Citations

Abstract Health and biomedical science-related academic societies have played significant roles in the development and evolution of science and medicine, as well as the evolution of disciplines, including the diversification of medicine into specialties and subspecialties. They have also had formative roles in the development of clinical practice, professionalism, and training standards. The communities they establish promote knowledge creation and dissemination, provide career and professional development opportunities, articulate professional matters, offer networking opportunities, provide recognition, support members, and perform public engagement and advocacy work. They also play increasingly important roles in educating the public and disseminating objective, evidence-based medical and scientific information. Academic societies face challenges related to membership (recruiting new members and engaging and retaining current members), technology, hosting meetings and conferences, generational shifts (e.g., in demographics and attitudes toward working conditions, career paths, work-life integration), costs and logistics related to operations, and morale within institutions and professions. The Council of Faculty and Academic Societies of the Association of American Medical Colleges plays a unique role in supporting academic medical and related societies by providing an interprofessional forum for their interaction and dialogue, and is a vehicle for asserting their collective voice. To the extent that past is prologue, future advances in health care and science will depend, in part, on the resilience of academic societies and on the health professional workforces that they nourish.

Low diagnostic yield of presurgical genetic testing in adult patients with epilepsy Jünemann C, Stuart A, Kaur N, Wiebe S, Jette N, Singh S, Borlot F, Knake S; Calgary Comprehensive Epilepsy Program Collaborators; Billie Au PY, Klein KM. Epilepsia . 2026 May 20. doi: 10.1002/epi.70291. Epub ahead of print. PMID: 42157695. Objective: To determine the diagnostic yield of genetic testing in patients undergoing presurgical evaluation for epilepsy. Methods: We conducted a cohort study including 115 adult patients who underwent presurgical evaluation in the Calgary Epilepsy Program between 2019 and 2023 and who had undergone research exome sequencing. A curated epilepsy gene panel comprising 765 Online Mendelian Inheritance in Man (OMIM)-listed epilepsy-associated genes was applied. Variants were classified according to American College of Medical Genetics and Genomics guidelines and assessed for clinical relevance and association with postsurgical outcomes. Results: Pathogenic or likely pathogenic variants in DEPDC5, NPRL2, KCNT2, and PRRT2 were identified, respectively, in 4 individuals (3.5%, 4/115). All variants met stringent quality criteria with high pathogenicity scores (Combined Annotation Dependent Depletion (CADD) 34–37) and absent or extremely low population frequencies in gnomAD v4.1. None of these patients had intellectual disability, and only 1 patient (PRRT2) had a positive family history. The patient with the KCNT2 variant underwent epilepsy surgery with good outcome (Engel class ID). Significance: This presurgical cohort demonstrates a low diagnostic yield of genetic testing in adult epilepsy surgery candidates. However, 3 of 4 patients with (likely) pathogenic variants did not have features that would have prompted clinical genetic testing, indicating that their genetic diagnosis would have been missed based on typical clinical genetic testing criteria in many jurisdictions.

Purpose To prospectively investigate subjective anterior groin pain, patient‐reported outcome measures, complications, reoperation rates, and hip flexion strength after arthroscopic iliopsoas fractional lengthening. Methods From 2023 to 2025, patients with persistent groin pain after total hip arthroplasty refractory to conservative management undergoing arthroscopic iliopsoas fractional lengthening were prospectively identified at 2 tertiary referral centers. Pre‐ and postoperative outcomes at a minimum 6‐month follow‐up including the Visual Analog Scale, Tegner activity scale, Single Assessment Numeric Evaluation, and subjective anterior groin pain and hip flexion strength were analyzed. Results Fifty‐nine hips in 56 patients were included (age: 64.9 ± 9.8 years, 59% women, body mass index: 30.0 ± 5.8 kg/m 2 ) and followed for 10.0 ± 6.9 months postoperatively (range: 4‐25 months). Patients experienced significant ( P < .001) postoperative improvements in the Visual Analog Scale at rest (1.4 ± 2.2 vs 2.8 ± 2.1), Visual Analog Scale with use (3.0 ± 2.9 vs 7.8 ± 1.8), Tegner activity scale (2.8 ± 1.2 vs 2.0 ± 1.0), and Single Assessment Numeric Evaluation score (73.8 ± 22.5 vs 47.7 ± 22.2). Postoperative surgical satisfaction was 8.0 ± 2.7 (scale: 0‐10). Nearly 90% of patients reported feeling much or slightly better regarding their anterior groin pain postoperatively at 2‐week (91%), 6‐week (88%), 3‐month (91%), and final follow‐up (92%). Regarding hip flexion strength, ≥66% reported feeling much or slightly better at 2‐week (73%), 6‐week (95%), 3‐month (89%), and final follow‐up (66%). Three hips (6%) underwent reoperation at the final follow‐up (1 acetabular screw removal with open revision release, 1 revision total hip arthroplasty for loosening, and 1 two‐stage exchange for nonacute periprosthetic joint infection). Conclusions Nearly 90% of patients who underwent arthroscopic iliopsoas fractional lengthening after primary total hip arthroplasty reported improved anterior groin pain, whereas two‐thirds reported increased subjective hip flexion strength throughout the follow‐up. Of note, clinically meaningful improvement in pain at rest was achieved by 50% of patients based on cohort‐specific minimal clinically important difference criteria. Level of Evidence Level IV, retrospective therapeutic case series.

PURPOSE EA1181 (ClinicalTrials.gov identifier: NCT04266249 ) is a single-arm trial evaluating neoadjuvant taxane, trastuzumab, and pertuzumab (THP) in patients with clinical stage II/IIIa human epidermal growth factor receptor 2 (HER2)–positive breast cancer. This report focuses on the secondary end points of pathologic complete response (pCR) rates and associated factors. The primary end point—3-year recurrence-free survival among patients achieving a pCR (ypT0/Tis, ypN0)—will be reported when data mature. METHODS Patients received four cycles of trastuzumab and pertuzumab (HP) with either once per week paclitaxel (12 weeks) or docetaxel (every 3 weeks for four cycles), followed by surgery. Clinicopathologic characteristics were assessed in all patients. The HER2DX pCR score was determined using diagnostic biopsy samples in a representative subset. Logistic regression models identified factors associated with pCR. RESULTS A total of 2,175 patients were enrolled (781 HER2+/estrogen receptor‑negative [ER–]; 1,394 HER2+/ER+). Of 2,141 patients who initiated THP, the overall pCR rate was 43.8%: 63.7% in HER2+/ER– and 32.4% in HER2+/ER+ tumors. Higher pCR rates were observed in tumors that were ER-negative or low ER expressing, progesterone receptor-negative or low expressing, HER2 immunohistochemistry (IHC) 3+, and in patients treated with once per week paclitaxel. T3 disease was associated with a lower pCR rate in HER2+/ER– tumors; otherwise, tumor (T) and nodal (N) stage did not significantly affect pCR. Among 569 patients assessed for HER2DX pCR scores, a high score was independently associated with higher pCR rates, after adjustment for clinicopathologic variables. CONCLUSION Neoadjuvant THP achieved pCR in nearly two-thirds of patients with HER2+/ER– and one third with HER2+/ER+ breast cancer. Low hormone receptor expression, HER2 IHC 3+ status, once per week paclitaxel use, and a high HER2DX pCR score were independent predictors of pCR. These findings should help optimize risk stratification and treatment personalization for patients with HER2-positive breast cancer.

Importance Many patients are diagnosed with atypical lesions or lobular carcinoma in situ (LCIS); however, evidence- and consensus-based guidelines for the management of many of these lesions are limited. Observations The American Society of Breast Surgeons, in collaboration with the Society of Breast Imaging and College of American Pathology, assembled a steering group to create guidelines for the management of atypical lesions and LCIS, inclusive of flat epithelial atypia (FEA), atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), classic LCIS (C-LCIS), and the variant LCIS forms pleomorphic LCIS (P-LCIS) and florid LCIS (F-LCIS). The natural history of ADH, ALH, and C-LCIS suggests that these lesions are associated with an elevated future breast cancer risk; therefore, patients diagnosed with these lesions should be recommended to undergo comprehensive risk assessment and counseling about breast cancer risk-reducing strategies. The magnitude of future breast cancer risk associated with P-LCIS and F-LCIS remains uncertain, yet if these lesions are determined to be hormone receptor positive, risk-reducing medications should be considered. There is no evidence that FEA is associated with an elevated future breast cancer risk. A second pathology review confirmation is recommended for ADH, should be considered for FEA, and is not necessary for ALH or LCIS. Currently available evidence supports the need to diagnostically excise most ADH, P-LCIS, and F-LCIS cases identified on core biopsy, although some ADH cases fulfilling strict criteria and multidisciplinary consensus can be observed. P-LCIS and F-LCIS require a negative margin, but ADH does not. ALH and C-LCIS can be safely observed if the core biopsy diagnosis is concordant with imaging features (ie, radiographic-pathologic concordance is established). Provided radiologic-pathologic concordance is confirmed, diagnostic excision is generally not indicated after a diagnosis of FEA alone. Conclusions and Relevance These guidelines provide evidence-informed, consensus-based recommendations for the management of atypical lesions of the breast, including ADH, ALH, FEA, C-LCIS, P-LCIS, and F-LCIS. Practicing clinicians who treat patients with atypical breast lesions or LCIS should consider integrating these guidelines into clinical management.

Breast cancer incidence rises with age and peaks across the menopausal transition, yet why some postmenopausal lobules persist, and why that persistence predicts cancer risk, remains unresolved. Incomplete age-related lobular involution is one of the strongest tissue-level predictors of subsequent breast cancer, but it is still commonly viewed as passive failure of hormonally driven regression. This Review proposes a different framework: persistent lobules are maintained by an active reserve niche that outlasts its reproductive function. By integrating breast epidemiology, mammary stromal biology, cellular senescence, immune surveillance, and comparative reserve systems in skeletal muscle, hematopoiesis, and postmenopausal endometrium, we argue that menopause is a biological control point at which tissue fate diverges. Efficient clearance of senescent cells permits lobular regression to complete, whereas impaired immune surveillance may allow inflammatory paracrine signaling, macrophage reprogramming, and immune evasion to create a self-sustaining senescent-immune niche lock. This framework explains why persistent lobules are biologically active, shifts attention from epithelial quantity to microenvironmental state, and identifies the perimenopausal window as a promising interval for biomarker-guided risk stratification and prevention.

Breast cancer incidence rises with age and peaks across the menopausal transition, yet why some postmenopausal lobules persist, and why that persistence predicts cancer risk, remains unresolved. Incomplete age-related lobular involution is one of the strongest tissue-level predictors of subsequent breast cancer, but it is still commonly viewed as passive failure of hormonally driven regression. This Review proposes a different framework: persistent lobules are maintained by an active reserve niche that outlasts its reproductive function. By integrating breast epidemiology, mammary stromal biology, cellular senescence, immune surveillance, and comparative reserve systems in skeletal muscle, hematopoiesis, and postmenopausal endometrium, we argue that menopause is a biological control point at which tissue fate diverges. Efficient clearance of senescent cells permits lobular regression to complete, whereas impaired immune surveillance may allow inflammatory paracrine signaling, macrophage reprogramming, and immune evasion to create a self-sustaining senescent-immune niche lock. This framework explains why persistent lobules are biologically active, shifts attention from epithelial quantity to microenvironmental state, and identifies the perimenopausal window as a promising interval for biomarker-guided risk stratification and prevention.