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PURPOSE: The Targeted Agent and Profiling Utilization Registry Study is a phase II basket trial evaluating the antitumor activity of commercially available targeted agents in patients with advanced cancer and genomic alterations known to be drug targets. Results from cohorts of patients with metastatic breast cancer (BC) with FGFR1 and FGFR2 alterations treated with sunitinib are reported. METHODS: Eligible patients had measurable disease, Eastern Cooperative Oncology Group performance status 0-2, adequate organ function, and no standard treatment options. Simon's two-stage design was used with a primary end point of disease control (DC), defined as objective response (OR) or stable disease of at least 16 weeks duration (SD16+) according to RECIST v1.1. Secondary end points included OR, progression-free survival, overall survival, duration of response, duration of stable disease, and safety. RESULTS: Forty patients with BC with FGFR1 (N = 30; amplification only n = 26, mutation only n = 1, both n = 3) or FGFR2 (N = 10; amplification only n = 2, mutation only n = 6, both n = 2) alterations were enrolled. Three patients in the FGFR1 cohort were not evaluable for efficacy; all patients in the FGFR2 cohort were evaluable. For the FGFR1 cohort, two patients with partial response and four with SD16+ were observed for DC and OR rates of 27% (90% CI, 13 to 100) and 7% (95% CI, 1 to 24), respectively. The null hypothesis of 15% DC rate was not rejected (P =.169). No patients achieved DC in the FGFR2 cohort (P = 1.00). Thirteen of the 40 total patients across both cohorts had at least one grade 3-4 adverse event or serious adverse event at least possibly related to sunitinib. CONCLUSION: Sunitinib did not meet prespecified criteria to declare a signal of antitumor activity in patients with BC with either FGFR1 or FGFR2 alterations. Other treatments and clinical trials should be considered for these patient populations. Sunitinib did not demonstrate antitumor activity in patients with FGFR1-/2-amplified or -mutated breast cancer. @ASCO #TAPUR [ABSTRACT FROM AUTHOR]

Purpose: Chemotherapy-induced alopecia (CIA) is a stigmatizing and psychologically devasting side effect of cancer treatment. Scalp cooling therapy (SCT) is the most effective method to reduce CIA, yet it is underutilized. We investigated factors that may impact scalp cooling discussion and use.Methods: We performed a retrospective review of cancer patients from 2000 to 2019 who had documentation of SCT discussion in the electronic medical record. The University of Michigan Rogel Cancer Center registry was used to identify the total number of cancer patients eligible for SCT during 2015-2019. Chi-square tests were used for outcome and patient characteristic comparisons (p < 0.05).Results: From 2000 to 2019, 194 patients had documentation of SCT discussion. Of those, 72 (43.6%) used SCT, 93 (47.9%) did not use SCT, and the remaining 29 (17.8%) had unknown SCT use. A total of 5615 cancer patients were eligible for SCT from 2015 to 2019. As compared to those who did not have documented SCT discussions, patients who had documentation of SCT discussions in that period (n = 161, 3.0%) were more likely to be female, have breast cancer, be less than 45 years old, and live in a zip code with average income > US $100,000 (all p < 0.0001). Between 2015 and 2019, 57 patients (1.02%) used SCT. On univariate analysis, patient-initiated conversation about SCT (p = 0.01) and age less than 65 (p = 0.03) were significantly associated with decision to use SCT.Conclusion: There were distinctions in the types of patients who have documented discussions about SCT. Improving patient knowledge about the availability of SCT and increasing access to this technology for all eligible cancer patients may enable more patients to achieve improved quality of life by reducing or preventing CIA. [ABSTRACT FROM AUTHOR]

Aims: Chemotherapy‐induced peripheral neuropathy (PN) is a treatment limiting toxicity of paclitaxel. We evaluated if EPHA genetic variation (EPHA4, EPHA5, EPHA6, and EPHA8) is associated with PN sensitivity by accounting for variability in systemic paclitaxel exposure (time above threshold). Methods: Germline DNA from 60 patients with breast cancer was sequenced. PN was measured using the 8‐item sensory subscale (CIPN8) of the patient‐reported CIPN20. Associations for 3 genetic models were tested by incorporating genetics into previously published PN prediction models integrating measured paclitaxel exposure and cumulative treatment. Significant associations were then tested for association with PN‐related treatment disruption. Results: EPHA5 rs7349683 (minor allele frequency = 0.32) was associated with increased PN sensitivity (β‐coefficient = 0.39, 95% confidence interval 0.11–0.67, p = 0.007). Setting a maximum tolerable threshold of CIPN8 = 30, optimal paclitaxel exposure target is shorter for rs7349683 homozygous (11.6 h) than heterozygous (12.6 h) or wild‐type (13.6 h) patients. Total number of missense variants (median = 0, range 0–2) was associated with decreased PN sensitivity (β‐coefficient: −0.42, 95% confidence interval −0.72 to −0.12, P =.006). No association with treatment disruption was detected for the total number of missense variants or rs7349683. Conclusion: Isolating toxicity sensitivity by accounting for exposure is a novel approach, and rs7349683 represents a promising marker for PN sensitivity that may be used to individualize paclitaxel treatment. [ABSTRACT FROM AUTHOR]