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Pharmacy School 2015-16 > PHAR 737 Midterm 2 > Flashcards

PHAR 737 Midterm 2 Flashcards

1
Q

Describe CYP P450s (structure, functions, importance)

A

Heme-containing superfamily of enzymes. Metabolize drugs, hormones, cholesterol and arachadonic acid. Regulate blood homestasis.

At least 80 percent are involved in phase 1 metabolism.

These are important targets for pharmacogenetics and pharmacogenomics.

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2
Q

Describe CYP2Cs

A

Most abundantly expressed enzyme in the human liver and responsible for metabolism of 15-20% of prescribed OTCs

Highly variant enzyme, and metabolizes drugs such as warfarin, tramadol, and codeine.

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3
Q

What is the importance of CYP2C9/2* and /3* defective variants?

A

Defective alleles associated with reduced S-warfarin hydroxylation, making these patients prone to bleeding events

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4
Q

The estimated variance in antidepressant response due to genetic variants is around _____

A

50 percent

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5
Q

Describe CYP2D6

A

Most polymorphic P450 with over 75 different alleles with variation in metabolism rates (5-10% whites and higher percentage of Asians are poor metabolizers)

Located in cells of instestinal wall, endothelium, liver, etc. and is missing in 7% of caucasians and 2% of non-caucasians (hyperactive in 30% of East Africans)

Deletion occurs in 3-5% worldwide, with duplications resulting in 2 pseudogenes and more than 80 possible polymorphisms in coding or promoter regions.

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6
Q

Describe CYP3A4

A

Most abundant P450 in human liver, metabolizing over 120 drugs.

Common substrates include: 
>Acetaminophen
>Codeine
>Erythromycin
>Warfarin
>Lovastatin
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7
Q

Describe UGTs

A

Uridine Diphosphoglucuronosyltransferases (catalyze the glucuronidation of polar aglycones)

Active on a diverse range of drugs and xenobiotics. UGT1, UGT2 and 130 structurally and functionally different variants

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8
Q

Describe SULTs

A

Sulfotransferases catalyze the transfer of the sulfonyl group from 3’-phosphoadenosine 5’-phosphosulfate (PAPS) to various compounds to make them readily excreted in urine.

There are membrane bound SULTS in golgi for sulfonation of proteins, lipids and glycosaminoglycans.

Cytosolic SULTs for sulfonation of drugs, xenobiotics, and endogenous substrates (bile, acids, steroids, neurotransmitters)

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9
Q

Describe NATs

A

Utilize the acetyl CoA to acetylate drugs and xenobiotics that contain amino and hydrazine substitutes to the corresponding amides and hydrides respectively.

NAT1 is broadly expressed
NAT2 is expressed in liver, small intestine and colon

Large allele variation globally

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10
Q

For 27 drugs frequently cited in adverse drug reaction studies, ____ are metabolized by at least one enzyme with a variant allele associated with decreased drug metabolism

A

59%

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11
Q

____ to _____ % of randomly selected drugs are metabolized by enzymes known to exhibit functional genetic polymorphisms

A

7-20

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12
Q

During which phase of clinical trials are genomic analyses common?

A

3rd (FDA recommends collection of DNA samples from all, but PK and PD outliers at the least)

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13
Q

How long should DNA in clinical trials be retained for postmarket analysis?

A

15 years at least

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14
Q

What main reactions make up Phase 1 metabolism? Phase 2?

A

Oxidation, reduction, hydrolysis

Acetylation, glucuronidation, sulfation, methylation

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15
Q

A SNP in CYP3A5 creates a non-functional enzyme by introduction of a _____

A

early stop-codon

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16
Q

Describe regulation of CYP3A4

A

Can give a drug (from cell or xenobiotic) to initiate CYP3A4 production by causing PXR and RXR together to form heterodimer which promotes production of CYP3A4, which can metabolize warfarin, doxorubicin, atorvastatin and many other drugs.

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17
Q

Describe GSTs

A

Glutathione-S-transferases

7 cytosolic families (A, M, T, P, S, O and Z) that participate in xenobiotic biotransformation

Mitochondrion (K family)

Play a role in detoxification of highly reactive drug metabolites

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18
Q

Describe drug transporters in the human body

A

Membrane proteins throughout body working in a coordinated fashion for drug disposition, therapeutic efficacy, adverse drug reactions, and drug-drug interactions.

SLCs (passive and active that rely on gradients) and ABCs (are ATP dependent)_

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19
Q

What are biomarkers?

A

Can be a gene, protein, or other change that indicates a biochemical phenotype before that phenotype is clinically apparent.

Important for diagnosing disease or determining risk of disease, establishing and/or predicting drug response and toxicity

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20
Q

Describe the difference between bimodal and unimodal distribution of drug-related polymorphisms

A

Biomodal represents mutations that eliminate activity of drug-clearing enzymes, while unimodal represents polymorphisms that cause small (basically no) variation in drug-clearing enzyme activity

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21
Q

Ideal Marker for Diagnosis

A

Sensitivity, specificity, accuracy, prognostic or outcome and treatment

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22
Q

Describe the ideal biomarker for screening

A

Highly specific (minimize false positives and negatives), able to clearly reflect the different stages of the disease, easily detected without complicated medical procedures, and cost effective method for screening

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23
Q

Describe Warfarin

A

Most commonly prescribed anticoagulant (2M people start taking every year in US) and is the 2nd most common drug implicated in emergency room visits for ADRs next to insulin.

Synthetic derivative of coumarin, originally developed as rat poison, and belongs to a class of Vitamin K antagonists

Common indications include: atrial fibrillations, deep venous thrombosis, pulmonary embolism, etc.

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24
Q

Warfarin is metabolized primarily by ________ and inhibits _____________________________

A

CYP2C9

Vitamin K epoxide reductase complex subunit 1 (VKORC1)

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25
Q

What test is available to determine the main mutation in CYP2C9 or VKORC1?

A

TherapID

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26
Q

Which warfarin isomer is most potent?

A

S is five times more potent than R

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27
Q

Up to ____ percent of the population inherits a form of the CYP2C9 gene which result in deficiency of the enzyme

A

35%

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28
Q

Which CYP2C9 variants require a lower warfarin maintenance dose?

A

CYP2C9*2 and *3

*3 being the more pronounced form (higher deficiency)

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29
Q

How does warfarin work?

A

Inhibits formation of clotting factors by inhibiting vitamin K epoxide reductase complex subunit 1 (VKORC1)

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30
Q

Polymorphisms in VKORC1 gene explain _____ of all dose variation between patients, and about _____ of all variance in warfarin dose can be attributed to VKORC1 and CYP2C9 combined

A

30%

40%

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31
Q

Which ethnicity is most affected by CYP2C9 variance? VKORC1 variance?

A

Whites (8-18% have *2 variant and 5-13% have *3 variant)

Asians (90-95% VKORC1)

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32
Q

What is clopidogrel? Why is it significant?

A

Antiplatelet drug for stent associated thrombosis

Up to 30% of patients do not display adequate antiplatelet response to clopidogrel

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33
Q

Describe clopidogrel metabolism

A

Absorbed in intestines - 85% converted to inactive carboxylic acid metabolite by esterases, 15% converted to active thiol metabolite.

Metabolized by: CYP3A4/A5, CYP2C19, CYP2C9, CYP1A2, CYP2B6 (all of these CYPs have many other substrates that can induce/inhibit them)

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34
Q

Which enzymes are the key players in clopidogrel metabolism for platelet aggregation

A

CYP3A4/A5 - you need at least one of them to be “free” and able to metabolize clopidogrel for platelet aggregation not to occur. When they are both “busy,” you will get aggregation.

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35
Q

Define Statins

A

Used to reduce the risk of cardiovascular even ts by 20-30% through the reduction of LDL cholesterol

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36
Q

What is the major metabolizer of Statins?

A

CYP3A4

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37
Q

Describe Alzeimer’s disease

A

Deficit in cholinergic neurotransmission

ApoE4 in chromosome 19 is associated with late onset of Alzeimer’s. Other susceptibility could include locus on 12 and 9

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38
Q

Describe a polymorphism important to ApoE4 carriers

A

Glutathione S-transferase polymorphism in gene regulating the rate of cognitive decline

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39
Q

Describe G6PD deficiency

A

African-American soldiers taking antimalarial drugs primaquine developed hemolytic anemia and were found to have decreased G6PD activity in affected RBCs.

Gene is X linked

G6PD catalyzes process leading to NADPH source for RBCs, a process that reduces oxidative damage

200-400 million people have variants that increase risk of hemolysis, with over 70 mutations being reported.

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40
Q

NAT2 polymorphism leading to slow acetylation will mostly impact which drugs?

A

Anti-TB drug isoniazid (INH), caffeine and sulfamethoxazole

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41
Q

What are some risks of NAT2 polymorphisms?

A

Cancer of lung, bladder, colon - resulting from acetlyation of aromatic amines found in tobacco smoke and cooked foods

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42
Q

Describe the Isoniazid pathway to get to Diacetyl Hydrazine

A

Isoniazid –> Acetyl isoniazid (via NAT2) —> Monoacetly hydrazine —> Diacetyl hydrazine (non-toxic)

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43
Q

Excretion of isoniazid from the body occurs via

A

hydrolysis

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44
Q

Which age group is most at risk of developing hepatitis?

A

50-64, followed by 35-47, 20-34 and under 20

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45
Q

INH (isoniazid hydrazine) for how many months reduces risks of active TB in persons with positive TB skin test?

A

6-12

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46
Q

How prevelant is deveoping irreversible hepatic failure from NAT polymorphism

A

1/10000

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47
Q

Describe somatic mutations

A

Occur in nongermline tissues, are nonheritable, and acquired alterations common for all cancers

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48
Q

Dihydropyrimidin mutation causing aberrant splicing and myelosuprression impacts which drug?

A

5-fluorouracil dehydrogenase (possible neurotoxicity)

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49
Q

Thiopurin methyltransferase SNP leading to instability affects which drug?

A

Mercaptopurine (may lead to myelosuppression or secondary tumors)

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50
Q

Glucuronosyl transferase SMP varying number of TA repeats in promoter impacts which drug?

A

Irinotecan (increasing risk of diarrhoea and myelosupression)

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51
Q

Describe PSA

A

Prostate Cancer Biomarker

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52
Q

Familial Adenomatous Polyposis (FAP) represents ____ percent of all colon cancers

A

1

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53
Q

Treatment options for Colon Cancer include

A

5-flurouracil (5FU) and Capecitabine

Irinotecan

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54
Q

Describe HNPCC (Colon Cancer)

A

Hereditary Non-polyposis Colon Cancer - represents 4-13% of all colon cancers

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55
Q

Describe Malignant conversion in Colon Cancer

A

Over 50 percent of tumors greater than 1cm have RAS mutation

Over 75 percent of tumors have p53 mutation with DCC mutations in up to 80%

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56
Q

What are the Amsterdam Criteria for determining if HNPCC

A

Three or more relatives with colon cancer, two generations and one or more diagnosed cases before the age of 50

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57
Q

What are fluoro-pyrimidines?

A

Developed in the late 50’s, 3rd most commonly prescribed chemo agent and used for single-agent activity against colorecatal carcinoma. Used in combination for breast, head/neck and other adult solid tumors. Belongs to class of chemo agents known as anti-metabolites

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58
Q

Describe the metabolism of 5-flurouracil (5FU)

A

metabolized (80%) in liver by dihydropyrimidine dehydrogenase. Remaining binds to thymidylate synthase to inhibit DNA synthesis

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59
Q

What happens when a patient has low hepatic DPD activity?

A

Cannot efficiently metabolize 5-FU and its accumulation will cause toxicity

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60
Q

In DPD, what substitution in exon 14 causes synthesis of non-functional protein?

A

G to A

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61
Q

Three tandem repeats of TS gene causes…

A

Over-expression of TS, leading to poor antitumour response to 5-FU

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62
Q

Two tandem repeats of TS gene causes…

A

Under-expression of TS causing good antitumour respsonse to 5-FU

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63
Q

Describe Irinotecan

A

A topoisomerase inhibitor used in colon cancer.

Is activated by carboxylesterase (CE) to SN38 which blocks DNA replication

64
Q

Describe SN38 inactivation

A

Inactivated by glucuronidation (UGT1A1) to SN-38-G which is eliminated in bile

65
Q

Low UGT1A1 leads to…

A

SN-38 accumulation causing diarrhea and leucopenia

66
Q

Which enzyme inactivates ironotecan

A

CYP3A, through oxidation

67
Q

Which polymorphism of UGT1A1 leads to reduced expression of the gene?

A

UGT1A1*28

68
Q

TPMT catalyzes _________________

A

S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP)

69
Q

Describe activation and inactivation of mercaptopurine (MP)

A

MP is converted by hypoxanthine phosphoribosyl transferase (HPRT) to its active metabolites, thioguanine nucleotides.

TPMT competes for MP substrate, catabolizing it to methyl-mercaptopurine, an inactive metabolite

70
Q

TPM deficiency is an _______________________ trait which determines _____ drug toxicity

A

autosomal recessive trait, 6MP

71
Q

90% WT/WT TPMT results in

A

Inactive metabolite decreased to chemo (by 6MP)

72
Q

10% WT/MUT TMPT results in

A

Intermediate 6MP activity

73
Q

0.3% MUT/MUT TMPT results in

A

High risk of severe bone marrow toxicity upon administration of 6MP

74
Q

What does the FDA recommend for 6-PM

A

That a patient TPMT genotype or phenotype status be determined before 6MP administration to prevent life-threatening effects

75
Q

How is chronic myelogenous leukemia treated?

A

With allogenic bone marrow transplantation (15-20% of patients) and treatment with Bcr-Abl inhibitor STI571 (Gleevec)

76
Q

What are the phases of chronic myelogenous leukemia?

A

Chronic phase - migration of chromosome 9 and 22 to form Bcr-Abl fusion protein and blast crisis

77
Q

Describe Gleevec (how it works)

A

AKA Imanitib, occupies ATP binding pocket of the kit kinase domain on Bcr-Abl, preventing substrate phosphorylation and signaling, which in turn prevents proliferation and survival

78
Q

What is the significance of breast cancer (prevalence, incidence, mortality)?

A

Most prevalent type in women (31%), median age 40 with 210,000 new cases every year. 71,000 deaths in women (33%) every year

79
Q

Treatment options for breast cancer

A

surgery, radiation, chemo

80
Q

Breast cancer chemo agents

A

Cyclophosphamide (Cytoxan)
Doxorubicin (Adriamycin)
Paclitaxel (Taxol)
Tamoxifen (Nolvadex)

Trastuzumab (Herceptin) - KNOW THIS ONE

81
Q

Side effects of cancer treatment agents

A

Nausea/vomiting, anemia, immune system compromised, pain

82
Q

Doxorubicin + Digoxin = ____ digoxin effects

A

decrease

83
Q

tamoxifen + warfarin = ___ warfarin effects

A

increase

84
Q

cyclophosphamide + aprepitant = ___ chemo efficacy

A

decrease

85
Q

paclitaxel + doxorubicin = ____________

A

cardiotoxicity

86
Q

trastuzumab + cyclo/dox = ______________

A

cardiotoxicity

87
Q

What is Herceptin used for

A

Herceptin, aka Trastuzumab, is the first humanized antibody for treatment of HER2 (human epidermal growth factor receptor 2) positive metasatic breast cancer; blocks function of HER2

88
Q

What is the difference between HER2 positive and HER2 negative breast cancer

A

HER2 positive: more aggressive disease, greater likelihood of recurrence, poorer prognosis, half the life expectancy

89
Q

Combo that FDA approved for treatment of metastatic breast cancer whose tumors over-express HER2

A

Herceptin and paclitaxel (only if they haven’t received chemo for the disease)

90
Q

Only humanized antibody that has demonstrated a “survival benefit” for metastatistic breast cancer

A

Herceptin

91
Q

Herceptin attaches to _____ receptors

A

HER2

92
Q

Describe Target selection in drug development

A

Discovery of biomarker

Involves proteomics, genomics, metabolomics, and imaging technologies

93
Q

Describe lead identification

A

Confirmation of biomarker and development of assay

Involves integrated technologies and multi-analyte assays

94
Q

Describe pre-clinical validation

A

Biomarker validation

Involves robust validated high-throughput assays and the development of a clinical assay

95
Q

Describe regulatory clinical trials (Phases 1, 2, and 3)

A

Used for clinical validation and utility

96
Q

Describe product launch marketing

A

Regulatory approval of drug and clinical adoption

Involves the use of a clinical assay

97
Q

As the drug discovery process advances, the number of analytes __________ while the number of samples (sample size) _________

A

Decreases, increases

98
Q

What is gene therapy?

A

Introducing normal genes into cells containing defective genes to reconstitute a missing protein product; correction of a deficient phenotype to improve a genetic disorder

99
Q

Why are somatic cell modifications necessary in gene therapy?

A

Inserted genes won’t be carried over to next generation (unlike germline)

100
Q

How is gene editing performed?

A

Engineered, non-specific nucleases are fuse to sequence-specific DNA binding domains

101
Q

These are notable inherited/monogenic disorders

A

Parkinson’s, Hunter syndrome, cystic fibrosis

102
Q

Define somatic gene therapy

A

The recipient’s genome is changed, but the change is not passed along to the next generation

103
Q

Define germline gene therapy

A

Sex cells are changed with the goal of passing these changes to their offspring; comes with major ethical issues

104
Q

Define CRISPR

A

Culstered, regularly interspaced, short, palindromic repeats

105
Q

Define CAS

A

CRISPR-associated systems

106
Q

Define CRISPR

A

Culstered, regularly interspaced, short, palindromic repeats

107
Q

Define CAS

A

CRISPR-associated systems

108
Q

What is the CRISPR/CAS system?

A

RNA-based bacterial defense mechanism designed to recognize and eliminate foreign DNA from invading bacteriophage and plasmids; CAS endonuclease cleaves target sequence by guide RNA (gRNA)

109
Q

What encodes for CAS endonuclease and gRNA in bacterial genome?

A

CRISPR/array

110
Q

What is the significance of the CRISPR/CAS system?

A

Plasmid (CAS 9) can be introduced in cells to cut the genome wherever, providing us with a huge tool for gene editing.

Can be done in LIVE cells

111
Q

What is the name of the location that the CAS9 protein complex binds in DNA?

A

PAM

112
Q

Describe the difference between “in vivo” and “ex vivo” gene delivery

A

In vivo delivery takes place in the body

Ex vivo delivery takes place out of the body and then the cells are placed back in the body

113
Q

Describe the details of “In vivo” delivery systems

A

Utilize viral vectors.

Virus is the carrier of the desired gene but is usually crippled to disable its ability to cause disease. Viral methods are currently the most efficient and many exist for stable integration of viral gene into genome.

114
Q

Problem(s) associated with in vivo viral delivery system

A

> replication of defective viruses adversely affect the virus’ normal ability to spread genes
reliant on diffusion and spread
hampered by small intracellular spaces for transport
restricted by viral-binding ligands on cell surface, and cannot advance far as a result

115
Q

What are retroviruses, how are they made and how do they operate?

A

dsDNA copies made from RNA genome use reverse transciptase and RNA. dsDNA viral genome integrates into human genomes with integrase, possibly resulting in insertional mutagenesis.

116
Q

Which retro-virus is currently being tested for safety in humans?

A

HIV

117
Q

Define Adenovirus

A

dsDNA genome that causes respiratory, intestinal and eye infections

118
Q

How does the Adenovirus infection spread?

A

Inserted DNA is NOT incorporated into the genome and must be reinserted when more cells divide (since its not replicated with the genome upon division)

119
Q

Where do retroviruses incroporate dsDNA viral genome?

A

Randomly in host cell genome through use of integrase

120
Q

How are Adenoviruses used for gene therapy?

A

A viral vector is used to insert genetic material into the target cell, Functional proteins are then created from the therapeutic gene causing the cell to return to a “normal” state

121
Q

List the gene therapy, Ex vivo delivery systems (6)

A 
>electroporation
>liposomes
>calcium phosphate
>gold bullets (fired with helium pessurized gun)
>retro-transposons
>human artificial chromosomes
122
Q

What are the various non-viral options for gene delivery

A

Direct introduction of therapeutic DNA (only works with certain tissues and requires a lot of DNA)

Liposome (artificial lipid sphere with aqueous core, carries therapeutic DNA through membrane)

Chemically linking DNA to molecule that will bind to special receptors (DNA is then engulfed by the cell membrane, however, this method isn’t overly effective)

Introduce a 47th chromosome to exist alongside the other 46 (can carry a lot of information but getting a molecule this large through the membrane is a challenge)

123
Q

What is the general principle of the antisense approach?

A

Using gene therapy to turn genes OFF

124
Q

How does the antisense approach work? What are the various methods available?

A

Antisense complements mRNA (sense) and prevents protein expression; utilizes small interfering RNA molecules (siRNA) and ribozymes

125
Q

List the main limitations of gene therapy

A

Gene delivery, duration of gene activity, patient safety, expense

126
Q

How is gene delivery limited in gene therapy?

A

Most viral vectors are unable to accommodate full length human genes containing all of their original regulatory sequences; some viral vectors also depend on the cell cycle

127
Q

Describe duration of gene activity as a gene therapy limitation

A

Non-integrating delivery will only last a short amount of time, whereas integrated delivery will be stable.

Regulatory information can be lost, for example, promoters can be substituted

128
Q

Describe patient safety as it relates to gene therapy limitations

A

Some patients experience immune hyper-responsiveness and random integration can result in adverse gene expression (i.e. insertion near highly methylated heterogenous DNA may silence certain genes)

129
Q

Describe expense as a limitation for gene therapy

A

ex vivo techniques are costly as are virus cultures for in vivo delivery

130
Q

How many patients have been treated (using gene therapy) in the past 12 years

A

5000

131
Q

Explain OTC deficiency

A

Ornithine Transcarbamylase Deficiency (urea cycle disorder resulting in ammonia accumulation in blood and brain, x linked)

132
Q

How severe is “Severe OTC Deficiency?”

A

Newborns are in a coma within 72 hours, most suffer severe brain damage, 1/2 die in first month, 1/2 of survivors die by age 5

133
Q

What is used for early-treatment of OTC?

A

Low-protein formula called “keto-acid”

Modern treatment is sodium benzoate or another sodium derivative that binds ammonia and helps eliminate it from body

134
Q

Which gene appears to be defective in most human cancers?

A

p53

135
Q

20-30% of human cancers have an abnormal _____ gene

A

ras

136
Q

What is the normal function of ras in human cells? What is different in cancer cells?

A

Tells cells when to divide normally; mutant ras is stuck on causing uncontrolled proliferation, as in cancers

137
Q

Which protein/receptor on tumors may be necessary to provide the second signal required for cytotoxic T cell activation?

A

B7 - improves the antigen presenting properties of tumor cells

138
Q

What is gene therapy (ex vivo) doing for HIV?

A

T lymphocytes are treated with rev and env defective mutant HIV strains ex vivo and are then injected back into patient, causing the stimulation of good cytotoxic T cell responses

139
Q

Broad definition of a stem cell (2 functions)

A

A single cell that can replicate itself or differentiate into many cell types

140
Q

Every cell in the human body can be traced back to a ___________

A

fertilized egg

141
Q

Differentiate between totipotent, pluripotent and multipotent stem cells

A

Totipotent - each cell can develop into a new individual

Pluripotent - cells can form any cell type

Multipotent - differentiated cells that can form other tissues

142
Q

Totipotent stem cells go on to form the ____________

A

blastocyst containing pluripotent stem cells

143
Q

Define embryonic stem cells

A

Derived from very early stage in human development and have the potential to produce all of the body’s cell types

144
Q

Explain the process of nuclear transfer

A

Inserting the nucleus of an already differentiated adult cell into an egg which will form a blastocyst from whcih ESCs will be derived (ESCs are copies or clones of the original adult cell because their nuclear DNA matches that of the adult)

145
Q

Explain the basic principles of reproductive cloning

A

donor nucleus taken from cell and implanted in egg cell that has had the nucleus removed. Fused cell is then implanted in a surrogate mother.

146
Q

Nuclear transfer is sometimes called

A

Research cloning or therapeutic cloning

147
Q

What are the common locations of adult stem cells?

A

Blood, skin, and lining of the gut

Some in the brain

148
Q

The main difference between embryonic and adult stem cells is

A

That adult stem cells are already somewhat specialized

149
Q

Neural Stem Cells go on to form which specialized cells?

A

Neurons, interneurons, oligodendrocytes, Type 2 astrocytes, Type 1 astrocytes

150
Q

Gut stem cells go on to form which specialized cells?

A

Paneth cells, goblet cells, endocrine cells, columnar cells

151
Q

Mesenchymal stem cell go on to form these specialized cells

A

Bone (osteoblasts), cartilage (chondrocytes) and fat (adipocytes)

152
Q

What is the purpose of induced pluripotent stem cells?

A

to make mature cells behave like embryonic stem cells

153
Q

Cancer stem cells can result from 3 lineages. Name them.

A

Stem cells, progenitor cells and differentiated cells

154
Q

What is the general difference between specific and unspecific cancer therapy?

A

Specific therapy targets the cancer stem cells, non-specific does not and kills tumor cells randomly, leaving room for the cancer stem cell to survive and continue proliferating.

155
Q

What are some primary applications of stem cells? (provide details)

A

Tissue repair (spinal cord injuries, heart tissue, etc.)

Heart disease (improvement of cardiac function)

Leukemia-Cancer (Leukemia patients treated with stem cells can emerge disease free; stem cell injections have also helped pancreatic cancer patients)

Rheumatoid Arthritis (repair of eroded cartilage)

Diabetes Type 1 (ESC may be able to become pancreatic islets cells needed to secrete insulin)

156
Q

Explain altered nuclear transfer

A

An alternative to using an embryo in stem cell research.

Blastocyst whose genetic material has been altered is created and used as a source of pluripotent stem cells

Pharmacy School 2015-16 (34 decks)

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