Erdafitinib treatment in metastatic urothelial carcinoma: a real-world analysis.

Background: Erdafitinib, a fibroblast growth factor receptor (FGFR) inhibitor is a standard post chemotherapy advanced treatment line for metastatic urothelial carcinoma harboring FGFR2/3 genomic alterations. It was approved based on a phase 2 clinical trial, revealing a 40% response rate, and 13.8 months overall survival. These FGFR genomic alterations are uncommon. Thus, real-world data on erdafitinb use is scant. We herein describe erdafitinib treatment outcome in a real world patient cohort. Methods: We retrospectively reviewed the data of patients treated with erdafitinib from 9 Israeli medical centers. Results: Twenty-five patients with metastatic urothelial carcinoma (median age 73, 64% male, 80% with visceral metastases) were treated with erdafitinib between January 2020 to October 2022. A clinical benefit (complete response 12%, partial response 32%, stable disease 12%) was seen in 56%. Median progression-free survival was 2.7 months, and median overall survival 6.73 months. Treatment related toxicity ≥ grade 3 occurred in 52%, and 32% discontinued therapy due to adverse events. Conclusions: Erdafitinib therapy is associated with a clinical benefit in the real world setting, and associated with similar toxicity as reported in prospective clinical trials.

Activity of cabazitaxel after docetaxel and abiraterone acetate therapy in patients with castration-resistant prostate cancer.

BACKGROUND: Cabazitaxel and AA have been approved by the US Food and Drug Administration for use after docetaxel in mCRPC. Recently, CAB appeared to be active when given after AA. AA is capable of inducing AR splice variants that confer ligand-independent AR transactivation. Because microtubule-targeting agents impair AR nuclear transport and activity, we raised concerns about CAB efficacy after AA failure in mCRPC. PATIENTS AND METHODS: One hundred thirty mCRPC patients received AA after docetaxel treatment in compassionate programs. Of them, 24 (18.4%) subsequently received CAB. We retrospectively reviewed their data using conventional methods. RESULTS: Twenty-four patients received a median of 4 (range, 1-13) CAB cycles. Nineteen (79.1%) of them received primary prophylaxis with growth factors. Median patient characteristics were: age 65 (range, 57-85) years; Gleason score: 8 (range, 6-10); and PSA: 128.1 (range, 0.01-1700) ng/mL. A PSA response (≥ 50% decrease from baseline) occurred in 6 (31.5%) of 19 evaluable patients (95% confidence interval [CI], 11.8-54.2%). CAB therapy obtained a partial response in 2 of the 13 (15.3%) evaluable patients (95% CI, 2.9-45.4%). Median survival from initiation of CAB was 8.2 (95% CI, 3.34-13.05) months, from AA 16.1 (95% CI, 11.56-20.64) and from docetaxel 32.0 (95% CI, 11.56-39.69). CONCLUSION: A limited number of patients with mCRPC received CAB after docetaxel and AA treatment. In this selected population, CAB was active.

Lack of HER-2 gene amplification in non-Hodgkin lymphoma using chromogenic in situ hybridisation test.

HER-2 is overexpressed in 25% of breast cancers and provides a poor prognostic factor, affecting treatment decisions including administration of trastuzumab. Single reports show a lack of HER-2 in non-Hodgkin lymphomas (NHLs) using immunohistochemical (IHC) test. The present study evaluates HER-2 in NHLs using the chromogenic in situ hybridisation (CISH) test, which is more accurate than IHC, to seek new prognostic factors. The secondary aim of the study is to investigate efficacy of using trastuzumab in the treatment of NHLs in future studies. Fifty eight formalin-fixed, paraffin-embedded tissue specimens presenting various NHLs were examined using CISH test. Sixty six percent of all patients were diagnosed at stages III and IV. Histologically, 30 (52%) were low grade and 28 (48%) were intermediate and high grade. HER-2 was negative in all NHLs. Because there is no HER-2 gene amplification in NHL, HER-2 cannot be used as a prognostic factor and should not play a role in biological targeting therapy in non-Hodgkin lymphoma.