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Purpose Pituitary neuroendocrine tumors (pitNETs) are benign tumors that may recur after surgical resection or persist following medical management. The objective of this study was to evaluate outcomes and toxicities of patients with pitNETs treated with stereotactic radiosurgery (SRS) at a single institution. Methods We completed a retrospective, single-institution study of patients with pitNETs treated with frame-based, single-fraction, cobalt-60 SRS between September 2005 and June 2023. The primary endpoint was local tumor control. Secondary endpoints included endocrine control (for functional tumors), overall survival, and toxicities. Results A total of 88 lesions in 83 patients were treated with SRS. Most lesions (70%) were non-functional tumors. Of the 26 functioning tumors, 6 patients achieved endocrine remission with SRS alone (23%), and the remainder achieved remission with combined medical management. With a median patient follow-up of 4.7 years, no local tumor recurrences were observed with an estimated local control probability of 100%. Two- and five-year overall survival estimates were 97% (95% confidence interval [CI] 89–99) and 95% (95% CI 84–98), respectively. Causes of death were unrelated to PitNET or SRS. Twelve patients (14%) developed hypopituitarism after SRS. Despite the 34 lesions that were ≤ 3 mm from optic structures, no patients developed any optic neuropathy or visual decline post SRS. Conclusions SRS is a highly effective modality for recurrent or residual pitNETs. This study observed a local control of 100% with no cases of optic toxicities after a median follow-up of 4.7 years. These observed findings suggest that dose de-escalation may be possible for future treatment of pitNETs.

Most women with estrogen receptor expressing breast cancers receiving anti-estrogens such as tamoxifen may not need or benefit from them. Besides the estrogen receptor, there are no predictive biomarkers to help select breast cancer patients for tamoxifen treatment. CCND1 (cyclin D1) gene amplification is a putative candidate tamoxifen predictive biomarker. The RSF1 (remodeling and spacing factor 1) gene is frequently co-amplified with CCND1 on chromosome 11q. We validated the predictive value of these biomarkers in the MA.12 randomized study of adjuvant tamoxifen vs. placebo in high-risk premenopausal early breast cancer. Premenopausal women with node-positive/high-risk node-negative early breast cancer received standard adjuvant chemotherapy and then were randomized to tamoxifen (20 mg/day) or placebo for 5 yrs. Overall survival (OS) and relapse-free survival (RFS) were evaluated. Fluorescent in-situ hybridization was performed on a tissue microarray of 495 breast tumors (74% of patients) to measure CCND1 and RSF1 copy number. A multivariate Cox model to obtain hazard ratios (HR) adjusting for clinico-pathologic factors was used to assess the effect of these biomarkers on Os and RFS. 672 women were followed for a median of 8.4 years. We were able to measure the DNA copy number of CCND1 in 442 patients and RSF1 in 413 patients. CCND1 gene amplification was observed in 8.7% and RSF1 in 6.8% of these patients, preferentially in estrogen receptor-positive breast cancers. No statistically significant interaction with treatment was observed for either CCND1 or RSF1 amplification, although patients with high RSF1 copy number did not show benefit from adjuvant tamoxifen (HR = 1.11, interaction p = 0.09). Unlike CCND1 amplification, RSF1 amplification may predict for outcome in high-risk premenopausal breast cancer patients treated with adjuvant tamoxifen.

BackgroundTo investigate the relationship between attendance to a pre-treatment psychoeducational intervention (prehab) with treatment outcomes and toxicities in patients receiving radiotherapy for head and neck cancers (HNCs).MethodsPatients were included from prehab inception in 2013 to 2017, comparing overall survival (OS), locoregional recurrence-free survival (LRFS), and locoregional recurrence (LRR) between prehab attendees (PA) and non-attendees (PNA). Multivariable analysis was performed for OS and LRFS.ResultsAmong 864 PA and 1128 PNA, 2-year OS was 88% vs 80% (p < 0.001), and LRFS was 84% vs 75% (p < 0.001). On multivariable analysis (MVA), OS and LRFS were independently and unfavourably associated with PNA. The PA cohort had a lower frequency of a “rocky treatment course” compared with the PNA cohort (52/150, 35% vs 71/150, 47%; p = 0.034).ConclusionsPrehab at our institution is associated with improved long-term oncologic outcomes. Prospective data is needed to better understand this association.

Several molecular factors have been associated with the sensitivity of breast cancer to tamoxifen (T): Pax2 can mediate the repression of ERBB2 expression by the tamoxifen-ER complex; TC21 is a member of the Ras superfamily associated with increased recurrence in tamoxifen-treated patients; CCND1 (Cyclin D1) is frequently amplified in breast cancers resistant to this drug; and RSF1 is often co-amplified with CCND1 on chromosome 11q. Here, validation of the predictive value of these biomarkers is explored in the MA.12 trial, in which premenopausal women with node-positive/high-risk node-negative early breast cancer, of any hormonal status, were randomized to T (20 mg/day) or P for 5 years after receiving adjuvant chemotherapy. Overall survival (OS) and relapse-free survival (RFS) were evaluated. Pax2 and TC21 (measured via IHC) expression were not associated with OS or RFS. However, in the ER+ subgroup, patients with low TC21 expression derived greater benefit from T compared with P than patients with high TC21 expression, as measured by RFS. No significant interaction with treatment was observed with CCND1 or RSF1 amplification (measured via FISH), although patients with high RSF1 copy number showed a trend toward no benefit from T. Although none of the 4 biomarkers for T response were completely validated in this clinical trial, the predictive effect of TC21 expression and RSF1 amplification deserve further study.

Most women with estrogen receptor expressing breast cancers receiving anti-estrogens such as tamoxifen may not need or benefit from them. Besides the estrogen receptor, there are no predictive biomarkers to help select breast cancer patients for tamoxifen treatment. CCND1 (cyclin D1) gene amplification is a putative candidate tamoxifen predictive biomarker. The RSF1 (remodeling and spacing factor 1) gene is frequently co-amplified with CCND1 on chromosome 11q. We validated the predictive value of these biomarkers in the MA.12 randomized study of adjuvant tamoxifen vs. placebo in high-risk premenopausal early breast cancer. Premenopausal women with node-positive/high-risk node-negative early breast cancer received standard adjuvant chemotherapy and then were randomized to tamoxifen (20 mg/day) or placebo for 5 yrs. Overall survival (OS) and relapse-free survival (RFS) were evaluated. Fluorescent in-situ hybridization was performed on a tissue microarray of 495 breast tumors (74% of patients) to measure CCND1 and RSF1 copy number. A multivariate Cox model to obtain hazard ratios (HR) adjusting for clinico-pathologic factors was used to assess the effect of these biomarkers on Os and RFS. 672 women were followed for a median of 8.4 years. We were able to measure the DNA copy number of CCND1 in 442 patients and RSF1 in 413 patients. CCND1 gene amplification was observed in 8.7% and RSF1 in 6.8% of these patients, preferentially in estrogen receptor-positive breast cancers. No statistically significant interaction with treatment was observed for either CCND1 or RSF1 amplification, although patients with high RSF1 copy number did not show benefit from adjuvant tamoxifen (HR = 1.11, interaction p = 0.09). Unlike CCND1 amplification, RSF1 amplification may predict for outcome in high-risk premenopausal breast cancer patients treated with adjuvant tamoxifen.