflammatory Compounds
stanford.edu
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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
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Mechanisms of anti-inflammatory action Related
abstracts
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Mechanisms of killing lymphoid cells Related
abstracts
Overview & side
effects About.com
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