For a 60-year-old asymptomatic patient with KRAS wild-type disease and unresolved peripheral neuropathy, I would probably administer FOLFIRI and bevacizumab.

I would offer FOLFIRI and bevacizumab to the 60-year-old asymptomatic patient with KRAS-mutant mCRC. Recent data have shown a benefit from the use of bevacizumab beyond disease progression. I am familiar and comfortable with bevacizumab. I am not convinced by the available data with aflibercept that it’s necessarily better as second-line therapy.

For a 60-year-old patient with KRAS wild-type disease, I would consider treatment with FOLFIRI/bevacizumab or irinotecan/bevacizumab. I would explain to the patient that continuing 5-FU may not add much benefit to irinotecan.

I would consider administering FOLFIRI and bevacizumab to this 60-year-old patient with asymptomatic KRAS-mutant mCRC.

Independent of whether the patient has KRAS wild-type or mutant mCRC, I would stop treatment with oxaliplatin if the peripheral neuropathy has not resolved. I would treat with FOLFIRI/bevacizumab. I have treated other diseases with aflibercept on clinical trials, but I’ve not used it for colon cancer yet.

I would administer FOLFIRI/bevacizumab to the 60-year-old patient with asymptomatic, KRAS wild-type disease. I prefer to use EGFR antibodies in later lines of therapy.

At this juncture, I am not using aflibercept off study. Therefore, I would administer FOLFIRI/bevacizumab to the 60-year-old patient with asymptomatic, KRAS-mutant mCRC.

I would administer FOLFIRI/bevacizumab to the 60-year-old patient with asymptomatic, KRAS wild-type or KRAS-mutant mCRC.

When you view the cross-trial comparison of the data with aflibercept in patients who previously received bevacizumab, the toxicity profile is clearly in favor of bevacizumab beyond disease progression versus aflibercept. More diarrhea, febrile neutropenia and asthenia occur with aflibercept. Overall, we have much more experience with bevacizumab beyond disease progression than with aflibercept, and it’s difficult to find a niche for aflibercept in this scenario right now.

For the patient with KRAS wild-type disease you could use an EGFR antibody, but antibodies maintain their efficacy even in later lines of therapy. We want to preserve the active lines of therapy that work for a patient. In these palliative scenarios, I normally opt for bevacizumab beyond disease progression followed by an EGFR antibody.

If the patient had KRAS wild-type mCRC, I would administer irinotecan with an EGFR antibody, usually cetuximab.

For the 60-year-old patient with KRAS-mutant mCRC, I would switch to irinotecan at this point. Recent data support switching to irinotecan/bevacizumab in this clinical scenario, so I may consider adding bevacizumab to irinotecan. However, for a patient who’s received a fluoropyrimidine for more than 1 year, I probably would discontinue the bevacizumab. I might consider treatment with aflibercept, but I have not used it much.

In general, I would continue bevacizumab beyond disease progression rather than switching to aflibercept. If the patient is not experiencing significant peripheral neuropathy, I would probably add oxaliplatin back into the regimen. I believe the questions to ask are, how much neuropathy is the patient experiencing and how many more doses of oxaliplatin can be administered at this point?

For a 60-year-old patient with asymptomatic, KRAS wild-type mCRC, I opt for FOLFIRI and an EGFR antibody-based therapy over a bevacizumab-based regimen approximately 70% of the time. I have a modest data-driven preference for panitumumab in the second-line setting. In certain areas of the country, like the one I live in, we see a high infusion reaction rate. For this reason, I would choose to administer panitumumab.

My first and preferred treatment choice for this 60-year-old patient with asymptomatic, KRAS-mutant mCRC would be FOLFIRI/bevacizumab. My second choice would be FOLFIRI/aflibercept. I would elect to use bevacizumab first as the biologic versus aflibercept based on data from the TML and VELOUR studies, in which the efficacy of the 2 agents appears to be similar but less toxicity is apparent with bevacizumab. I say “apparent” because a difference could exist in the toxicity profiles of the chemotherapy regimens used in those trials. My feeling is that if bevacizumab and aflibercept were compared head to head, they would not be as different as they appear.

For a 60-year-old patient with asymptomatic, KRAS wild-type mCRC, I would recommend treatment with FOLFIRI in combination with the EGFR-targeting antibody cetuximab. This patient has not been previously exposed to an EGFR antibody, and the Phase III EPIC trial showed that cetuximab is effective in the second-line metastatic setting. I believe that the argument to switch over to an EGFR monoclonal antibody rather than continuing bevacizumab beyond progression in KRAS wild-type disease makes a lot of sense.

I would administer FOLFIRI/bevacizumab to a 60-year-old patient with asymptomatic, KRAS-mutant mCRC. Although the efficacy results are similar with bevacizumab and aflibercept, the toxicity profile with aflibercept is clearly worse and I would not consider using it in this particular scenario. Also, aflibercept is not a drug that I am familiar with. I was not involved in any of the clinical trials, and I have never used aflibercept. However, if the patient had KRAS-mutant disease and experienced rapid disease progression on first-line FOLFOX/bevacizumab, I would consider aflibercept in that scenario.