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Pharmacology II > Anti-Neoplastics #4 > Flashcards

Anti-Neoplastics #4 Flashcards

1
Q

Define personalized or precision medicine.

A

Separates patients into different groups with medical decisions, practices, interventions
being tailored to the individual patient based on their predicted response or risk for disease

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2
Q

Why is diagnostic testing used in precision medicine?

A

In PM, diagnostic testing is employed for selecting appropriate or optimal therapies based on the context of a patient’s genetic content or other molecular or cellular analysis. Enzymes especially b/c?

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3
Q

What is the benefit of analyzing a patient’s genes in the field of precision medicine?

A

In PM, by analyzing patient’s genes, you can identify certain drugs that may be dangerous/toxic or completely ineffective

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4
Q

How can you identify mutations linked to specific diseases?

A

To identify mutations linked to certain disease, GWASs (genome-wide association study) are performed: sequencing the genome of many patients in the particular disease

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5
Q

Define pharmacogenetics.

A

Pharmacogenetics is the study of genetic causes of individual variations in DRUG RESPONSE

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6
Q

Define pharmacogenomics.

A

Pharmacogenomics: is the study of the role of the genome in DRUG RESPONSE

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7
Q

What is targeted therapy?

A

Targeted Therapy: targeting specific molecules and/or signaling pathways
Essential part of precision medicine

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8
Q

Precision medicine was further advanced by?

A

Advances in DNA sequencing technology and Human Genome Project (1990 -2003)

International HapMap Project (2002 -2010): identification of genetic variations that contribute to human disease (s)

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9
Q

Previous observations that were not fully understood.

A

Observations:
➢ Certain drugs are more effective in some patients and others
➢ In response to certain drugs, some patients experience unusually severe side effects

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10
Q

Progress in understanding the molecular factors responsible for differences in drug response became possible by developing two new fields in pharmacology: Pharmacogenetics and Pharmacogenomics

A
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11
Q

What is the importance of health information technology?

A

Health Information Technology (Electronic Health Records: history, family history, medications, test results, demographics)

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12
Q

What are some of the challenges in achieving more personalized medicine?

A

Challenges: >106 variation, multiple disciplines analysis, geographic and ethnic differences, ethical problems

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13
Q

What does inter-patient variability in drug response result from?

A

Interpatient variability in drug response may result primarily from genetically determined differences in drug metabolism, drug distribution, and drug target proteins

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14
Q

What is the long term goal of both pharmacogenetics and pharmacogenomics?

A

Long-term goal: to help doctors select the drugs and doses best suited for each person

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15
Q

Is personalized medicine used in veterinary medicine?

A
  • Personalized medicine, which has seen success in humans, is now flourishing in veterinary medicine
  • Conditions from canine cancers to drug and anesthesia sensitivity are being studied in new ways
  • The AKC CHF is focusing on personalized medicine to unlock new treatment methods
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16
Q

What is the benefit of conducting genetic testing in dogs?

A

Genetic testing reveals which targeted therapies might work. The information provided by genomic testing in conjunction with tumor type helps to identify possible cancer-causing mutations and then suggests targeted therapy to precisely attack the cancer cells.

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17
Q

What is the significance of MDR1?

A

MDR1 gene: the single most “Very Important Pharmacogene (VIP) in dogs

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18
Q

MDR-1 gene mutations produces a?

A

Mutations results in a non-functional P-glycoprotein transporter protein

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19
Q

MDR-1 gene mutation results in ?

A

A decrease in function alters the safety and efficacy of drugs in affected patients

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20
Q

Dogs suffering from the MDR-1 gene mutation demonstrate what clinical signs?

A

Affected dogs show extreme sensitivity (toxicity) to Vincristine and Doxorubicin

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21
Q

Is testing for the MDR-1 gene mutation common?

A

▪ It is a standard practice in Vet Med to test for the MDR mutation prior to using P-glycoprotein transported drugs in dogs

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22
Q

What dog breeds are most likely to suffer from the MDR-1 gene mutation?

A

Shetland sheepdogs (Shelties), Australian shepherds, old English sheepdogs, English shepherds, German shepherds, long-haired whippets, silken windhounds, Collies, Waller

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23
Q

What is the KIT oncogenic receptor tyrosine kinase?

A

The KIT oncogenic receptor tyrosine kinase has been implicated in the pathogenesis of
several neoplastic diseases

▪ cutaneous mast cell tumors (MCTs) in dogs & cats
▪ Canine gastrointestinal stromal tumors
▪ Canine oral melanomas b/c genetic defects are noticed in about 30% of dogs and this mutation makes uncontrolled divisional cells. So we can apply the drug, Palladia, to target MUTATED c-kit.

24
Q

What medication is used to treat cancers caused by KIT oncogenic tyrosine kinase mutation?

A

Constitutive activation of KIT due to genetic defect (30%) results in uncontrolled mast cell proliferation
PalladiaR (Toceranib) targets MUTATED c-Kit
Mutational profiles of canine lymphoma and other cancers

25
Define hormone therapy.
Drugs in this category are sex hormones, or hormone-like drugs, that are used to slow the growth of mammary gland, prostate, and endometrial (uterine) cancers. They work by making the cancer cells unable to use the hormone they need to grow, or by preventing the body from making the hormone. Depend on hormones such as estrogen and androgens to grow. Once these hormones encourage proliferation of mammary gland or prostate gland -> bad. Similar to targeted therapy but it is more specific.
26
Define targeted therapy.
Targeted therapies attack cancer cells more specifically than traditional chemotherapy drugs. These drugs can be used as part of the main treatment, or they may be used after treatment to keep the cancer under control or keep it from coming back
27
Define immunotherapy
Some treatments are given to people/animals with cancer to help their immune systems recognize and attack cancer cells
28
What function do cancer vaccines serve?
Activate bodies immune system to recognize and kill cancer cells
29
30
Hormone therapy utilizes what type of drugs? What is the MOA?
Hormone therapy: - Steroidal or non-steroidal hormone-like drugs, that are used to slow the growth of breast and prostate cancers Two major mechanisms of action: * Preventing the body from making hormone * Preventing cancer cells from using hormone for their growth
31
What are the two major approaches in hormone therapy?
32
SERMs - selective estrogen receptor modulators SARMs - selective androgen receptor modulators Do not have to remember.
33
What are SERMs?
▪ SERMs are a new class of drugs, which have a tremendous impact in breast cancer treatment and prevention and hold promise for preventing several other disorders in women. ▪ The most interesting characteristic of pharmacology of SERMs is that they can be estrogenic in some tissues and anti- estrogenic in others. ▪ The molecular mechanisms responsible for this selectivity are unknown
34
What is benign prostatic hypertrophy (BPH)? How is it treated? What are the potential side effects?
Finasteride is a form of hormone deprivation therapy.
35
Wor when hormone is bound to receptor inside cells. Enza = metastatic prostate cancer in dogs RELISTE#N
36
What purpose does standard chemotherapy serve?
▪ Chemo drugs reduce tumor by killing fast-dividing cells, may cause considerable damage to normal cells. ▪ Some treatments may increase the incidence of second-site cancers ▪ Traditional predictors, such as age, tumor size, status of LNs, pathological grade, hormone-receptor status – do not predict outcome ▪ Although 15% will develop metastatic disease – all patients are treated aggressively
37
What purpose does targeted therapy serve?
▪ To develop molecular targets that enable oncologist to distinguish between indolent and aggressive tumors ▪ To develop drugs that interact with specific targets and cancer pathways ▪ Targets are chosen very carefully, with great precision so, they may cause little or no damage to normal cells
38
What are the differences between targeted therapy and standard chemotherapy?
See below
39
Explain the MOA of targeted therapy.
❖ Block or turn off chemical signals that tell the cancer cell to grow and divide ❖ Change proteins within the cancer cells so the cells die ❖ Stop making new blood vessels to feed the cancer cells ❖ Trigger the immune system to kill the cancer cells ❖ Carry toxins to the cancer cells to kill them, but not normal cells
40
What are the best targets for targeted therapy?
▪ Molecular Signaling pathways present in cancer and absent in normal cells (only attack cancer cells) ▪ Molecule that is present more frequently in cancer cells than in normal cells (possible to adjust dose of the drug)
41
What are the differences between druggable and undruggable targets?
▪ Druggable: has a structure indicating that it should be vulnerable to attack and inhibition by low-molecular weight compounds Example: kinases that have well-defined catalytic cleft that can bind small organic molecules in a highly specific manner. ▪ Undruggable: transcription factors, protein-protein interactions; much more difficult to drug. AR and ER are transcription facotrs enter cell nuc and bind to DNA seq to trigger transcription of genes but we know that they can bind to different ligands and ?? RELISTEN **Major exceptions: nuclear hormone receptors (ER, AR) with hormone-binding domains**
42
What are the different types of targeted drugs?
Small molecules Antibodies vaccines
43
Small molecules are capable of?
are just peptides ✓ Travel across the cell membranes ✓ Bind to proteins inside or outside of cells ✓ Interact with specific areas of protein/enzymes
44
Antibodies are capable of?
✓ Outside the cells: they interfere with receptor binding and block the signaling pathway ✓ Delivery vehicles: antibodies are attached to toxins or radioactive molecules ✓ Trigger immune response: reactivating T-cells or B-cells to attack cancer
45
Vaccines acts as ?
preventative and Therapeutic
46
What are the different cancer cell signaling pathways? What are their functions?
47
What is the difference between the normal growth signaling pathway and cancer-effected growth signaling pathway?
GF bind to TKR and trigger cell proliferation. Cancer cells are Constitutively active; does not care if ligand is there, it can do whatever it wants
48
What is the goal of targeted growth signaling?
The Goal: Block any part of dysregulated growth signaling pathway ▪ Drugs that bind to the growth factor receptors and prevent their interaction with other receptors and dimerization ▪ Drugs that keep receptors in “OFF” position ▪ Drugs that prevent from transmitting phosphorylation pathway (kinase inhibitors). Phosphorylation is important for signal propagation
49
Explain how Erlotinib acts as a small molecule inhibitor.
EGFR is either overexpressed or mutated in lung cancer, specifically small cell lung cancer. NSCLC= non-small cell lung cancer
50
Explain how Herceptin (Transtuzumab) acts as a monoclonal antibody?
MAB = molecular antibody HER 2 is more aggressive than Lam? B and A.
51
Are EGFR and HER2 present in non-human animals?
Both EGFR and HER2 have structural homologs in various canine cancers, and chimeric versions of these antibodies speciated to the dog have been developed. Canine anti-EGFR was shown to decrease canine mammary carcinoma cell proliferation by 40%–60% and to mediate tumor cell killing by macrophage phagocytosis in vitro
52
Overexpression of HER2 has also been identified in ?
spontaneous feline mammary carcinomas; however, feline specific antibodies have yet to be developed
53
Ongoing and future clinical studies will continue to evaluate the in vivo efficacy of these compounds and their effects on the adaptive immune response.
54
The KIT oncogenic receptor tyrosine kinase has been implicated in?
The pathogenesis of several neoplastic diseases, particularly cutaneous mast cell tumors (MCTs) in dogs. Constitutive activation of KIT due to genetic defect (30%) results in uninhibited mast cell proliferation
55
Describe Palladia and Masitinib's MOA
NIB is for protein
56
Toceranib Therapeutic uses? Adverse effects? Animals?
57
Masitinib Therapeutic uses? Adverse effects? Animals?

Pharmacology II (27 decks)

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