Chapter 34 — Anti-Cancer Drugs Part II — Module 2 — Targeted Small Molecule Inhibitors: Foundational Recall
1. A patient with BRAF V600E melanoma is receiving combination dabrafenib (a BRAF inhibitor) plus trametinib (a MEK inhibitor). During therapy the clinician must arrange baseline and periodic ophthalmologic examination specifically because of a toxicity that belongs to the MEK inhibitor component rather than the BRAF inhibitor. Which ocular toxicity is the class effect of MEK inhibitors that drives this monitoring requirement?
A) Acute angle-closure glaucoma from pupillary block
B) Serous retinal detachment (chorioretinopathy) with associated retinal vein occlusion and blurred vision
C) Bacterial keratitis from corneal surface breakdown
Serous retinal detachment, also termed MEK-inhibitor-associated chorioretinopathy, is the class ocular toxicity of MEK inhibitors and, together with retinal vein occlusion and blurred vision, is the reason baseline and periodic ophthalmologic evaluation is required during combination therapy. It is distinct from the dermatologic and pyrexia effects that dominate the BRAF inhibitor side of the combination. This is the correct toxicity.
Option A: Option A is incorrect because angle-closure glaucoma is not a recognized MEK inhibitor class effect and is not the basis for retinal monitoring.
Option C: Option C is incorrect because MEK inhibitors do not characteristically cause infectious keratitis.
Option D: Option D is incorrect because cataract is not the signature MEK inhibitor ocular toxicity and would not be detected by the retinal surveillance these drugs require.
Option E: Option E is incorrect because optic neuritis is not the class effect; the monitored lesion is at the level of the retina, not the optic nerve.
2. Three CDK4/6 inhibitors (cell-cycle kinase inhibitors used in hormone-receptor-positive breast cancer) — palbociclib, ribociclib, and abemaciclib — share neutropenia as their dominant on-target toxicity, but one of the three is set apart by a markedly higher rate of diarrhea and by a continuous twice-daily dosing schedule rather than a three-weeks-on, one-week-off cycle. Which agent shows this distinguishing profile?
A) Palbociclib, because it is dosed continuously and causes the most diarrhea
B) Ribociclib, because it is dosed continuously and causes the most diarrhea
C) All three are identical in dosing schedule and diarrhea rate
D) Abemaciclib, because it is dosed continuously twice daily and causes substantially more diarrhea than the other two
E) None of the three causes clinically significant diarrhea
ANSWER: D
Rationale:
Abemaciclib is distinguished from palbociclib and ribociclib by continuous twice-daily dosing (rather than the three-weeks-on, one-week-off schedule used by the other two) and by a much higher rate of diarrhea, driven by CDK4/6 inhibition in intestinal crypt cells; early loperamide and dose reduction for persistent diarrhea are standard. Abemaciclib is also active as monotherapy. Option D correctly identifies the agent and both distinguishing features.
Option A: Option A is incorrect because palbociclib uses the intermittent schedule and is not the high-diarrhea agent.
Option B: Option B is incorrect because ribociclib likewise uses the intermittent schedule; its distinguishing concerns are QTc prolongation and hepatotoxicity, not diarrhea.
Option C: Option C is incorrect because the three agents differ meaningfully in both schedule and gastrointestinal profile.
Option E: Option E is incorrect because diarrhea is clinically significant and, with abemaciclib in particular, is a defining toxicity.
3. A postmenopausal woman with hormone-receptor-positive, HER2-negative breast cancer is started on ribociclib (a CDK4/6 inhibitor) with an aromatase inhibitor. Ribociclib is the CDK4/6 inhibitor that prolongs the QTc interval (the heart-rate-corrected electrical recovery time on the ECG) and therefore requires a defined electrocardiographic monitoring protocol. Which management step correctly reflects this requirement?
A) Obtain a baseline ECG, repeat it early in treatment, and withhold ribociclib if the QTc exceeds the protocol threshold
B) No ECG is needed because QTc prolongation is not a concern with any CDK4/6 inhibitor
C) Obtain a single baseline ECG only, with no further monitoring regardless of symptoms
D) Add a second QTc-prolonging antiarrhythmic to stabilize the rhythm during therapy
E) Monitor liver enzymes instead of the ECG, since QTc is unaffected
ANSWER: A
Rationale:
Ribociclib is the CDK4/6 inhibitor with the most stringent cardiac monitoring requirement: a baseline ECG, a repeat ECG early in cycle one and at the start of cycle two, and withholding of the drug when the QTc exceeds the protocol threshold. Concurrent QTc-prolonging drugs should be avoided. The correct choice states this accurately.
Option B: Option B is incorrect because ribociclib specifically does prolong the QTc, which is the entire basis for the protocol.
Option C: Option C is incorrect because a single baseline ECG is insufficient — repeat monitoring is mandated.
Option D: Option D is incorrect and dangerous because adding another QTc-prolonging agent compounds the risk rather than stabilizing the rhythm.
Option E: Option E is incorrect because, although ribociclib can also raise liver enzymes, that does not replace the required ECG monitoring for QTc prolongation.
4. Two PI3K inhibitors target different isoforms of the enzyme: idelalisib inhibits PI3K-delta (the isoform B lymphocytes depend on) and alpelisib inhibits PI3K-alpha (the isoform insulin uses for glucose uptake). A clinician must match each drug to its characteristic dose-limiting toxicity. Which pairing is correct?
A) Idelalisib causes hyperglycemia; alpelisib causes immune-mediated colitis
B) Both drugs cause hyperglycemia as their dominant toxicity
C) Idelalisib causes hepatotoxicity and immune-mediated colitis with opportunistic infection; alpelisib causes hyperglycemia
D) Both drugs cause immune-mediated colitis as their dominant toxicity
E) Neither drug has a characteristic isoform-specific toxicity
ANSWER: C
Rationale:
The toxicity of each PI3K inhibitor follows from the isoform it blocks. Idelalisib (PI3K-delta) produces immune-mediated injury — hepatotoxicity, colitis, and an excess of opportunistic infections requiring Pneumocystis prophylaxis — because PI3K-delta is central to normal immune-cell signaling. Alpelisib (PI3K-alpha) produces hyperglycemia because PI3K-alpha mediates insulin-driven glucose uptake. Option C matches each drug to its correct toxicity.
Option A: Option A is incorrect because it reverses the two, attributing hyperglycemia to idelalisib and colitis to alpelisib.
Option B: Option B is incorrect because only the alpha-isoform inhibitor causes prominent hyperglycemia.
Option D: Option D is incorrect because only the delta-isoform inhibitor causes the immune-mediated colitis.
Option E: Option E is incorrect because each drug has a clear, isoform-specific signature toxicity, which is the basis of the distinction.
5. A patient on everolimus (an mTOR inhibitor) develops a dry cough and exertional breathlessness, and imaging shows bilateral ground-glass opacities without an identified pathogen. This presentation is consistent with the non-infectious pneumonitis characteristic of mTOR inhibitors. What is the appropriate management?
A) Start broad-spectrum antibiotics and continue everolimus unchanged
B) Start an antifungal agent and increase the everolimus dose
C) Ignore the findings, as everolimus does not affect the lungs
D) Begin inhaled bronchodilators alone and continue everolimus at full dose
E) Hold everolimus and give corticosteroids if the patient is symptomatic
ANSWER: E
Rationale:
mTOR inhibitor pneumonitis is a non-infectious inflammatory process, so the correct response is to interrupt the drug and treat symptomatic patients with corticosteroids, not to escalate antimicrobials. The same corticosteroid-based, anti-inflammatory logic applies to mTOR-inhibitor stomatitis, which is treated with a corticosteroid mouthwash rather than an antifungal. This is the management given in the correct choice.
Option A: Option A is incorrect because antibiotics do not treat a non-infectious inflammatory pneumonitis, and continuing the drug unchanged ignores its causative role.
Option B: Option B is incorrect because there is no fungal infection to treat and raising the dose would worsen the toxicity.
Option C: Option C is incorrect because mTOR inhibitors clearly do cause pulmonary toxicity that requires intervention.
Option D: Option D is incorrect because bronchodilators do not address an inflammatory infiltrative process, and the drug should be held rather than continued at full dose.
6. A patient taking acalabrutinib (a second-generation BTK inhibitor) for chronic lymphocytic leukemia also takes a daily proton pump inhibitor (a strong gastric acid suppressant) for reflux. Acalabrutinib has pH-dependent solubility, so this combination raises a specific pharmacologic concern. What is the concern and the preferred adjustment?
A) The proton pump inhibitor increases acalabrutinib absorption, risking toxicity; reduce the acalabrutinib dose
B) The proton pump inhibitor reduces acalabrutinib absorption and can lower its efficacy; an H2-receptor antagonist taken separated in time is preferred
C) The proton pump inhibitor has no effect on acalabrutinib because absorption is pH-independent
D) The proton pump inhibitor accelerates acalabrutinib metabolism through CYP induction; double the dose
E) The two drugs form an inactive chelate; separate them by giving the proton pump inhibitor intravenously
ANSWER: B
Rationale:
Acalabrutinib requires an acidic gastric environment for dissolution, so a proton pump inhibitor that durably raises gastric pH reduces acalabrutinib absorption and can compromise efficacy. The preferred approach is to avoid the proton pump inhibitor and instead use an H2-receptor antagonist dosed with appropriate time separation, or an antacid separated from acalabrutinib. The correct choice states both the concern and the adjustment.
Option A: Option A is incorrect because acid suppression decreases, not increases, absorption.
Option C: Option C is incorrect because acalabrutinib absorption is specifically pH-dependent.
Option D: Option D is incorrect because the interaction is one of pH-dependent solubility, not CYP induction, and doubling the dose is not the recommended fix.
Option E: Option E is incorrect because the problem is reduced dissolution at high gastric pH, not chelate formation, and changing the proton pump inhibitor route does not resolve it.
7. A patient on ibrutinib (a first-generation BTK inhibitor) for chronic lymphocytic leukemia develops new atrial fibrillation and now requires anticoagulation. Ibrutinib inhibits CYP3A4 and P-glycoprotein (a drug efflux transporter) and independently causes platelet dysfunction. Applying these interactions, which anticoagulation approach is most appropriate?
A) Use warfarin, because ibrutinib has no effect on its metabolism
B) Add aspirin to the regimen to enhance clot prevention
C) Avoid anticoagulation entirely, since atrial fibrillation on ibrutinib never warrants it
D) Avoid warfarin (ibrutinib elevates INR via CYP3A4 inhibition) and prefer a direct oral anticoagulant with awareness that ibrutinib's P-glycoprotein inhibition raises its levels; consider switching to a more selective BTK inhibitor
E) Use a high warfarin dose to overcome the interaction
ANSWER: D
Rationale:
Managing anticoagulation on ibrutinib requires applying its interaction profile. Ibrutinib inhibits CYP3A4, elevating warfarin levels and the INR, so warfarin is avoided; a direct oral anticoagulant is generally preferred, but because ibrutinib also inhibits P-glycoprotein and raises direct oral anticoagulant exposure, dose awareness is needed, and switching to a more selective second-generation BTK inhibitor reduces both the arrhythmia risk and platelet dysfunction going forward. The correct choice captures this reasoning.
Option A: Option A is incorrect because ibrutinib's CYP3A4 inhibition does affect warfarin, elevating the INR.
Option B: Option B is incorrect because adding aspirin to a BTK inhibitor compounds bleeding risk through additive platelet impairment.
Option C: Option C is incorrect because atrial fibrillation with appropriate stroke risk does warrant anticoagulation; the task is choosing it safely, not withholding it.
Option E: Option E is incorrect because escalating the warfarin dose does not resolve the interaction and increases bleeding danger.
8. A patient receiving venetoclax (a BCL-2 inhibitor) for acute myeloid leukemia is also given posaconazole, an azole antifungal that is a strong CYP3A4 inhibitor (CYP3A4 being the enzyme that clears venetoclax). Applying this interaction, what is the correct management of the venetoclax dose?
A) Substantially reduce the venetoclax dose, because the strong CYP3A4 inhibitor markedly increases venetoclax exposure
B) Increase the venetoclax dose, because the antifungal accelerates its clearance
C) Make no change, because azole antifungals do not interact with venetoclax
D) Stop venetoclax permanently, because the combination is absolutely contraindicated under all circumstances
E) Replace venetoclax with a higher-dose proteasome inhibitor
ANSWER: A
Rationale:
Because venetoclax is cleared by CYP3A4, a strong inhibitor such as posaconazole sharply raises venetoclax exposure, increasing the risk of toxicity and tumor lysis; the established management is a substantial venetoclax dose reduction when the strong inhibitor is co-administered, with particular caution during the ramp-up phase. This is the management given in the correct choice.
Option B: Option B is incorrect because an inhibitor slows clearance and raises levels rather than accelerating clearance.
Option C: Option C is incorrect because azole antifungals interact strongly with venetoclax through CYP3A4.
Option D: Option D is incorrect because the combination is managed by dose reduction rather than being absolutely prohibited; azole antifungals are frequently needed in these patients and are used with adjusted venetoclax dosing.
Option E: Option E is incorrect because there is no rationale for replacing venetoclax with a proteasome inhibitor, which treats a different disease context and does not address the interaction.
9. Among the PARP inhibitors (DNA-repair enzyme inhibitors) olaparib, rucaparib, and niraparib, one agent is distinguished both by a notably high rate of thrombocytopenia requiring weekly blood-count monitoring early in therapy and by being metabolized predominantly by carboxylesterases rather than by CYP3A4, giving it fewer CYP-based drug interactions. Which agent is this?
A) Olaparib, because it is metabolized by carboxylesterases and causes the most thrombocytopenia
B) Rucaparib, because it is metabolized by carboxylesterases and causes the most thrombocytopenia
C) All three are metabolized identically and carry equal thrombocytopenia risk
D) None of the three causes clinically important thrombocytopenia
E) Niraparib, because it is metabolized chiefly by carboxylesterases and is distinguished by a high rate of thrombocytopenia
ANSWER: E
Rationale:
Niraparib stands apart from olaparib and rucaparib on two counts: it is metabolized predominantly by carboxylesterases rather than CYP3A4, so it has fewer CYP-mediated interactions, and it carries a distinctly high rate of thrombocytopenia, prompting weekly blood-count monitoring during the first month and dose reduction for significant drops. The correct choice identifies the agent and both features.
Option A: Option A is incorrect because olaparib is metabolized primarily by CYP3A4 and is not the high-thrombocytopenia agent.
Option B: Option B is incorrect because rucaparib is also subject to CYP-based interactions and is not distinguished by the thrombocytopenia profile that defines niraparib.
Option C: Option C is incorrect because the three agents differ meaningfully in metabolism and hematologic toxicity.
Option D: Option D is incorrect because thrombocytopenia is clinically important, particularly with niraparib.
10. Two FLT3 inhibitors (FLT3 is a receptor tyrosine kinase mutated in about a third of acute myeloid leukemias) are used in different clinical settings: one is a multi-kinase inhibitor given with standard induction chemotherapy for newly diagnosed FLT3-mutant disease, and the other is a more selective oral agent used for relapsed or refractory FLT3-mutant disease. Which pairing of agent to setting is correct?
A) Gilteritinib is the multi-kinase agent for newly diagnosed disease; midostaurin is the selective agent for relapsed disease
B) Both agents are interchangeable and approved only for relapsed disease
C) Midostaurin is the multi-kinase agent given with induction chemotherapy for newly diagnosed disease; gilteritinib is the more selective agent for relapsed or refractory disease
D) Both agents are given only as monotherapy for newly diagnosed disease
E) Neither agent has a defined role in FLT3-mutant acute myeloid leukemia
ANSWER: C
Rationale:
Midostaurin is a multi-kinase inhibitor approved for newly diagnosed FLT3-mutant acute myeloid leukemia in combination with standard induction chemotherapy, whereas gilteritinib is a more selective FLT3 inhibitor used as therapy for relapsed or refractory FLT3-mutant disease. Option C matches each agent to its correct setting.
Option A: Option A is incorrect because it reverses the two agents and their roles.
Option B: Option B is incorrect because the agents are not interchangeable and midostaurin has a defined frontline role.
Option D: Option D is incorrect because midostaurin is given with chemotherapy rather than as monotherapy, and gilteritinib's role is in the relapsed or refractory setting.
Option E: Option E is incorrect because both agents have well-defined roles in FLT3-mutant disease.
11. A clinician is selecting the route of administration for bortezomib (a proteasome inhibitor) in a patient with multiple myeloma who has early sensory symptoms and is at risk for peripheral neuropathy. Knowing that the two available routes produce equivalent systemic drug exposure, which choice best limits the risk of higher-grade neuropathy?
A) Intravenous administration, because it produces lower systemic exposure and spares the nerves
B) Subcutaneous administration, because it lowers the rate of higher-grade peripheral neuropathy while delivering equivalent systemic exposure
C) Intravenous administration at double the dose to shorten the course
D) Either route, because the route has no effect on neuropathy risk
E) Oral administration of bortezomib, because the oral route eliminates neuropathy
ANSWER: B
Rationale:
At equivalent systemic exposure, subcutaneous bortezomib produces a markedly lower rate of peripheral neuropathy than the intravenous route — roughly halving higher-grade neuropathy — which is why the subcutaneous route is preferred in all eligible patients, and especially in a patient already showing early sensory symptoms. The correct choice states this and its rationale.
Option A: Option A is incorrect because the two routes give equivalent exposure; the intravenous route does not lower exposure and in fact carries the higher neuropathy rate.
Option C: Option C is incorrect because doubling the intravenous dose increases cumulative neurotoxicity.
Option D: Option D is incorrect because the route does substantially affect neuropathy risk — that is the basis for preferring the subcutaneous route.
Option E: Option E is incorrect because bortezomib has no oral formulation; the oral proteasome inhibitor is ixazomib, a different agent.
12. Carfilzomib (a second-generation proteasome inhibitor) is being considered for a patient with relapsed multiple myeloma. Because of carfilzomib's distinguishing toxicity, which baseline factor and supportive measure most directly govern whether and how it is given?
A) Baseline hearing assessment, with audiometry before each dose
B) Baseline thyroid function, with levothyroxine before each infusion
C) Baseline bone density, with a bisphosphonate before each cycle
D) Baseline cardiac status — advanced heart failure (New York Heart Association class III or IV) excludes the patient — with careful intravenous hydration around infusions
E) Baseline visual acuity, with an eye examination before each dose
ANSWER: D
Rationale:
Carfilzomib is distinguished from other proteasome inhibitors by cardiovascular toxicity, including cardiomyopathy, heart failure, and hypertension, so its use is governed by baseline cardiac assessment: patients with advanced (New York Heart Association class III or IV) heart failure are excluded, and careful intravenous hydration before and after infusions is a standard supportive measure. The correct choice gives both the governing baseline factor and the supportive measure.
Option A: Option A is incorrect because hearing loss is not the carfilzomib-defining toxicity.
Option B: Option B is incorrect because thyroid dysfunction is not its characteristic concern.
Option C: Option C is incorrect because, although bone disease is relevant in myeloma generally, it is not what governs carfilzomib administration.
Option E: Option E is incorrect because visual toxicity is not the distinguishing carfilzomib effect; the cardiovascular profile is.
13. A patient with newly diagnosed multiple myeloma is starting lenalidomide (an immunomodulatory drug) combined with high-dose dexamethasone and has a prior history of deep vein thrombosis. Immunomodulatory drugs require risk-stratified thromboprophylaxis. Applying the risk tiers, which prophylaxis is appropriate for this patient?
A) A therapeutic anticoagulant (low-molecular-weight heparin or a direct oral anticoagulant), because multiple high-risk features are present
B) Aspirin alone, because aspirin is adequate for every patient on an immunomodulatory drug
C) No prophylaxis, because the risk applies only to thalidomide
D) An antiplatelet agent only, with no anticoagulant regardless of risk
E) Prophylaxis is unnecessary because dexamethasone lowers clot risk
ANSWER: A
Rationale:
Immunomodulatory-drug thromboprophylaxis is chosen by risk tier: aspirin is appropriate for lower-risk patients, while patients with multiple risk factors — here high-dose dexamethasone in combination plus a prior venous thromboembolism — require a therapeutic anticoagulant such as low-molecular-weight heparin or a direct oral anticoagulant. The correct choice applies the high-risk tier.
Option B: Option B is incorrect because aspirin is not adequate for this high-risk profile.
Option C: Option C is incorrect because venous thromboembolism risk is a class-wide effect of immunomodulatory drugs, not limited to thalidomide.
Option D: Option D is incorrect because an antiplatelet agent alone is insufficient for a high-risk patient who needs anticoagulation.
Option E: Option E is incorrect because dexamethasone increases, rather than lowers, the thrombotic risk of these regimens.
14. A patient with multiple myeloma and reduced kidney function (creatinine clearance is the estimate of renal filtration used to guide dosing) is to receive an immunomodulatory drug. Lenalidomide and thalidomide differ importantly in how the kidney affects their dosing. Which statement correctly applies this difference?
A) Thalidomide must be dose-reduced for low creatinine clearance, while lenalidomide needs no renal adjustment
B) Both drugs are cleared entirely by the liver, so renal function never affects dosing of either
C) Both drugs require an increased dose when creatinine clearance is reduced
D) Neither drug is affected by renal function under any circumstances
E) Lenalidomide is predominantly renally eliminated and requires dose reduction as creatinine clearance falls, whereas thalidomide is largely non-renally cleared and is less dependent on renal function
ANSWER: E
Rationale:
Lenalidomide is eliminated predominantly unchanged by the kidney, so its dose must be reduced as creatinine clearance falls, with avoidance in severe impairment absent dialysis. Thalidomide, by contrast, is largely non-renally cleared and is therefore less dependent on renal function for dosing. The correct choice states this difference accurately.
Option A: Option A is incorrect because it reverses the two drugs.
Option B: Option B is incorrect because lenalidomide is renally, not hepatically, eliminated, so renal function clearly matters.
Option C: Option C is incorrect because reduced clearance calls for a lower lenalidomide dose, not a higher one.
Option D: Option D is incorrect because renal function meaningfully affects lenalidomide dosing.
15. A patient on enasidenib (an IDH2 inhibitor) for acute myeloid leukemia develops fever, dyspnea, and bilateral pulmonary infiltrates at week six, consistent with differentiation syndrome. Applying the grade-based management of this complication, which approach is correct?
A) Permanently discontinue enasidenib immediately and withhold corticosteroids until cultures return
B) Continue enasidenib unchanged and give no corticosteroids, since the syndrome resolves on its own
C) Start systemic corticosteroids promptly; continue enasidenib through mild-to-moderate differentiation syndrome and hold it only for severe manifestations
D) Treat with antibiotics alone and avoid corticosteroids entirely
E) Increase the enasidenib dose to accelerate resolution
ANSWER: C
Rationale:
Differentiation syndrome is managed by prompt initiation of systemic corticosteroids (such as dexamethasone) without waiting for confirmation, because delayed treatment raises mortality; the IDH inhibitor is continued through mild-to-moderate syndrome with steroid coverage and held only for severe manifestations such as respiratory failure or severe renal failure. The correct choice states this grade-based approach.
Option A: Option A is incorrect because corticosteroids should be started promptly rather than withheld, and the drug is not automatically discontinued for milder disease.
Option B: Option B is incorrect because differentiation syndrome can be life-threatening and requires corticosteroids rather than observation.
Option D: Option D is incorrect because antibiotics alone do not treat differentiation syndrome and corticosteroids are essential, even though infection must also be considered.
Option E: Option E is incorrect because raising the dose does not resolve the syndrome and would be expected to worsen it.
16. A patient with BRAF V600E-mutant colorectal cancer is being evaluated for targeted therapy. Applying what is known about BRAF-directed treatment in colorectal cancer, which approach is correct?
A) Confirm RAS wild-type status, then treat with encorafenib (a BRAF inhibitor) combined with cetuximab (an anti-EGFR antibody), rather than using BRAF inhibitor monotherapy
B) Treat with single-agent BRAF inhibitor monotherapy, which is the standard for colorectal cancer
C) Use a BRAF inhibitor only if the tumor is also RAS-mutant
D) Avoid all targeted therapy, since BRAF V600E has no treatment implications in colorectal cancer
E) Give a MEK inhibitor alone, with no BRAF inhibitor and no anti-EGFR antibody
ANSWER: A
Rationale:
In BRAF V600E colorectal cancer, BRAF inhibitor monotherapy is not used because of limited efficacy and paradoxical pathway concerns; the established approach is combination therapy with encorafenib plus the anti-EGFR antibody cetuximab, and RAS wild-type status should be confirmed because a concurrent RAS mutation predicts lack of benefit and paradoxical activation. This is what the correct choice states.
Option B: Option B is incorrect because single-agent BRAF inhibition is specifically not the colorectal standard.
Option C: Option C is incorrect because a RAS mutation argues against BRAF inhibitor use rather than being a prerequisite for it.
Option D: Option D is incorrect because BRAF V600E is an actionable target in colorectal cancer with a defined combination regimen.
Option E: Option E is incorrect because MEK inhibitor monotherapy is not the regimen; the standard pairs a BRAF inhibitor with an anti-EGFR antibody.
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