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101 Cards in this Set

  • Front
  • Back
What are the 4 basic tissue types from which tumors arise?
1. Epithelial tissue
2. Connective tissue
3. Lymphoid tissue
4. Nerve tissue
Malignancy on surface epithelium
carcinoma
Malignancy on glandular tissue
adenocarcinoma
Malignancy on fibrous tissue
fibrosarcoma
Malignancy on bone
osteosarcoma
Malignancy on smooth muscle
leiomyosarcoma
Malignancy on striated muscle
rhabdomyosarcoma
Malignancy on fat
liposarcoma
Malignancy on bone marrow elements
leukemias
Malignancy on lymphoid tissue
Hodgkin's and non-Hodgkin's lymphoma
Malignancy on plasma cell
multiple myeloma
Malignancy on glial tissue
glioblastoma multiforme, astrocytoma
Malignancy on nerve sheath
neurofibrosarcoma
Malignancy on melanocytes
malignant melanoma
Malignancy on gonadal tissue
teratocarcinoma
Tissue of origin of carcinoma
surface epithelium
Tissue of origin of adenocarcinoma
glandular tissue
Tissue of origin of fibrosarcoma
fibrous tissue
Tissue of origin of osteosarcoma
bone
Tissue of origin of leiomyosarcoma
smooth muscle
Tissue of origin of rhabdomyosarcoma
striated muscle
Tissue of origin of liposarcoma
fat
Tissue of origin of leukemias
bone marrow elements
Tissue of origin of Hodgkin's and non-Hodgkin's lymphoma
lymphoid tissue
Tissue of origin of multiple myeloma
plasma cell
Tissue of origin of glioblastoma multiforme, astrocytoma
glial tissue
Tissue of origin of neurofibrosarcoma
nerve sheath
Tissue of origin of malignant melanoma
melanocytes
Tissue of origin of teratocarcinoma
gonadal tissue
Benign tumor characterisitics
noncancerous, localized, seldom metastasize, once removed they rarely recur
Malignant tumor characteristics
invade and destroy surrounding tissue, genetically unstable, atypical of their tissue of origin, metastasize frequently, recurrences are common after removal
What are the 7 warning signs of cancer?
1. Change in bowel or bladder habits
2. A sore that does not heal
3. Unusual bleeding or discharge
4. Thickening or lump in breast or elsewhere
5. Indigestion or difficulty in swallowing
6. Obvious change in wart or mole
7. Nagging cough or hoarseness
What are the principles of tumor growth?
In early stages tumor growth is exponential. It takes a constant amount of time to double its size. This is called the growth fraction. When the growth fraction is high the tumor is most sensitive to chemotherapy.
List out the cell cycle
1. Mitosis - cell division occurs
2. G0 - dormant phase
3. G1 - first gap phase, prepares for DNA synthesis
4. S - DNA synthesis, can be used to determine aggressiveness of tumors
5. G2 - second gap phase, prepares for mitosis and produces RNA
Are the cell cycle specific agents schedule or dose dependent?
schedule dependent
Are the cell cycle nonspecific agents schedule or dose dependent?
dose dependent
What drugs work in the G1 phase of the cell cycle?
aspariginase
What drugs work in the S phase of the cell cycle?
Antimetabolites
-methotrexate
-cytarabine, fluorouracil, gemcitabine, capecitabine
-mercaptopurine, fludarabine
What drugs work in the G2 phase of the cell cycle?
-bleomycin
-etoposide
What drugs work in the M phase of the cell cycle?
-vincristine, vinblastine, vinorelbine
-paclitaxel, docetaxel
Malignancy on plasma cell
multiple myeloma
Malignancy on glial tissue
glioblastoma multiforme, astrocytoma
Malignancy on nerve sheath
neurofibrosarcoma
Malignancy on melanocytes
malignant melanoma
Malignancy on gonadal tissue
teratocarcinoma
Tissue of origin of carcinoma
surface epithelium
Tissue of origin of adenocarcinoma
glandular tissue
Tissue of origin of fibrosarcoma
fibrous tissue
Tissue of origin of osteosarcoma
bone
Tissue of origin of leiomyosarcoma
smooth muscle
What are the cell-cycle phase-nonspecific agents?
-alkylating agents
-anthracycline antibiotics
-dacarbazine
-cisplatin
-nitrogen mustards
What are the stages of carcinogenesis?
1. Initiation - exposure of normal cells to carcinogenic substance; irreversible cellular mutations occur
2. Promotion - growth of mutated cell population, reversible process
3. Progression - spread to distant sites
What are the two major classes of genes involved in carcinogenesis?
oncogenes and tumor suppressor genes
What are oncogenes and how do they become carcinogens?
They develop from normal genes called protooncogenes. Protooncogenes are present in all cells and help regulate normal cellular function. Genetic alterations of protooncogenes via point mutations, chromosomal rearrangement, or gene amplification activates them into oncogenes. This can be caused by carcinogens, radiation, chemicals, viruses, or genetics.
What are tumor suppressor genes and how do they become carcinogens?
They regulate and inhibit inappropriate cellular growth and proliferation. They promote programmed cell death. Tumors may lack or have a defect in this gene.
Which viruses are linked to cancers?
Herpesviruses (simplex 1 and 2, cytomegalovirus, Epstein-Barr virus, roseolovirus)
Hepatitis B and C
HTLV (T cell lymphoma)
HIV
What types of cancer can HSV1 and HSV2 lead to?
Kaposi's sarcoma
Carcinoma of lip and cervix
What types of cancer can HHV5 (cytomegalovirus) lead to?
Kaposi's sarcoma
Prostatic cancer
What types of cancer can HHV4 (Epstein-Barr virus) lead to?
Burkitt's lymphoma
PTLD lymphoma
Nasopharyngeal carcinoma
What types of cancer can HHV6 (roseolovirus) lead to?
lymphoproliferative disorders
What types of cancer can hepatitis B lead to?
hepatocellular disorder
What types of cancer can hepatitis C lead to?
hepatocellular carcinoma
What types of cancer can HTLV lead to?
T cell lymphoma
What types of cancer can HIV lead to?
Kaposi's and lymphomas
What is the MOA of direct-acting carcinogens?
electrophile, organic compound, genotoxic; interacts with DNA
What is the MOA of procarcinogens?
Requires conversion ghrough metabolic activation by host or in vitro to type 1
What is the MOA of a hormone carcinogen?
Mainly alters the endocrine system balance and differentiation; often acts as promoter; usually not genotoxic
What is an example of a hormone carcinogen?
estradiol
diethylstilbestrol
What is the MOA of an immunosuppressor carcinogen?
Mainly stimulates "virally induced", transplanted, or metastatic neoplasms; usually not genotoxic
What is the MOA of a cocarcinogen?
Not genotoxic or carcinogenic, but enhances effect of type 1 or type 2 agent when given at the same time; may modify conversion of type 2 to type 1
What is the MOA of a cytotoxin?
Not genotoxic or carcinogenic; above specific dosages kills cells, increases regeneration and cell cycling
What is the MOA of a promoter?
Not genotoxic or carcinogenic, but enhances effect of type 1 or type 2 agent when given subsequently
What is an example of a promoter?
phorbol esters, phenol, bile acids, sodium saccharin
What are the genotoxic carcinogens?
-direct acting agents
-procarcinogens
What are the epigenetic carcinogens?
-hormones
-immunosuppressor
-cocarcinogen
-cytotoxin
-promoter
What is responsible for 1/3 of all US cancer deaths?
smoking
What are the most common sites of secondary tumors?
breast, prostate, or colon
What are the common sites of metastatic disease?
liver, brain, bone, lung, spleen, adrenal glands
How big must tumors get before they are detectable?
greater than 10^9 cells
What is the Fractional Cell Kill Hypothesis?
a given concentration of drug for a given time period kills a constant fraction of the cell population
When using the Fractional Cell Kill Hypothesis, what is the frequency limited by?
the dose limiting toxicity (bone marrow suppression or GI toxicity)
How can resistance to cancer drugs develop?
1. alteration in membrane transport
2. depleted activating enzymes
3. changes in target enzymes
4. new alternative pathways
5. altered binding of drugs to macromolecules
6. multi-drug resistance
Describe multi-drug resistance and how it can be inhibited.
Many tumors develop resistance to a number of unrelated naturally occurring chemotherapy agents. The mechanism of the resistance is the presence of an intercellular pump, p-glycoprotein. The pump can be inhibited by a number of agents such as verapamil.
What are some ways to overcome drug resistance?
1. Change method of drug administration (dose, schedule, route)
2. Change the drug preparation
3. Use combination products and combined modalities
What is rationale behind combination chemotherapy?
-some cells may be resistant to a single agent
-prevent the development of resistance
-by using different agents one can increase efficacy without increasing toxicity
What should you look for when selecting agents to be in a combination chemo regimen?
Drugs that are active against tumor, have different mechanisms, lack cross resistance, and have different toxicities.
How to space out a chemo regimen.
-Start with cell cycle nonspecific agents to reduce tumor bulk and recurit cells into cycle
-follow with cycle specific agents
-use non-myelosuppressive durgs during "off" period to suppress tumor growth
Dose modification of methotrexate in renal failure or decreased creatinine clearance.
decrease dose in proportion to decrease in creatinine clearance (normal is 60)
Dose modification of cis-Platinum (cisplatin) in renal failure.
decrease dose in proportion to creatinine clearance
Dose modification of cyclophosphamide in renal failure (creatinine clearance below 25)
50% decrease
Dose modification of bleomycin in renal failure (creatinine clearance below 25)
50-75% decrease
Dose modification of streptozotocin in renal failure (creatinine clearance below 25)
50-75% decrease
Dose modification of carboplatin in renal failure
decrease in proportion to creatinine clearance
Dose modification of hydroxyurea, VP-16, and deoxycoformycin in renal failure
decrease in proportion to creatinine clearance
Dose modification of mAMSA, doxorubicin, daunorubinin, vincristine, and vinblastine in hepatic dysfunction
1. for bilirubin greater than 1.5mg/100ml, reduce initial dose by 50%
2. for bilirubin greater than 3.0mg/100ml, reduce initial dose by 75%
What is the therapy and probable cure rate of diffuse histiocytic lymphoma?
Therapy is combination chemotherapy
Cure rate is greater than 50%
What is the therapy and probable cure rate for Hodgkin's disease?
Therapy is combination chemotherapy
Cure rate is greater than 50%
What is the therapy and probable cure rate for Testicular carcinoma?
Therapy is combination chemotherapy plus surgery
Cure rate is greater than 75%
What is the therapy and probable cure rate for Gestational choriocarcinoma?
Therapy is methotrexate plus actinomycin D
Cure rate is 90%
What is the therapy and probable cure rate for Ovarian carcinoma?
Therapy is combination chemotherapy
Cure rate is 10-20%
What is the therapy and probable cure rate for AML?
Therapy is combination chemotherapy
Cure rate is 20%