Oncology 4 Flashcards

1
Q

What are the five pillars of cancer care?

A

radiotherapy
surgery
traditional chemotherapy
precision therapy
immunotherapy

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2
Q

Which pillar of cancer care has a durable response in patients who respond to therapy?

A

immunotherapy

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3
Q

What is immuno-oncology?

A

development and delivery of therapies that improve immune response against cancer
-provides immune system with tools to recognize tumours and strengthen tumour attack

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4
Q

What is the goal of immuno-oncology?

A

restore or enhance anti-tumour immune responses

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5
Q

What are the side effects of immuno-oncology agents related to?

A

immune-related and can affect any organ
-may include colitis/diarrhea, rash, hepatitis, endocrinopathies, uveitis, nephritis

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6
Q

What are the types of IO therapy?

A

monoclonal antibodies:
-bind specific targets to cause immune responses to destroy cancer cells
adoptive T-cell transfer:
-isolates and modifies T cells from tumor for enhanced immune response against cancer cell
cytokines:
-role in normal immune response and immune system response to cancer
treatment vaccines:
-enhance immune system response against cancer cells
Bacillus Calmette-Guerin:
-weakened form of TB bacteria, used in bladder cancer to cause immune response against cancer cells
toll-like receptor agonists:
-bind toll-like receptors on immune cells to cause immune response against cancer cells

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7
Q

Describe how IO differs from chemotherapy and targeted therapy.

A

chemotherapy:
-acts directly on cancer cells that are actively reproducing
-often causes tumour cell death vs simply inhibiting tumour growth
targeted therapy:
-inactivates specific proteins in tumour cells that are involved in growth, progression, and spread of cancer
IO:
-triggers the immune system to destroy cancer cells
-considered a type of targeted therapy

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8
Q

What are some inhibitory cells found on T cells?

A

CTLA-4
PD-1

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9
Q

What is an example of a CTLA-4 inhibitor?

A

ipilimumab

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10
Q

What are examples of PD-1 inhibitors?

A

pembrolizumab
nivolumab

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11
Q

What are examples of PD-L1 inhibitors?

A

durvalumab
atezolizumab
avelumab

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12
Q

What is the site of activity of CTLA-4 inhibitors?

A

lymph node

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13
Q

What is the site of activity of PD-1 inhibitors?

A

cancer cell

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14
Q

What are the indications for CTLA-4 inhibitors?

A

melanoma (ipi, ipi + nivo)
kidney cancer (ipi+nivo)
small cell lung cancer (ipi+nivo)

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15
Q

True or false: PD-1 and PD-L1 inhibitors are used for a small range of cancers

A

false
used for a super broad range of cancer

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16
Q

True or false: the current IOs are monoclonal antibodies

A

true

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17
Q

How is IO administered?

A

IV

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18
Q

What is generally done for IO toxicity?

A

doses are NOT reduced for toxicity, either hold or give full dose

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19
Q

What is the response rate to chemotherapy in metastatic melanoma?

A

only 1-2% of pts achieve a durable long-term response to chemotherapy, which is no longer considered as valid treatment

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20
Q

What was OS for metastatic melanoma prior to introduction of immunotherapy?

A

about 6 months

21
Q

True or false: the response rate to ipilimumab for metastatic melanoma is worse than it was for chemotherapy

A

false
much better survival rates with ipilimumab

22
Q

How was NSCLC once considered as a disease?

A

was once considered a single disease, until distinct subtypes, characteristics identified
-subtype characteristics are clinically relevant for treatment planning from diagnosis

23
Q

What was found with the CheckMate 003 trial?

A

people who responded to the checkpoint inhibitor (nivo) had a long-term durable response vs cytotoxic therapy

24
Q

What was found with the KeyNote-024 trial?

A

pembrolizumab is superior to CT in patients with TPS > 50%

25
Q

Why do different forms of cancer therapies lead to different toxicities?

A

different MOA leads to different toxicities

26
Q

Which chemotherapy-related and immune-related adverse effects tend to overlap?

A

NVD
fatigue
symptoms may overlap but mediated through different pathways

27
Q

What happens with irAEs without appropriate management?

A

irAEs tend to self-perpetuate without appropriate management

28
Q

What are the risk factors for irAEs?

A

personal/family hx of autoimmune diseases
tumor infiltration
concomitant medications and occupational exposures

29
Q

What are the key factors for prevention of irAEs?

A

HCP and patient education
-awareness of risks of IO agents
patient reporting
-immediate reporting of signs and sx
call-back program
-regular calls to pt to assess irAEs

30
Q

Describe proper irAE follow-up before and after treatment.

A

during IO treatment:
-lab tests before every IO administration
-compare values to baseline
after IO treatment termination:
-lab tests/evaluation on 3 month basis during 1st year and then every 6 months

31
Q

True or false: irAEs can develop even after discontinuation of IO treatment

32
Q

What are the potential etiologies of adverse effects?

A

disease-related
incidental event
immune-related adverse event

33
Q

Which body systems might be impacted during an irAE via IOs?

A

skin
hepatic
gastrointestinal
renal
eye
endocrine
cardiac
pulmonary
neurologic

34
Q

When do the irAEs tend to appear?

A

rash, pruritis: ~ 4 wks
liver: ~6 wks
diarrhea, colitis: ~5 wks
hypophysitis: ~6 wks

35
Q

Describe the management of irAE according to the severity of symptoms.

A

grade 1:
-supportive care; +/- withhold drug
grade 2:
-withhold drug, consider restart if toxicity resolves to grade < 1
-initiate low dose steroids (prednisone 0.5 mg/kg/day or ~) if sx do not resolve within 1 week
grade 3/4:
-d/c drug
-high dose steroids (prednisone 1-2 mg/kg/day or ~) taper once grade < 1
severe or steroid-refractory:
-no response to steroids within 48-72h
-additional immune suppressive agents

36
Q

What do most irAEs resolve with?

A

temporary or permanent d/c of IO treatment
temporary immunosuppression

37
Q

How long does it take for irAEs to resolve?

A

depends on nature of toxicity
-immunosuppression can rapidly improve GI, hepatic, and renal toxicities
-skin and endocrine toxicities require more time for resolution

38
Q

What is the impact of immunosuppression on IO efficacy?

A

no negative impact on treatment efficacy

39
Q

What is the optimal steroid dosing regimen for irAEs?

A

not yet established
-prolonged, high-dose steroid use has been associated with additional risks
-confirmed risk of opportunistic infection from steroid use in irAE management

40
Q

Describe proper management of steroid-related complications.

A

monitor for signs and sx of steroid-related AEs
antibiotic prophylaxis may be warranted
gradual steroid tapering is important
-taper over at least 1 month before resuming IO therapy
additional considerations:
-vitamin D and calcium (osteoporosis)
-PPI (gastritis)

41
Q

What are the toxicities of CAR-T?

A

B-cell aplasia
cytokine release syndrome
-frequently begins with fever, may develop unstable hypotension and hypoxia
-potentially fatal, may require ICU care
neurotoxicity
-tremor, dysgraphia, impaired attention, speech difficulty, seizures

42
Q

What is a common complication of both cancer and treatment?

A

thrombosis
-higher mortality among cancer pts
-2nd leading cause of death in cancer pts

43
Q

What are the risk factors for cancer-associated thrombosis?

A

patient related
cancer related
treatment-related

44
Q

Differentiate when to use LMWH or a DOAC in cancer-associated thrombosis.

A

LMWH preferred in pts:
-at high risk of bleeding
-with unresected GI or GU cancer
-significant DDI with DOACs
DOACs preferred in pts:
-at low risk of bleeding
-with other cancer types
-without significant DDIs

45
Q

How long is duration of therapy for cancer-associated thrombosis?

A

initial 6 months

46
Q

What is cancer related fatigue?

A

cancer-related fatigue is a distressing, persistent, subjective sense of physical, emotional, and/or cognitive tiredness or exhaustion related to cancer or cancer tx that is not proportional to recent activity and interferes with usual functioning

47
Q

What is the most commonly reported side effect of cancer treatment with chemotherapy, RT, or selected biologic response modifiers?

A

cancer related fatigue
14-96% of pts undergoing cancer tx and in 19-82% of pts post-tx

48
Q

What generally occurs to cancer fatigue once treatment is complete?

A

generally improves but some fatigue may persist for months or years following tx

49
Q

How is cancer related fatigue managed?

A

manage precipitating factor
-rarely an isolated symptom
energy conservation
exercise with moderate intensity
limit naps
reduce stress
food and water intake
use distractions