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PHAR359 > Oncology 1 > Flashcards

Oncology 1 Flashcards

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1
Q

What is the lifetime probability of developing cancer?

A

both sexes: 45% (1 in 2.2)
males: 45% (1 in 2.2)
females: 44% (1 in 2.2)

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2
Q

What are the 5 most common cancer deaths?

A

lung (23.5%)
colorectal (10.7%)
pancreas (6.9%)
breast (6.2%)
prostate (5.7%)

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3
Q

How much higher are cancer death rates in males compared to females?

A

37% higher in males than in females

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4
Q

What is the leading cause of death in Canada?

A

cancer

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5
Q

What is the most commonly diagnosed cancer?

A

lung
-remains leading cause of cancer death in Canada

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6
Q

What are the most commonly diagnosed cancers in 2024?

A

males:
-prostate (21.9%)
-lung (11.6%)
-colorectal (11.1%)
-bladder (7.3%)
females:
-breast (25.4%)
-lung (14.4%)
-colorectal (9.3%)
-uterine (7.2%)

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7
Q

True or false: survival increases with increasing stage at diagnosis

A

false
survival decreases with increasing stage at diagnosis

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8
Q

Describe the economic impacts of cancer in Canada in 2024.

A

total cost of cancer to society projected to be $37.7 billion
-$30.2 billion health system, $7.5 billion to pts/caregivers
patients and caregivers pay the most in the first 12 months after diagnosis
OOP costs account for 49% of costs to pts and caregivers
lifetime avg costs to pts and caregivers is ~ $33,000
cost of cancer to society in next 10 yrs will increase 23%

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9
Q

What are the key measures used to describe the occurrence of cancer?

A

incidence
- # of new cases diagnosed with cancer in a specific period
mortality
- # of cancer deaths in a specific period
rates
-divide by population (expressed per 100,000)
-for rates to be comparable over time or between different populations, statistics are adjusted for age
prevalence
-total # of people with cancer at a specific time

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10
Q

What has occurred to cancer rates dating back to 2011?

A

cancer rates have declined by 1.2% annually since 2011 for males and 0.4% annually since 2012 for females

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11
Q

What has occurred to the number of cancer cases diagnosed each year?

A

number of cases diagnosed each year has been increasing because of growing and aging population
-when effect of age and population size are removed, risk of cancer has been decreasing
-rate of new cancers increases with age

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12
Q

Which cancers have seen increased rates?

A

melanoma and cervical

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13
Q

What are the non-modifiable risk factors for cancer?

A

age
-seniors > 65 are the fasting growing group
sex
genetics

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14
Q

What are the modifiable risk factors for cancer?

A

tobacco
sun exposure
alcohol consumption
physical inactivity
diet
obesity
vaccination (HPV, hepatitis)
minimizing exposure to radiation, air pollution, radon gas

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15
Q

What is cancer?

A

generic term used to describe a larger number of neoplastic diseases affecting various parts of the body

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16
Q

What are cancer cells?

A

abnormal human cells and can arise from any cell type

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17
Q

What are the characteristics of cancer cells?

A

exhibit uncontrolled growth:
-malignant cells are unresponsive to normal feedback mechanisms that regular cellular proliferation in normal tissue
ability to invade surrounding tissue:
-malignant cells can penetrate adjacent tissues
exhibit decreased cellular differentiation:
-malignant cells generally are not capable of performing the physiologic functions of their tissue of origin
-atypical of cell of origin, anaplastic
ability to metastasize:
-malignant cells have a unique ability to break away and spread via blood, lymph system, or seed body cavities and establish new, secondary growths in other tissues

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18
Q

What are the most common sites of metastases?

A

liver
lung
bone
brain

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19
Q

Do metastatic growths have different characteristics from the original cancer tissue?

A

secondary, metastatic growth retains the characteristics of the original cancer tissue

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20
Q

What is often the “lethal” effect of many solid tumor cancers?

A

metastases

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21
Q

Different benign and malignant tumors.

A

benign:
-some degree of growth control
-encapsulated (non-invasive)
-localized
-typical of cell of origin (differentiated)
-indolent (slow growth)
-non-recurrent
malignant:
-uncontrolled growth
-invasive
-metastatic
-atypical (anaplastic, less differentiated)
-aggressive (faster growth)
-recurrent

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22
Q

What determines aggressiveness?

A

tumor grading
-“how bad does it look?”

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23
Q

What is tumor grading based on?

A

primarily based on degree of differentiation of malignant cells and secondarily on estimate of growth rate (mitotic rate)
-the less a tumor cell resembles a normal cell and the more cells that are active in cell division, the higher the grade - indicates more aggressive tumor cell & often correlates with poorer prognosis

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24
Q

What determines extent of disease?

A

tumor staging
-“how far has it spread?”

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25
What is tumor staging based on?
primary lesion (T), presence of lymph node involvement (N), presence of identifiable metastases (M) -TNM staging system divides tumors in stages 0-IV
26
What is cancer grading and staging important for?
prognosis treatment planning exchange of information evaluation of treatment
27
Where are biomarkers found?
found in tissue (incl. cancer), blood, urine, and other bodily fluids
28
What is the use of biomarkers?
diagnostic, prognostic, predictive, or used to monitor response (or a combination) -predictive: identify pts likely to benefit from a specific tx
29
What are the four pillars to cancer therapy?
surgery radiation cytotoxic & targeted therapies immunotherapy *surgery, radiation, and cytotoxic & targeted therapies work at the tumor level whereas immunotherapy works at the patient level*
30
What is the most effective cancer treatment for solid tumors?
surgery
31
When is surgery ineffective for cancer?
largely ineffective for metastasized or disseminated cancers often not feasible for very large tumors
32
Why does radiation work for cancer?
rapidly dividing cells are very sensitive to ionizing radiation; cancer cells preferentially destroyed due to higher growth rate
33
When is drug (systemic) therapy used for cancer?
utilized for disseminated/metastasized cancers and for treatment of micro-metastatic disease high dose chemotherapy & stem cell transplant: -utilized primarily for hematologic cancers
34
What is the principle of immunotherapy?
engages the patients own immune system to destroy cancer cells
35
What are the different terminology for cancer drugs and their associated definitions?
cytotoxic drugs (traditional "chemotherapy"): -interferes with or damage DNA targeted drug therapy: -block, inhibit, attack specific proteins that are involved in the molecular processes driving tumor cell growth immunotherapy: -activate ones immune system against a cancer
36
What is the growth fraction?
cells in cycle/total # cells in tissue
37
When is the growth fraction higher? When is it decreased?
higher growth fraction early in tumor growth growth fraction decreases as tumor gets larger -cells become farther away from blood vessels and nutrient supply; accumulation of toxic metabolites; less cell to cell communication = may not be able to divide
38
What is the MOA of cytotoxic drugs?
interfere with synthesis or function of DNA/RNA causing 'apoptosis' or programmed cell death -target is the processes within the cell cycle -cause crosslinking and DNA strand breaks, leading to abnormal base pairing, inhibiting transcription of DNA to RNA, and stopping protein synthesis and cell division -occurs in all cells, but primary effects on rapidly dividing cells which do not have time for DNA repair -cancer cells are among the most affected because they are among the most rapidly dividing cells
39
What is apoptosis?
programmed cell death -occurs naturally when DNA abnormalities detected -end result of irreparable damage to DNA caused by cytotoxic drugs
40
What is p53?
guardian of the genome -senses genomic damage; halts cell cycle and initiates DNA repair; if irreparable damage, p53 initiates cell death process or apoptosis
41
What is cycle specificity important for with cytotoxic drugs?
dosing and scheduling
42
Differentiate cell cycle specific drugs and cell cycle non-specific drugs.
cell cycle specific drugs: -effective against cells in process of division -most effective in tumors with high growth fraction cell cycle non-specific drugs: -some activity against resting cells -dose-dependent -used in large tumors with low growth fraction
43
Differentiate the two types of cell cycle specific drugs.
phase-specific drugs: -schedule-dependent drugs -most effective in repeated doses phase non-specific drugs: -can inflict damage at any point in cell cycle -dose-dependent
44
What are the goals of systemic therapy?
cure -elimination of all known tumor cells improve survival -tumor control -delay time to recurrence palliation -reduce tumor-related symptoms; improve QoL; some tumor control
45
What are the common clinical trial endpoints?
response rate (RR) -CR, PR, SD, PD survival -overall survival is the gold standard -surrogates: PFS, DFS, RFS quality of life safety
46
Describe induction chemotherapy.
primary treatment usually applied in hematologic malignancies; also applicable for advanced disease (1st line)
47
Describe adjuvant chemotherapy.
drug treatment given after primary tumor is controlled by definitive local treatment (e.g. surgery or radiation) pt is clinically free of cancer, but at high risk for relapse (tumor re-growth) goal is CURE - destroy undetectable cancer cells clinical trial evidence for benefit of adjuvant therapies would evaluate relapse-free or disease-free survival
48
What is the premise of adjuvant chemotherapy?
microscopic, clinically undetectable cancer cells remain after surgery or radiation or at a distant metastatic site these smaller populations of cancer cells are more susceptible to chemo and may be eradicated -better vascular supply for penetration -higher growth fraction -not as diverse genetically, less resistance
49
How aggressive are the treatments used for adjuvant chemotherapy?
aggressive chemotherapy treatments often used
50
What are the disadvantages of adjuvant chemotherapy?
cannot assess response short and long-term risk of aggressive chemo
51
Describe consolidation therapy.
treatment of subclinical, residual disease term often applied in treatment of hematologic malignancies after induction therapy has produced a complete remission
52
Describe neo-adjuvant chemotherapy.
use of drug therapy prior to local treatment goal: -increase effectiveness of local treatment by reducing tumor burden and destroying undetectable cancer cells susceptible to chemotherapy that may have metastasized early advantage: can evaluate response to chosen drugs adjuvant therapy may or may not follow neoadjuvant tx and surgery/radiation
53
Describe maintenance therapy.
longer term, usually lower dose therapy, used to decrease recurrence rate, or progression rate can be used in both curative and non-curative settings
54
Describe salvage therapy.
treatment of relapsed (recurrent after previous control) or refractory (unresponsive to treatment) disease
55
What is local chemotherapy?
local instillation of anticancer drugs -e.g. CSF, bladder instillation, intra-cavitary for malignant effusions, chemo-embolization of hepatic artery purpose: -deliver chemotherapy to relatively inaccessible sites -provide high local [ ] -avoid systemic toxicity
56
What are high doses of chemotherapy lethal to?
bone marrow -rescue with SCT with WBC growth factor support
57
What is the premise of SCT?
high doses overcome resistance of tumor to chemotherapy
58
What are the barriers to SCT?
patient age/fitness toxicities (acute and long-term)
59
Describe lymphodepleting therapy prior to CAR T-cell.
reduces the number of existing lymphocytes in the patients body, creating space for the infused CAR-T cells to effectively expand and fight cancer cells
60
What are common chemotherapy toxicities?
bone marrow suppression, risk of infection (neutropenia) mucositis, stomatitis hair loss or thinning (alopecia) nausea or vomiting -dose and drug dependent fatigue
61
Which chemotherapy drug is most emetogenic?
cisplatin
62
Which drugs can be used to help with nausea and vomiting caused by chemotherapy?
5HT3 antagonist NK1 antagonists
63
What are the advantages of combination chemotherapy?
higher cell kill different MOA: heterogeneity of tumor prevent or slow development of tumor resistance
64
What are the disadvantages of combination therapy?
multiple toxicities may have to dose reduce in combination -compromised efficacy? more complicated to administer
65
What is the goal of combination therapy?
balanced increased efficacy with tolerable toxicity
66
List some considerations when determine the drug selection for combination therapy.
show clinical activity against tumor alone different MOA; more effective minimal overlapping toxicities no cross resistance between drugs synergistic in combination
67
How are many chemotherapy drugs dosed?
based on BSA (mg/m2)
68
How are many monoclonal antibodies dosed?
mg/kg; many flat dosing
69
What is the goal of dosing with cancer drugs?
attempt to deliver maximum dose for maximum efficacy
70
What are some factors that may cause modification of initial protocol doses?
curability of tumor (less aggressive if non-curable) overall performance status renal/liver function prior therapies
71
What are the usual reasons for dose modifications as a patient proceeds through treatment?
usually for toxicity/tolerability concerns -possible reduced efficacy?
72
What is taken into account when planning the interval between doses?
recovery of host tissue toxicity how fast the tumor is growing MOA of drug: cell cycle specificity *depending on drug, may be given on a cyclic schedule or more typical daily dosing*
73
What is the difference between duration of therapy for adjuvant therapy and advanced disease?
adjuvant: -prescribed # of cycles and duration advanced disease: -commonly given until evidence of disease progression or as long as toxicity can be managed
74
Why does chemotherapy treatment sometimes fail?
toxicity to normal cells - dose limiting patient comorbidities limit effective dosing first order kinetics of cell kill -constant % of cells killed, not constant # -theoretically cannot get 100% cell kill
75
Why does cancer treatment fail?
failure to detect tumor in early stage -tumor burden high - metastases present -growth fractions low - less sensitive to chemo drugs -compromised pt - limits effective dosing limited drug access to tumor site -perfusion to tumor is low main reason: drug resistance (inherent or acquired)
76
Describe tumor cell heterogeneity.
spontaneous genetic mutations occur in tumor cell populations without exposure to drugs larger tumor masses have more mutations and a higher probability of drug-resistant cell lines
77
What are some mechanisms of acquired drug resistance?
enzymes to inactivate drug p-glycoprotein: pump drug out of cell enzymes to repair drug damage to DNA mutations in protein receptor another molecular pathway becomes dominant
78
What is the first true 'target therapy'?
endocrine therapies -not cytotoxic
79
How does targeted endocrine therapy mediate its effects?
through hormone receptor or hormone deprivation
80
Which cancers are endocrine therapies useful for?
hormone-sensitive cancers -prostate cancer -breast cancer -uterine (endometrial) cancer
81
What are examples of therapies that block estrogen receptor?
tamoxifen fulvestrant
82
What are examples of therapies that block the aromatase enzyme?
anastrozole letrozole exemestane
83
What are examples of therapies that interfere with estrogen production?
GnRH analog megestrol
84
What are examples of therapies that block testosterone receptor?
bicalutamide enzalutamide apalutamide darolutamide
85
What are examples of therapies that inhibit testosterone production?
GnRH analog GnRH antagonist cyproterone abiraterone
86
What is molecular targeted drug therapy?
target specific molecules or signaling pathways involved in the growth and spread of cancer cells -takes advantage of understanding the cancer biology -highly selective, molecularly targeted treatments
87
What is the goal of molecular targeted drug therapy?
improve efficacy and avoid the severe toxicities to normal cells from traditional cytotoxic chemotherapy
88
What are the types of drugs used in molecular targeted drug therapy?
monoclonal antibodies targeting tumor receptors small molecule, tyrosine kinase inhibitors
89
What is the MOA of small molecule compounds?
act within a cancer cell to interfere with key proteins (produced by abnormal genes) in pathways essential to disease progression
90
What is the MOA of monoclonal antibodies?
block extra-cellular proteins (antigens) or receptors outside the cell or on the cell surface that are involved in essential cancer cell functions
91
What are the targeted drug approaches?
anti-receptor blocking antibodies anti-ligand blocking antibodies tyrosine kinase inhibitors ligand-toxin conjugates antibody-drug conjugates
92
What is required with targeted therapy?
the need for a "companion" molecular biomarker eligibility test -ex: HER2, EGFR, BRAF quality biopsies with enough tissue required
93
Why does our own immune system not target tumor cells?
they appear to be 'self' or cancer cells may send out signals to block host immune response against the abnormal cell
94
What are some forms of immunotherapy?
monoclonal antibody immune checkpoint inhibitors -take the breaks off the immune system, helps recognize and attack cancer cells "personalized" cellular therapy (e.g. CAR T-cell)
95
Describe T-cell checkpoint regulation.
T-cell responses are regulated through a complex balance of inhibitory ("checkpoint") and activating signals tumors can dysregulate checkpoint and activating pathways, and consequently the immune response targeting checkpoint and activating pathways is designed to promote an immune response against the tumor
96
What is the MOA of PD-1 inhibitors?
PD-1 inhibitors block the PD-1/PD-L1 interaction between tumor cells and T cells, thereby restoring T-cell mediated immunity
97
Describe the process of CAR T-cell therapy.
remove blood from patient to get T cells make CAR T cells in the lab grow millions of CAR T cells infuse CAR T cells into patient CAR T cells bind to cancer cells and kill them
98
Describe immunotherapy toxicities.
treated differently than usual chemo toxicities can affect multiple organ systems from immune effects requires prompt assessment and tx -interrup therapy, steroids, infliximab, tocilizumab life-threatening: CRS, ICANS

PHAR359 (28 decks)

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