Lucrezia Toppi

Background: This exploratory study assessed whether qualitative dynamic contrast-enhanced MRI (DCE-MRI) time–intensity curves (TICs) differentiate non-progressive treatment-related changes (NPTRC) from tumor progression after stereotactic radiotherapy for brain metastases. Methods: Thirty-two patients with 51 treated lesions underwent DCE-MRI. Five neuroradiologists independently delineated a volume of interest and classified the resulting TIC as Type A–D. Longitudinal clinical and MRI follow-up provided the reference outcome, which was recorded before the TIC framework was finalized. An A/B versus C/D grouping was evaluated as a secondary exploratory analysis. Results: Thirty-five lesions were classified as NPTRC and 16 as tumor progression. All 17 Type A lesions were NPTRC, whereas all 13 Type C/D lesions showed progression. Type B was observed in 21 of 51 lesions (41.2%), including 18 NPTRC and 3 progressive lesions, representing a substantial indeterminate subgroup. The exploratory A/B versus C/D grouping yielded 81.3% sensitivity and 100% specificity. The ordinal TIC analysis yielded an AUC of 0.952. Interobserver agreement was high within the present reader group (Fleiss’ κ = 0.889). Conclusions: Type A was associated with NPTRC, Types C/D were associated with progression, and Type B represented an indeterminate pattern. These descriptive findings require independent validation before clinical use.

Background: This exploratory study assessed whether qualitative dynamic contrast-enhanced MRI (DCE-MRI) time–intensity curves (TICs) differentiate non-progressive treatment-related changes (NPTRC) from tumor recurrence after stereotactic radiotherapy for brain metastases. Methods: Thirty-two patients with 51 treated lesions underwent DCE-MRI. Five neuroradiologists inde-pendently delineated a volume of interest and classified the resulting TIC as Type A–D. Longitudinal clinical and MRI follow-up provided the reference outcome, which was recorded before the TIC framework was finalized. An A/B versus C/D grouping was evaluated as a secondary exploratory analysis. Results: Thirty-five lesions were classified as NPTRC and 16 as tumor recurrence. All 17 Type A lesions were NPTRC, and all 13 Type C/D lesions showed recurrence. Type B occurred in both groups (18 NPTRC; 3 recurrences). The A/B versus C/D grouping yielded 81.3% sensitivity and 100% specificity. The ordinal TIC analysis yielded an area under the curve of 0.952. Interobserver agree-ment was high for the four TIC categories (Fleiss’ κ = 0.889). Conclusions: Type A was associated with NPTRC, Types C/D with recurrence, and Type B represented an indeterminate pattern. These descriptive findings require independent validation before clinical use.

Background: CDK4/6 inhibitor plus ET is a standard treatment for advanced HR+ BC. This study evaluates the efficacy and safety of CDK4/6 inhibitors with concurrent RT (SBRT and non-SBRT) in terms of pain, analgesic therapy changes, toxicities, and net clinical benefit (NCB). Methods: BC patients with bone metastases treated with RT and CDK4/6 inhibitor in the prospective observational COMBART study were analyzed. Pain was measured with the NRS. The NCB was defined by pain reduction (NRS), toxicity, and treatment changes. Adverse events (AEs) were graded per CTCAE v5.0. Statistical tests included chi-square and t-test. Results: Forty patients were treated with CDK4/6 inhibitor (palbociclib 30.8%, ribociclib 51.3%, abemaciclib 17.9%) and RT (131 lesions; 100 SBRT, 31 non-SBRT). The mean NRS score dropped from 3.52 (pre-treatment) to 1.31 (post-treatment) (p < 0.001), with better outcomes for patients treated with moderate hypofractionation (58.6% vs. 39.9% pain relief, p = 0.016). Pain relief was independent of the type of CDK4/6 inhibitor used (p = NS). Analgesic reduction was most common with palbociclib (35.4%, p = 0.001). Eight toxicities (grade 1–2) were reported. The NCB was 0.6 overall, higher with non-SBRT (0.74 vs. 0.52). Conclusions: RT plus CDK4/6 inhibitor, especially with moderate hypofractionation, significantly reduced pain with manageable toxicity. Analgesic therapy can often continue without stopping CDK4/6 inhibitor.