immunosupressants and anticancer Flashcards
Epidemiology of Cancer
# associated disease processes
leading cause of the death in the U.S.?
Nearly ? deaths a day
% of all deaths
Many causes of cancer are mediated by ?
theories on cancer pathophysiologic process?
150+ associated disease processes
Second leading cause of the death in the U.S.
Nearly 1,500 deaths a day
25% of all deaths
Many causes of cancer are mediated by the environment
and lifestyle of a person
Smoking
Obesity
Alcohol consumption
Multitude of theories on cancer pathophysiologic process
Neoplasia
Process of altered cell differentiation and growth
Uncoordinated
Autonomous
Lacks normal regulatory control
Neoplasm
New growth
“Tumor”
Cancer
Disease resulting from altered cell differentiation and growth
Review: Cell Growth & Proliferation
Cell Differentiation
Proliferating cells become progressively?
Cells have a specific set of?
As cells differentiate, what deminishes?
Undifferentiated cells are hallmark of?
Proliferating cells become progressively more specialized
Cells have a specific set of structural, functional, and life-expectancy characteristics
As cells differentiate, their capacity or proliferation diminishes
Undifferentiated cells are hallmark characteristic of cancer cells
Cell Growth Gone Wrong: Cancer
Unchecked growth that progresses toward limitless expansion
Abnormal and rapid proliferation
Loss of differentiation> anaplasia
Causation – genetic & external
Comparison of Characteristics: normal cells and cancer cells
Carcinoma
Carcinoma
Arise from the cells that cover external and internal body surfaces such as lung,
pancreatic, breast, and colon
Sarcoma
Arise from cells found in the supporting tissues of the body such as bone, cartilage,
fat, connective tissue, and muscle
Lymphoma
Arise in lymph nodes and tissues of the body’s immune system
Leukemia
Cancers of the immature blood cells that grow in the bone marrow
Invasion & Metastasis
Solid tumors secrete enzymes that break down proteins and contribute to infiltration, invasion, and penetration of surrounding tissues
Complete surgical removal difficult
Cancer cells may travel and “seed” into different body cavities where they can proliferate and cause tumor growth (metastasis)
Blood vessel and lymphatic spread
Finely orchestrated; selected cells only
Angiogenesis
Metastasis & Use of Bisphosphonates in Cancer
current tx guidelines
Metastasis & Use of Bisphosphonates in Cancer
Bone health?
bone pain?
Reduction of ?
Bone health maintenance
Reduce bone pain due to hypercalcemia
Reduction of bone metastasis (breast & prostate cancer)
bisphosphonates in prostate cancer
70% of breast and prostate cancer patients develop bone metastases
15-30% of other common solid cancers
bisphophonates in breast cancer
early onset and when metatstisized
bisphosphonate names
Clodronate
moa, route, potentcy
BP
given oral/IV
10 potentcy factor
Pamidronate
moa, route, potentcy
BP, IV, 100
Alendronate
moa, route, potentcy
BP ,oral, 500
Ibandronate
moa, route, potentcy
BP , oral/IV, 1000
Risedronate
moa, route, potentcy
BP, oral, 2000
Zoledronate*
moa, route, potentcy
BP, IV, 10000
MOA: Bisphosphonates
Inhibit osteoclast
Attach to bony surfaces undergoing active resorption
Bisphosphonates released during resorption by osteoclasts impairs ability of osteoclasts to form the ruffled border, to adhere to the bony surface
Reduce osteoclast genesis and recruitment
Promoting osteoclast apoptosis
Tumor Cell and Osteoclast Symbiotic Relationship
* tumor cell releases:
Tumor Cell and Osteoclast Symbiotic Relationship
* bone resobrtion releases:
Result of Tumor Cell and Osteoclast Symbiotic Relationship
Symbiotic relationship further increases bone destruction and
tumor growth.
[do not need to memorize hormones]
Tumor Cell and Osteoclast Symbiotic Relationship diagrammed
Dental Concerns: Bisphosphonates
associated with? mechanism? precipitated by?
risk factors of dental concerns for BP
Hx of bisphosphonates especially IV
Hx of Cancer
Corticosteroid therapy
Diabetes
Smoking
Alcohol use
Poor oral hygiene
Chemotherapuetic drugs
what often preceeds MRONJ
extractions
Study on ONJ Risk
increased incidence with increased duration of tx (1% per yr)
what bp has the highest risk for MRONJ
zolendronate
Non-Cancer pts on BP’s and dental tx
Low-risk for osteoporosis dosed bisphosphonates – 0.1%
ADA – “recommends that a patient with active dental or periodontal disease should
be treated despite the risk of developing ARONJ, because the risks and consequences
of no treatment likely outweigh the risks of developing ARONJ.”
Additional Considerations of BP’s
Education
drug holidays?
chlorohexidine use?
Prophylactic antibiotics?
Education
Avoid drug holidays
0.2% Chlorhexidine: rinse for 1-minute prior to dental treatment and
continue rinsing twice daily for 7-days after treatment
Prophylactic antibiotics: no specific dose/agent recommendations
Amoxicillin (Amoxil) or amoxicillin/clavulanic acid (Augmentin) has been successful in studies
Retrospective analysis for prevention of ONJ in multiple myeloma pts using abx prophylaxis?
abx used and dose?
Prospective case series, for prevention of ONJ in patient requiring tooth
extraction and on IV bisphosphonate
abx/dose?
Cancer pts ADA/AAOMS dental tx and using BP’s
High-risk for oncologically dosed bisphosphonates – 2-18%
ADA – does not address
AAOMS – “procedures that involve direct osseous injury should be avoided.
Nonrestorable teeth may be treated by removal of the crown and endodontic
treatment of the remaining roots. Placement of dental implants should be avoided in
the oncologic patient receiving IV antiresorptive therapy”
BP duration and MRONJ
increased incicdence when used over longer times
Mechanism of Action: Denosumab (Xgeva, Prolia)
Inhibit osteoclast activation
RANKL is secreted by bone marrow cells and osteoblasts
RANKL binds to the RANK receptor on osteoclasts and promotes osteoclast
differentiation and activity.
Denosumab is a fully human monoclonal antibody that binds to RANKL
Bound RANKL cannot attach to RANK receptors (i.e. inhibiting activation of
osteoclast)
Monocolonal Antibodies: Denosumab
production
Murine antibody that recognizes specific antigen
Murine Antibody:
induce a human anti-mouse antibody immune response
activate human immune effector mechanisms poorly
short t1/2 in humans
Chimerized by substituting major portions of the human IgG molecule
Ab types and immunogenicity scale
Toxicities – Infusion Reactions with Ab’s
Typical symptoms?
time frame
Premedication
Typical include fever, chills, nausea, dyspnea, and rashes
within 30 minutes to two hours of initiation of drug infusion, symptoms may be
delayed for up to 24 hours
Premedication with diphenhydramine and acetaminophen is indicated
Denosumab Risk of MRONJ
high and low doses
High Dose Denosumab : High prevalence (2-5% Osteonecrosis)
Mechanism of MRONJ
Profound and prolonged inhibition of bone resorption with over-suppression of bone remodeling (ie, low bone turnover), and infection are the main mechanisms
Postulated that MRONJ is a form of avascular necrosis, possibly caused by inhibition of angiogenesis.
MRONJ and inhibition of angiogenesis
In vitro experiments consistently demonstrate inhibition of angiogenesis by zoledronic
acid, and cancer patients treated with this agent have decreased circulating VEGF levels
Growing body of evidence linking MRONJ to antiangiogenic drugs, including
bevacizumab and orally active tyrosine kinase inhibitors.
Angiogenesis and Cancer
Angiogenesis =
Key factor in the?
Solid tumors secrete ?
stimulates?
Angiogenesis = the development of new blood vessels
Key factor in the growth and metastasis of certain solid tumors
Solid tumors secrete proangiogenic factors, vascular endothelial growth factor (VEGF)
stimulate new vessel development via downstream signaling pathways
inhibitors of angiogenesis introduced into oncology
practice
monoclonal antibodies against VEGF (e.g., bevacizumab),
tyrosine kinase inhibitors (e.g., sorafenib, sunitinib),
mammalian target of rapamycin (mTOR) pathway inhibitors (e.g., everolimus)
immunomodulatory agents (e.g., thalidomide, lenalidomide).
bevacizumab
monoclonal antibodies against VEGF
sorafenib
tyrosine kinase inhibitors
sunitinib
tyrosine kinase inhibitors
everolimus
mammalian target of rapamycin (mTOR) pathway inhibitors
thalidomide
immunomodulatory agents
lenalidomide
immunomodulatory agents
Bevacizumab moa
used in what cancers?
Bevacizumab (Avastin)- humanized; binds VEGF-A
Used in solid tumor cancers
Specifically recognize and bind to VEGF.
Once bound, the complex is unable to activate the VEGF receptor.
Bevacizumab
Most effective when?
kills tumors? role?
Reduces?
possible adrs?
Most effective when combined with additional
therapies, especially chemotherapy.
Do not necessarily kill tumors; they instead may
prevent tumors from growing.
Reduce formation of new blood vessels; reduce
nutrient delivery
Increases in bleeding and reduced wound healing
Note on ONJ and antiangiogenic rx’s
Association of ONJ with therapies that target angiogenesis is?
Especially with?
Risk for MRONJ when recieiving both antiabsorb and antiangio?
Association of ONJ with therapies that target angiogenesis is more
controversial
Especially monotherapy with an antiangiogenic agent
Risk for MRONJ more clearly established for use of antiangiogenic
agents in patients ALSO receiving antiresorptive agents
International Task Force on Osteonecrosis of the Jaw
For patients whose cancer management includes treatment with denosumab or IV
bisphosphonates, recommends:
“a thorough dental examination with dental radiographs should be ideally completed prior to the initiation of antiresorptive therapy in order to identify dental disease before drug therapy is initiated”
“Any necessary invasive dental procedure including dental extractions or implants should ideally be completed prior to initiation of [bisphosphonate] or [denosumab] therapy.”
American Society of Clinical Oncology (ASCO) – 2017
“All patients should have what before using a Bone-modifying agent (BMA).”
“in the setting of invasive dental procedures, it is advisable, whenever possible to?
“If an invasive manipulation of the bone underlying the teeth is clinically indicated
before starting BMA therapy…initiation of BMA therapy should be ideally delayed for?
“All patients should have a dental examination and preventive dentistry before using a Bone-modifying agent (BMA).”
“in the setting of invasive dental procedures, it is advisable, whenever possible to delay the starting of therapy with BMA until the initial bone healing process of the tooth socket bone has taken place”
“If an invasive manipulation of the bone underlying the teeth is clinically indicated before starting BMA therapy…initiation of BMA therapy should be ideally delayed for 14 to 21 days to allow for wound healing, if the clinical situation permits.”
Cancer Treatment
Goal of therapy based on severity of illness:
Multiple modalities utilized:
Supportive care for ?
Goal of therapy based on severity of illness: Curative, Control, Palliative
Multiple modalities utilized: Surgery, Radiation therapy, Chemotherapy, Hormonal therapy, Biotherapy
Supportive care for clinical manifestations and/or treatment adverse reactions
Chemotherapy Agents
forms?
moa’s
Reaches
Adjuvant (given after therapy) vs. neoadjuvant (before tx to reduce size)
Various mechanisms of action> slow/stop cell proliferation
Reach ‘microscopic’ cancer cells
2 log kill desired
what limits chemotherapeutics use?
Adverse reactions limit use
GI disturbances (N/V/D)
Hair loss
Bone marrow suppression
(anemia, increased infection risk)
Antineoplastic Medications forms
Alkylating Agents
moa?
cell cycle specific?
Can be used in?
Directly damage cell DNA
Impairs replication & transcription= cell death
Work in all phases of the cell cycle
Can be used in many different cancers
* carbonium ion highly reactive>binds dna
alkylating agents ADRs/toxicity
oppurtunistic infections possible=thrush
alkylating agents classes
Nitrogen Mustards
Platinum Compounds
Nitrosoureas
Alkyl sulfonates
Triazines
Ethylenimines
Nitrogen Mustards:
cyclophosphamide, chlorambucil, ifosfamide, melphalan
cyclophosphamide class/moa
N mustard
akylarting agent
chlorambucil class/moa
N mustard
alk agent
ifosfamide class/moa
N mustard
alk agent
melphalan class/moa
N mustard
alk agent
Platinum Compounds:
cisplatin, carboplatin, oxaliplatin
cisplatin class/moa
Plat compound, alk agent
carboplatin class/moa
Plat compound, alk agent
oxaliplatin class/moa
Plat compound, alk agent
Nitrosoureas:
streptozocin, carmustine and lomustine
Nitrosoureas often used with?
brain tumors
streptozocin class/moa
nistrosourea, alk agent
carmustine class/,moa
nistrosourea, alk agent
lomustine class/moa
nistrosourea, alk agent
Alkyl sulfonates:
busulfan
busulfan class/moa
Alkyl sulfonates, alk agent
Triazines:
dacarbazine and temozolomide
dacarbazine (DTIC) class/moa
triazine, alk agent
temozolomide (Temodar®)
triazine, alk agent
Ethylenimines:
thiotepa and altretamine (hexamethylmelamine)
thiotepa class/moa
Ethylenimines, alk agent
altretamine (hexamethylmelamine) class/moa
Ethylenimines, alk agent
platinum compounds nn adr
Neurotoxicity
Drugs enter into the dorsal root ganglion and binds to DNA, causing apoptosis.
Platinum compounds form intrastrand adducts and interstrand crosslinks altering tertiary structure of DNA. This promotes alterations in cell-cycle kinetics, leading to an attempt of differentiated postmitotic dorsal root ganglion neurons to re-enter cell cycle, which leads to the induction of apoptosis
Regardless of the mechanism, apoptosis results in secondary damage to peripheral nerves
Oxaliplatin association with:
Cold-induced?
breathing?
Mm?
Jaw?
swallowing?
mm appearence?
Voice?
Ocular?
pain triggered by exposure to cold liquids
Cold-induced perioral paresthesias – 95%
Cold-induced pharyngolaryngeal dysesthesia – 92%
Dyspnea – 40%
Muscle cramps – 34%
Jaw stiffness – 34%
Dysphagia – 30%
Visible fasciculations – 30%
Voice changes – 6%
Ocular changes – 0.7%
Antimetabolites:
Antimetabolites are structurally related to normal compounds that exist
within the cell
antimetabolites moa
Antimetabolites interfere with DNA and RNA growth by substituting for or competing with the normal building blocks of DNA and RNA
i.e. the availability of normal purine or pyrimidine nucleotide precursors
May either by inhibiting the synthesis of normal nucleotides or compete with them in the formation of DNA or RNA
are antimetabolites cell phase specific
Their maximal cytotoxic effects are in S-phase
Synthesis – DNA replicates, yielding two separate sets
Antimetabolites types
Folate antagonists
Pyrimidine antagonists
Purine antagonist
Folate antagonists names
moa
methotrexate, pemetrexed
inhibit folate syn=no nucleic acids
methotrexate
folate antagonist
pemetrexed
folate antag
Pyrimidine antagonists:
5-Fluorouracil (5FU), Cytarabine, gemcitabine
5-Fluorouracil (5FU),
Pyrimidine antagonists:
Cytarabine
Pyrimidine antagonists:
gemcitabine
Pyrimidine antagonists:
Purine antagonists
Mercaptopurine, Fludarabine
Mercaptopurine
Purine antagonist:
Fludarabine
Purine antagonist
Folate antagonists, Pyrimidine antagonists, Purine antagonist moa
Inhibit precursors to DNA synthesis
Methotrexate
moa, used in? phase? affected tissues?
Antineoplastic; immunosuppressant (psoriasis; RA)
Target S-phase (DNA replication), inhibit rapid proliferating cells
Bone marrow and intestinal epithelium
Myelosuppression risk for hemorrhage and infection
methotrexate dental note
can cause?
what agents are most stomatotoxic
whiich rx known to be secreted into the saliva, result of this?
Dental Note: oral mucositis
Oral pain; Erythema; Difficulty opening the mouth
DNA cycle specific agents are most stomatotoxic
Methotrexate, etoposide known to be secreted into the saliva
further increasing stomato toxicity potential
DNA cycle specific agents associated with oral mucositits
Methotrexate
5FU
Cytarabine
Doxorubicin
Etoposide
Bleomycin
Cytotoxic Antibiotics moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
produce radicals
cytotoxic abx groups
Anthracyclines: Doxorubicin, daunorubicin, epirubicin, idarubicin.
Other: bleomycin, plicamycin, mitomycin
Doxorubicin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
daunorubicin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
epirubicin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
idarubicin moa
Bind to and break DNA inside cancer cell to keep them from growing and multiplying (via radical production)
Cytotoxic Antibiotics
bleomycin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
plicamycin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
mitomycin moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
what can be seen orally with cytotoxic abx?
mucositis
Mitotic Inhibitors
Work in M-Phase to prevent cell division
mitotic inhibitor groups include:
Vinca Alkaloids: Vincristine, Vinblastine
Taxanes: Paclitaxel, Docetaxel
Vincristine moa
Derived from ?
Derived from Madagascar periwinkle
MOA: bind β tubulin & block its polymerization with α tubulin into
microtubules
Cell division arrests in metaphase
Absence of intact mitotic spindle, chromosomes cannot align, disperse throughout the cytoplasm
Apoptosis
vinka alkloids/ vincristine toxicity
Peripheral neuropathy-numbness, tingling
Neurotoxicity may also be persistent, deep aching and burning pain that mimics a toothache
Side Effects: Cell Replication Inhibition
Primarily GI tract, Bone marrow, Oral cavity
Mucositis painful inflammation along GI
Develops within 1-week of chemotherapy initiation
Stomatotoxic (toxic effects on the oral tissues)
Impairment of bone marrow (myelosuppression)
suppressing white blood cells, red blood cells, and platelets
GET LABS THE DAY BEFORE ANY PROCEDURE
WBC >2000
ANC >2000
Platelets >75,000
Oral Complications Common to Chemotherapy & Radiation
Oral mucositis (20-40%)
Infection
Xerostomia/salivary gland dysfunction
Functional disabilities
Taste alterations
Nutritional compromise
Abnormal dental development
Oral mucositis with Chemotherapy & Radiation
inflammation and ulceration of the mucous membranes
can increase the risk for pain, oral and systemic infection, and nutritional compromise
Infection with Chemotherapy & Radiation
viral, bacterial, and fungal
from myelosuppression, xerostomia, and/or damage to mucosa from chemotherapy or radiotherapy
Xerostomia/salivary gland dysfunction with Chemotherapy & Radiation
dry mouth d/t thickened, reduced, or absent salivary flow
increases the risk of infection and compromises speaking, chewing, and swallowing
persistent dry mouth increases the risk for dental caries
Functional disabilities with Chemotherapy & Radiation
impaired ability to eat, taste, swallow, and speak
due to mucositis, dry mouth, trismus, and infection
Taste alterations with Chemotherapy & Radiation
changes in taste perception of foods, ranging from unpleasant to tasteless
Nutritional compromise with Chemotherapy & Radiation
eating difficulties due to mucositis, dry mouth, dysphagia, and loss of taste
Abnormal dental development with Chemotherapy & Radiation
altered tooth development, craniofacial growth, or skeletal
development in children secondary to radiotherapy and/or high doses of chemotherapy before age 9
Taste Alterations - Chemotherapy
Common occurrence following
chemotherapy administration
Lasts 3-4 weeks post-treatment
common meds of taste of alterations
Cisplatin
Cyclophosphamide
Doxorubicin
5-Fluorouracil
Methotrexate
Paclitaxel
Vincristine
Neurotoxicity of chemo
side effects of what rx’s
Persistent, deep aching and burning pain that mimics a toothache, but no dental or mucosal source can be found.
side effect of certain classes of drugs (vinca alkaloids; platinum compounds)
Bleeding with chemo
oral bleeding from the decreased platelets and clotting factors
Radiation caries:
Radiation caries: lifelong risk of rampant dental decay that may begin within
3 months of completing radiation treatment if changes in quality or quantity of saliva persist
Osteonecrosis with radiation
blood vessel compromise and necrosis of bone exposed to high-dose radiation therapy; results in decreased ability to heal if traumatized
Disease States for Immunosuppression
Autoimmune, collagen, connective tissue and inflammatory disorders
Systemic Lupus erythematosus
Rheumatoid arthritis
Chronic active hepatitis
Inflammatory bowel disease
Glomerulonephritis
Nephrotic syndrome
Myasthenia gravis
…among others…
Organ or tissue transplantation
Prevent rejection
Target of Immunosuppression
Inhibit mononuclear cells
(lymph and blood cells)
T-cell Inhibitors
Cyclosporine (Sandimmune)
Tacrolimus (Prograf; FK506)
Sirolimus (Rapamune)
Everolimus (Zortress)
Cyclosporine (Sandimmune)
t cell inhib
Tacrolimus (Prograf; FK506)
t cell inhib
Sirolimus (Rapamune)
t cell inhib
Everolimus (Zortress)
t cell inhib
T-cell and B-cell inhibitors
Azathioprine (Imuran)
Leflunomide (Arava)
Mycophenolate (Cellcept)
Azathioprine (Imuran)
b and t cell inhib
Leflunomide (Arava)
b and t cell inhib
Mycophenolate (Cellcept)
b and t cell inhib
Corticosteroids
Corticosteroids = Glucocorticoids
Prednisone, dexamethasone, prednisolone, et
t cell inhibitors moa
used for?
Downstream inhibit helper and killer T-cell activation
Actively attack/destroy any invading/invaded cell (each T-cell is specific to virus/bacteria/protein)
To prevent and treat rejection of organ and bone marrow transplants; RA; Psoriasis
Cyclosporine – Side Effects
suggested tx’s? avoid?
Cyclosporine AND Tacrolimus DDIs
Cimetidine (Tagamet)
Clarithromycin (Biaxin)
Erythromycin
Corticosteroids
Fluconazole (Diflucan)
Itraconazole (Sporanox)
Ketoconazole (Nizoral)
Cyclosporine AND Tacrolimus Cimetidine DDI
Reports implicate cimetidine and
famotidine as increasing
cyclosporine concentrations and/or
decreasing cyclosporine clearance
Clarithromycin and tarcolimus
One report describes 2 female patients (aged 37 and 69 years), who each experienced acute renal failure and more than a 2.3-fold increase in tacrolimus serum concentrations after 9 doses of clarithromycin therapy (250 mg daily)
Corticosteroids and cyclosporine
Toxic effects of prednisone and/or
cyclosporine, if agents combined
Azoles and cyclosporine concentrations
Serum cyclosporine concentrations have been reported to
increase as much as tenfold in transplant patients
following the initiation of azole antifungal agents
T-Cell and B-Cell Inhibitors moa
used for?
MOA: inhibit purine (azathioprine and mycophenolate) and pyrimidine (leflunomide) nucleotide synthesis for lymphocyte production (T and B)
Prevent and treat rejection of organ and bone marrow transplants; RA
b and t cell inhibitors dental notes:
what rx’s? can reduce effectiveness of mycophenolate
Risk for?
Antacids and PPIs can reduce effectiveness of mycophenolate
Risk for infection increased while taking
Directly damage cell DNA
Impairs replication & transcription= cell death
Work in all phases of the cell cycle
Can be used in many different cancers
Alkylating Agents
moa?
cell cycle specific?
Can be used in?
Nitrogen Mustards
Platinum Compounds
Nitrosoureas
Alkyl sulfonates
Triazines
Ethylenimines
alkylating agents classes
cyclophosphamide (Cytoxan®), chlorambucil, ifosfamide, melphalan
Nitrogen Mustards:
cisplatin, carboplatin, oxaliplatin
Platinum Compounds:
streptozocin, carmustine (BCNU), and lomustine
Nitrosoureas:
dacarbazine (DTIC) and temozolomide (Temodar®)
Triazines:
thiotepa and altretamine (hexamethylmelamine)
Ethylenimines:
interfere with DNA and RNA growth by substituting for or competing with the normal building blocks of DNA and RNA
i.e. the availability of normal purine or pyrimidine nucleotide precursors
May either by inhibiting the synthesis of normal nucleotides or compete with them in the formation of DNA or RNA
antimetabolites moa
Folate antagonists
Pyrimidine antagonists
Purine antagonist
Antimetabolites types
methotrexate, pemetrexed
Folate antagonists names
5-Fluorouracil (5FU), Cytarabine, gemcitabine
Pyrimidine antagonists:
Mercaptopurine, Fludarabine
Purine antagonists
Inhibit precursors to DNA synthesis
Folate antagonists, Pyrimidine antagonists, Purine antagonist moa
Bind to and break DNA inside cancer cell to keep them from growing
and multiplying
Cytotoxic Antibiotics
Anthracyclines: Doxorubicin, daunorubicin, epirubicin, idarubicin.
Other: bleomycin, plicamycin, mitomycin
cytotoxic abx groups
Work in M-Phase to prevent cell division
Mitotic Inhibitors
Vinca Alkaloids: Vincristine, Vinblastine
Taxanes: Paclitaxel, Docetaxel
mitotic inhibitor groups include:
Cisplatin
Cyclophosphamide
Doxorubicin
5-Fluorouracil
Methotrexate
Paclitaxel
Vincristine
common meds of taste of alterations
Cyclosporine (Sandimmune)
Tacrolimus (Prograf; FK506)
Sirolimus (Rapamune)
Everolimus (Zortress)
T-cell Inhibitors
Azathioprine (Imuran)
Leflunomide (Arava)
Mycophenolate (Cellcept)
T-cell and B-cell inhibitors
