Abstract 3568
Background
In CORRECT, REG significantly improved overall survival and PFS vs placebo in pts with treatment-refractory mCRC. We did a retrospective, exploratory subgroup analysis of REG-treated pts in CORRECT with PFS >4 m (long PFS) and ≤4 m (short PFS).
Methods
Pts with pretreated mCRC were randomized 2:1 to REG 160 mg or placebo QD for 3 weeks on/1 week off until disease progression, death, or unacceptable toxicity. PFS was the time from randomization to progression or death. Of 505 pts randomized to REG, 98 (19%) had long PFS and 407 (81%) had short PFS.
Results
Compared to short PFS pts, the long PFS group had a higher proportion of patients with ECOG PS0, 1–2 tumor sites, and ≥18 m since diagnosis of metastatic disease (Table). Long PFS pts received a median of 6 (1–12) cycles, short PFS pts a median of 2 (1–11). Mean actual daily doses were 138.7 mg (long PFS) and 149.2 mg (short PFS). Dose modifications occurred in 91% (long PFS) and 72% (short PFS). NCI-CTCAE (v3) grade (Gr) ≥3 REG-related treatment-emergent adverse events (TEAE) occurred in 64% (long PFS) and 53% (short PFS). Most common REG-related Gr ≥3 TEAEs included (long PFS, short PFS) hand–foot skin reaction (20%, 16%), hypertension (17%, 5%), fatigue (13%, 9%), diarrhea (16%, 5%), rash/desquamation (3%, 6%), and hypophosphatemia (5%, 3%). Gr ≥3 laboratory toxicities (long PFS, short PFS) included increased bilirubin (8%, 13%), ALT (6%, 5%), and AST (5%, 6%). Although REG-related TEAEs led to a higher dose modification rate in long PFS pts (71% vs 52% for short PFS), discontinuations due to REG-related TEAEs were similar (long PFS 5%; short PFS 9%).
| Long PFS (n = 98) | Short PFS (n = 407) | |
|---|---|---|
| Median age, yrs (range) | 61 (34–82) | 61 (22–82) |
| Male, % | 64 | 61 |
| Median body mass index, kg/m2 | 25.6 | 24.7 |
| ECOG PS, % 0 1 | 63 37 | 50 50 |
| No. of tumor sites, % 1 2 3 ≥4 | 30 38 16 16 | 17 35 30 18 |
| KRAS status, % mutant wildtype | 47 44 | 56 40 |
| Primary site of disease, % Colon Rectum Both | 52 37 10 | 67 28 5 |
| No. of prior regimens on or after diagnosis of metastatic disease, % 0–2 3 ≥4 | 22 22 55 | 28 25 47 |
Time since first diagnosis of metastatic disease to randomization, % ConclusionsThis exploratory analysis showed that pts with mCRC treated with REG who had PFS >4 m tended to have a better performance status, fewer metastatic tumor sites, and a longer time since diagnosis of metastatic disease, compared to pts with short PFS. Clinical trial identificationNCT01103323 Legal entity responsible for the studyBayer FundingBayer DisclosureA. Grothey: Advisory board: Bayer. Corporate-sponsored research: Bayer. A. Falcone: Advisory board: Amgen, Roche, Bayer, Lilly, Sanofi, Servier, Merck. Corporate-sponsored research: Roche, Amgen, Bayer, Merck, Sanofi. O. Bouche: Advisory board: Merck Serono, Roche. L. Mineur: Advisory board participation. A. Adenis: Corporate-sponsored research: Bayer, Sanofi Other substantive relationship: Bayer, Sanofi, Pfizer, Roche. J. Tabernero: Advisory board: Amgen, Bayer, Boehringer Ingelheim, Celgene, Chugai, Lilly, MSD, Merck Serono, Novartis, Roche, Sanofi, Symphogen, Takeda, Taiho. T. Yoshino: Corporate-sponsored research: GlaxoSmithKline K.K. Boehringer Ingelheim GmbH H-J. Lenz: Advisory board: Bayer. Lectures: Bayer. Clinical trial support: Bayer. R.M. Goldberg: Corporate-sponsored research: Bayer. L. Huang: Stock ownership: Bayer Other substantive relationships: Bayer (employee). A. Wagner: Other substantive relationships: Bayer (employee). E. Van Cutsem: Corporate-sponsored research: Bayer. All other authors have declared no conflicts of interest. Resources from the same session2354 - The clinicopathologic features and treatment of 607 hindgut neuroendocrine tumor (NET) patients at a single institutionPresenter: Seung Tae Kim Session: Poster Display Resources: Abstract 2594 - Neuroendocrine carcinomas of the colorectal origin - Polish experiencePresenter: Agnieszka Kolasińska-Ćwikła Session: Poster Display Resources: Abstract 2539 - Neuroendocrine neoplasms of the appendix including goblet cell carcinoidsPresenter: Agnieszka Kolasinska-Cwikla Session: Poster Display Resources: Abstract 1245 - Prognostic validity of AJCC staging system in neuroendocrine tumors of the appendixPresenter: Amir Mehrvarz Sarshekeh Session: Poster Display Resources: Abstract 3902 - Enhancer of zest homolog 2 (EZH2) expression in well and moderately differentiated pancreatic neuroendocrine tumor (pNET)Presenter: Riccardo Marconcini Session: Poster Display Resources: Abstract 3882 - Differential clinical and pathological characteristics of hereditary neuroendocrine pancreatic tumours (NEPT)Presenter: Gema Marín Zafra Session: Poster Display Resources: Abstract 2296 - Natural course of thyroid cancer nodules compared with benign thyroid nodulesPresenter: Kyung-Jin Yun Session: Poster Display Resources: Abstract 4083 - Reassessment of proliferative activity at disease progression in neuroendocrine neoplasmsPresenter: Noemi Cicchese Session: Poster Display Resources: Abstract 3866 - 18F-FDG-PET to predict disease progression in advanced digestive neuroendocrine neoplasmsPresenter: Maria Rinzivillo Session: Poster Display Resources: Abstract 3651 - UK phase IV, observational study to assess quality of life in patients (pts) with pancreatic neuroendocrine tumours (pNETS) receiving treatment with everolimus: The “real-world” OBLIQUE studyPresenter: John Ramage Session: Poster Display Resources: Abstract This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used. For more detailed information on the cookies we use, please check our Privacy Policy.
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