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Out‐of‐pocket costs are not the bottom line in financial toxicity
Fields, Brittany C. , Afolaranmi, Oluwasegun , Ohlsen, Timothy J. D. , Okoroh, Juliet S. , Lumati, Juliet S , Afolaranmi, Oluwasegun

Cancer | August 6, 2026 | Volume: 132 | Issue: 16 | Pages: No page available

10.1002/cncr.70561 | PMID 42559663 Get It

Health care–related out‐of‐pocket and indirect costs may create financial barriers to initial and/or continued receipt of care among patients with cancer, and subsequent financial toxicity is associated with worse oncologic and quality of life outcomes. Recognition and mitigation of risk factors for financial toxicity are essential to the provision of equitable, high‐quality care.
Implementing a Hospital Internal Medicine Interest Group - Innovative and Personalized Structured Support for Future Hospitalists
Gavrancic, Tatjana , Hill, Ebone D., Pagán, Ricardo J, Jackson, B.F. , Laenger, Jessica, Zuberi, Eric , Hedges, Mary S., Cowdell, J. Colt, Jackson, Brittany , Zuberi, Eric C. , Hill, Ebone, Pagán, Ricardo J. , Laenger, Jessica , Hedges, Mary S. , Cowdell, Jed C.

Journal of Medical Education and Curricular Development | July 28, 2026 | Volume: 13 | Issue: No issue available | Pages: No page available

10.1177/23821205261474676 | PMID 42534303 Get It

Hospital medicine offers diverse career opportunities, yet formal guidance for residents pursuing hospitalist careers is often lacking. To address this gap, the Hospital Internal Medicine Interest Group (HIMIG) was launched at an academic institution in the Southeastern United States to provide structured mentorship and professional development. Residents expressing interest completed an entry survey to identify career goals and areas of focus, informing a longitudinal curriculum that included education, leadership, research, quality improvement, and networking. Seventeen residents (≈25% of the IM residency program) joined HIMIG, and 88% completed the initial survey. Education, leadership, and quality improvement were top interests, while mentorship and career guidance were primary motivators. A post-implementation survey revealed all participants met mentors and felt HIMIG supported their career goals. HIMIG demonstrates a flexible, personalized approach to hospitalist career development that may serve as a model for other programs.
Reporting and Analysis of Sociodemographic Characteristics in High-impact Perioperative Medicine Studies: A Scoping Review
Kraus, Molly, Noss, Bryant, Burton, Brittany N., Maloney, Jillian, Warner, David O., Wang, Z, Mariano, Edward R., Boulware, Angel , Milam, Adam J. , Milam, Adam J , Kraus, Molly B., Burton, Brittany N. , Maloney, Jillian , Yu, Soojie , Warner, David O. , Mariano, Edward R.

Anesthesiology Open | July 24, 2026 | Volume: 1 | Issue: 2 | Pages: e0025

10.1097/ao9.0000000000000025 Get It

Cancer Risk After Simultaneous Pancreas‐Kidney Transplantation Compared With Kidney Transplant Alone: A Propensity‐Matched Cohort Study
Balloura, Mohamad Amir, Mawaldi, Mohammad, Johnson, Brittany, Ovincy, Cene, Fontánez, N. Camacho, Ingram, Demarcus, Me, Hay Me , Leeaphorn, Napat , Attieh, Rose Mary , Fontanez, Nicole Camacho

Clinical Transplantation | July 23, 2026 | Volume: 40 | Issue: 7 | Pages: No page available

10.1111/ctr.70621 | PMID 42489648 Get It

ABSTRACT Background Post‐transplant malignancy is a major determinant of long‐term outcomes after solid organ transplantation. Whether simultaneous pancreas–kidney (SPK) transplantation confers a differential post‐transplant cancer risk compared With kidney transplantation alone (KA) remains uncertain. Methods We conducted a retrospective propensity score–matched cohort study of adult transplant recipients at three Mayo Clinic sites between 2001 and 2017. SPK recipients ( n = 484) were matched 1:1 with KA recipients using propensity scores. The primary outcome was post‐transplant cancer incidence analyzed using Fine–Gray competing risks regression with death as a competing event. Standardized incidence ratios (SIRs) were calculated relative to the US general population. Cox proportional hazards models with cancer modeled as a time‐varying covariate evaluated associations with mortality and death‐censored graft failure. Results Over a median follow‐up of 10 years, overall cancer incidence was similar between SPK and KA recipients (subdistribution hazard ratio [sHR] 0.80, 95% CI 0.63–1.02; p = 0.07). The observed trend toward lower cancer incidence in SPK recipients was driven by a lower incidence of non‐melanoma skin cancer (NMSC) (sHR 0.72, 95% CI 0.53–0.97; p = 0.03), which was attenuated after age adjustment (sHR 0.76, p = 0.07). Incidence of other malignancies did not differ between groups. Compared with the US general population, cancer risk excluding NMSC was approximately twofold higher in both cohorts (SIR 2.18 for SPK vs. 2.23 for KA). Incident malignancy was strongly associated with increased mortality (HR 3.40 in KA and 2.07 in SPK) but not with a statistically significant increase in graft failure. Conclusions In this propensity score–matched cohort study, overall post‐transplant malignancy incidence was comparable between SPK and KA recipients. Both groups experienced substantially elevated cancer risk relative to the general population, and incident malignancy was strongly associated with mortality. These findings suggest that malignancy risk is driven primarily by shared immunologic and demographic factors rather than transplant type.
Abstract B054: Systemic Therapy and Outcomes in Patients with Intermediate or High-Risk Solitary Fibrous Tumor
Lin, Miranda, Siontis, Brittany, Robinson, S I, Okuno, Scott, Ho, Thanh, Siontis, Brittany L. , Robinson, Steven I. , Ho, Thanh

Cancer Research | July 18, 2026 | Volume: 86 | Issue: 14_Supplement | Pages: B054-B054

10.1158/1538-7445.rareca26-b054 Get It

Abstract Background: Solitary fibrous tumors (SFT) make up less than 5% of sarcomas. The Demicco model stratifies risk of metastasis based on age, tumor size, mitotic count, and necrosis. Patients (pts) with relapsed disease have limited options. We evaluated outcomes of systemic therapies (tx) to treat SFT. Methods: A retrospective analysis was performed of pts with intermediate-to-high risk SFT confirmed by soft tissue pathologists at a multi-site health system from 1999 – 2024. Demographics, tx, and pt outcomes were analyzed. Radiographic response was abstracted from documentation by treating provider. Results: Sixty pts had intermediate-to-high risk SFT, of which 21 pts received systemic tx. Of these, 12 were male, median age at diagnosis 62.8 years (41.0 – 82.7 yrs). Tumors originated from chest (11, 52.4%), abdomen (5, 23.8%), pelvis (4, 19.0%), and skull (1, 4.8%). All pts had surgery for primary tumor, median size 16.0 cm (7.8 – 43.0), and 14 (66.7%) had surgery at relapse. Eight pts (38.1%) had perioperative radiation therapy (RT); 12 (57.1%) had palliative RT. Five (23.8%) had ablation. Of the 21 pts, 2 (9.5%) had perioperative chemotherapy (chemo). Twenty pts (95.2%) received median 2 lines (1 – 6) of palliative systemic tx (1 pt did not pursue any). One pt had partial response on dacarbazine, otherwise best clinical response was stable disease (SD, 53.1% vascular endothelial growth factor inhibitors (VEGFi), 40% chemo) or disease progression (PD). Most pts received VEGFi: 11 pts had sunitinib (median 3.1 months, range 1.0 – 10.6 mo), 11 pts had pazopanib (4.1 mo, 0.1 – 38.7), and 10 pts had temozolomide/bevacizumab (5.6 mo, 1.0 – 15.8). VEGFi was dose reduced or held in 59.4% . Discontinuation due to toxicity occurred in 34.4% of pts treated with VEGFi vs 26.7% of pts treated with chemo. Five pts received liposomal doxorubicin (median 4.8 mo, range 3.5 – 11.3). Four pts had doxorubicin with dacarbazine, ifosfamide or olaratumab (2.8 mo, 0.7 – 8.5). Two pts received dacarbazine (1.9 and 9.6 mo, respectively), and 2 pts received gemcitabine/docetaxel (0.9 and 4 mo). Eribulin and trabectedin (1 pt, respectively) were used for less than 1 mo. Tx was held or dose reduced for 1 pt on doxorubicin/dacarbazine and 1 pt on gemcitabine/docetaxel. Three pts had immunotherapy (IO, 2 pts pembrolizumab, 1 pt nivolumab/ipilimumab) and stopped for PD (2 pts) or toxicity (1 pt) after 2 mo or less. Two pts participated in clinical trials. Median time from primary surgery to relapse was 2.0 yrs (0.0 – 12.3). Sixteen pts died (76.2%), 14 from SFT. Median time from relapse to death or last contact was 4.1 yrs (0.5 – 14.7). Median overall survival from diagnosis to death/last contact was 6.6 yrs (0.6 – 27.0). Conclusion: Perioperative chemo was rarely used to treat intermediate-to-high risk SFT. For relapse, VEGFi use was more common than chemo, with more pts achieving SD and receiving longer duration of tx. VEGFi had greater toxicity and subsequent discontinuation. No benefit was observed in few pts who received IO. Clinical trial participation was uncommon. Citation Format: Miranda Lin, Brittany Siontis, Steven Robinson, Scott Okuno, Thanh Ho. Systemic Therapy and Outcomes in Patients with Intermediate or High-Risk Solitary Fibrous Tumor [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Breaking Barriers in the Fight against Rare Cancers; 2026 Jul 18-20; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2026;86(14_Suppl):Abstract nr B054.
Unintentional Weight Loss Does Not Predict Poor Outcomes in Zenker Diverticulum
Allen, Jacqueline , Belafsky, Peter C., deSilva, Brad W. , Dhar, Shumon I. , Ekbom, Dale C. , Friedman, Aaron D. , Fritz, Mark A. , Gardner, Glendon M., Johnson, Christopher, Kasperbauer, Jan L. , Kim, Brandon , Kuhn, Maggie A. , Madden, Lyndsay L., Matrka, Laura , Piraka, Cyrus, Ramaswamy, Apoorva, Rosen, Clark A. , Sibley, Haley , Wright, Carter, Yang, Z. Mike, Young, VyVy N. , Postma, Gregory, Howell, Rebecca J. , Allen, Jacqui , Amin, Milan R , Bayan, Semirra L. , deSilva, Brad , Dhar, Shumon I , Ekbom, Dale , Fritz, Mark , Kasperbauer, Jan , Krekeler, Brittany N , Kuhn, Maggie , Ma, Yue , Matrka, Laura , Mayerhoff, Ross , Rosen, Clark , Sibley, Haley C , Tabangin, Meredith , Young, Vyvy , Howell, Rebecca , Schuman, Ari D. , Altaye, Mekibib , Belafsky, Peter C. , Gardner, Glendon M., Guardiani, Elizabeth , Madden, Lyndsay L. , Mayerhoff, Ross , Piraka, Cyrus , Ramaswamy, Apoorva Tewari , Tabangin, Meredith E. , Postma, Gregory

The Laryngoscope | July 18, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.1002/lary.70734 | PMID 42470432 Get It

ABSTRACT Objective Weight loss is frequently considered a cardinal presenting symptom for patients with Zenker diverticulum (ZD). We hypothesized that weight loss in patients with cricopharyngeal muscle dysfunction (CPMD), with or without diverticula, was associated with the length of symptoms and size of diverticulum. Methods Prospective, multicenter observational study of CPMD patients with and without diverticula reporting unintentional weight loss (+WL) or no weight loss (−WL) prior to enrollment in the Prospective Outcomes of Cricopharyngeal Hypertonicity (POuCH) database. Complications and symptom response using a patient reported outcome measure, the Eating Assessment Tool (EAT‐10), were compared. Results Of 427 patients, 101 (23.6%) were +WL. Median weight loss was 14 pounds (interquartile range [IQR] 10–25). +WL cohort had a mean age of 71.5 (standard deviation [SD] 11.5) vs. 67.9 in −WL (SD 11.6, p = 0.007). Mean preoperative EAT‐10 score was 24.7 in +WL (SD 9.7) and 14.8 in −WL (SD 8.8, p < 0.0001). Higher preoperative weight loss was associated with higher preoperative EAT‐10 ( p < 0.0001, Spearman's ρ = 0.43). Size of diverticulum was associated with WL ( p = 0.003), but weight loss was highest in both large diverticula and CP bars. Duration of symptoms was not associated with weight loss ( p = 0.30). Postoperative complications in +WL and −WL patients were similar ( p = 0.78). Conclusion Unintentional weight loss is common with ZD. Patients with worse dysphagia are more likely to have more weight loss. Weight loss does not increase with the size of the diverticulum or length of symptoms. Surgery has a similar safety profile with greater improvement in dysphagia in patients reporting weight loss. Level of Evidence 3.
Breast Cancer Follow-Up and Surveillance After Primary Treatment: ASCO Guideline Update
Nahleh, Zeina , Alfano, Catherine M. , Somerfield, Mark R. , Lee, Janie M. , Hieken, Tina J. , Magnuson, Allison , Rao, Ruta , Chew, Helen K., Chia, Stephen , Harvey, Brittany , Landsberger, Ellen , Mwanzi, Sitna , Parsons, Heather A. , Patt, DA , Sung, Hyuna , Rao, Ruta , Chia, Stephen K L , Harvey, Brittany E , Lim, Bora , Mwanzi, Sitna Ali , Parsons, Heather A , Sukumar, Jasmine S , Sung, Hyuna , Werutsky, Gustavo , Lustberg, Maryam , Hieken, Tina J , Alfano, Catherine M , Chew, Helen K. , Lim, Bora , Lustberg, Maryam B.

Journal of Clinical Oncology | July 16, 2026 | Volume: 44 | Issue: 30 | Pages: 2953-2971

10.1200/jco-26-01700 | PMID 42462191 Get It

ASCO Guidelines provide recommendations with comprehensive review and analyses of the relevant literature for each recommendation, following the guideline development process as outlined in the https://www.asco.org/practice-patients/guidelines/guideline-methodology . ASCO Guidelines follow the https://www.asco.org/about-asco/legal/conflict-interest-coi . Clinical Practice Guidelines and other guidance (“Guidance”) provided by ASCO is not a comprehensive or definitive guide to treatment options. It is intended for voluntary use by clinicians and should be used in conjunction with independent professional judgment. Guidance may not be applicable to all patients, interventions, diseases or stages of diseases. Guidance is based on review and analysis of relevant literature, and is not intended as a statement of the standard of care. ASCO does not endorse third-party drugs, devices, services, or therapies and assumes no responsibility for any harm arising from or related to the use of this information. See complete disclaimer in Appendix 1 and Appendix 2 (online only) for more . PURPOSE To offer clinicians recommendations concerning breast cancer follow-up and surveillance after primary treatment. METHODS ASCO convened an Expert Panel to develop recommendations based on a systematic review and a formal consensus process. RESULTS One randomized controlled trial (RCT) was identified and formed the evidentiary basis for the surveillance mammography guideline recommendation. No RCTs were identified that evaluated different follow-up approaches by risk of relapse in patients treated for early-stage breast cancer. Given the dearth of evidence identified in the systematic review of the literature, formal modified Delphi consensus-based recommendations were generated. RECOMMENDATIONS The guideline offers recommendations on the role of a risk-based approach to the frequency and intensity of follow-up among patients with breast cancer in the adjuvant setting. Regular history, physical examination, and mammography are recommended for breast cancer follow-up. Either virtual or in-person visits can be offered. Certain patients at a high risk of cancer recurrence warrant closer surveillance, such as those patients with locally advanced disease or residual disease following neoadjuvant chemotherapy. Recommendations on the use of blood-based biomarkers and supplemental imaging are provided. Guideline recommendations will be updated once additional evidence-based tools become available to better individualize surveillance. Additional information is available at www.ascopubs.org/topics/asco-guidelines/breast-cancer .
Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy
Miner, A, Zetterberg, Henrik, Blennow, Kaj, Groh, Jenna R., Singh, Alpana, Dieckhoff, Kari, Tripodis, Yorghos, Adler, Charles H., Balcer, Laura J. , Bernick, C L, Peskind, Elaine, Asken, Breton M., Tanner, Jeremy A., Rabinovici, Gil D., Banks, Sarah J., Barr, William B., Wethe, Jennifer V., Cantu, Robert C., Dodick, David W., Mez, Jesse, Palmisano, J, Martin, Brett, Stein, Thor D., McKee, Ann C., Cummings, Jeffrey L., Shenton, Martha E., Reiman, E Bieto, Rc, Stern, Ashton, Nicholas J., Alosco, Michael L., Chen, Kewei, Protas, Hillary, Su, Yi, Boker, Connie, Au, Rhoda, Farrer, Lindsay, Helm, Robert, Kowall, Neil, Mercier, Gustavo, Otis, James, Weller, Jason, Bragg, Tahlia, Simkin, Irene, Trujillo-Rodriguez, Diana, Amerongen, Suzan van , Andino, Alondra, Conneely, Shannon, Diamond, Courtney, Fagle, Tessa, Haller, Olivia, Hunt, Tennyson, Gullotti, Nicole, Kossow, Bailey, Kugelmass, Carrie, Mariani, Megan, Mayville, Brian, McLaughlin, Kathleen, Nanna, Mary, DiPopolo, Marty, Platt, Taylor, Rice, Fiona, Sestak, Madison, McClean, Michael, Annis, Douglas, Chaisson, Christine, Dixon, Diane, Finney, Carolyn, Gallagher, Kerrin, Hartlage, Kaitlin , Lu, Jun, Ojo, E O, Pine, Brittany, Ramachandran, Janani, Baucom, Zachary, Tuz‐Zahra, Fatima , Yhang, Eukyung , Bouix, Sylvain, Fitzsimmons, Jennifer, Lin, Alexander P., Koerte, Inga K., Pasternak, Ofer, Arciniega, Hector , Billah, Tashrif , Bonke, Elena, Breedlove, Katherine M. , Carrington, Holly, Coello, Eduardo , Coleman, Michael J., John, Omar , Jung, Leonard, Liao, Huijun, Loy, Maria, Rizzoni, Elizabeth, Schulz, V. D., Silva, Annelise, Vessey, Brynn, Wiegand, Tim L.T, Miller, Jason, Ritter, Aaron , Sabbagh, Marwan, Cruz, Raelynn de la, Durant, Jan, Golceker, Morgan, Harmon, Nicolette, Kaylegian, Jaeson, Long, Rachelle, Nance, Christine, Sandoval, Priscilla, Staples, Miranda, Clark, Emma F., Serrano, Andrew, Geda, Yonas, Duffy, Amy, Falk, Bryce, Howard, Marci, Montague, Michelle , Osgood, Thomas, Babcock, Debra, Bellgowan, Patrick, GOLDBERG, JUDITH, Joseph, Binu , Kirov, Ivan, Lui, Yvonne, Marmar, Charles, Wisniewski, T R, Al-Kharafi, Alhassan, George, Allan, Hasanaj, Lisena, Martin, Sammie, Riley, Edward, Runge, William, Serrano, Liliana , Iliff, Jeffrey, Li, Gail, Janssen, D, Meabon, James, Piantino, Juan, Schindler, Abigail, Thomas, Ronald, Colasurdo, Elizabeth , Shofer, Jane, Marcus, Daniel S., Gurney, Jenny , Greenwald, Richard, Johnson, Keith A., Singh, Alpana , Singh, Alpana , Miner, Annalise E., Zetterberg, Henrik , Blennow, Kaj , Groh, Jenna R. , Singh, Alpana, Tripodis, Yorghos , Adler, Charles H. , Bernick, Charles , Peskind, Elaine R. , Asken, Breton M. , Rabinovici, Gil D. , Banks, Sarah J. , Barr, William , Wethe, Jennifer V. , Cantu, Robert C. , Dodick, David W. , Mez, Jesse , Stein, Thor D. , McKee, Ann C. , Cummings, Jeffrey L. , Shenton, Martha E. , Reiman, Eric M. , Ashton, Nicholas J. , Alosco, Michael L. , Protas, Hillary , Au, Rhoda, Weller, Jason , Trujillo‐Rodriguez, Diana , Fagle, Tessa, Mariani, Megan, McLaughlin, Kathleen , Pulukuri, Surya Vamsi , Sestak, Madison, McClean, Michael D , Annis, Douglas, Finney, Carolyn, Lu, Jun, Pine, Brittany, Ramachandran, Janani , Baucom, Zachary, Bouix, Sylvain , Koerte, Inga K , Pasternak, Ofer , Bonke, Elena M. , Carrington, Holly , Coleman, Michael J. , Liao, Huijun, Schulz, Vivian, Wiegand, Tim L. T. , II, Robert W. Turner , Marek, Kenneth , Geda, Yonas E. , Howard, Marci, Montague, Michelle, Babcock, Debra, Bellgowan, Patrick S.F. , Kirov, Ivan, George, Allan, Meabon, James S. , Piantino, Juan , Thomas, Ronald G. , Colasurdo, Elizabeth A. , Shofer, Jane, Marcus, Daniel S., Johnson, Keith A.

JAMA Network Open | July 13, 2026 | Volume: 9 | Issue: 7 | Pages: e2622966

10.1001/jamanetworkopen.2026.22966 | PMID 42440317 Get It

Importance In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. Objective To evaluate the utility of plasma phosphorylated tau 217 (p-tau217), assess its performance as a beta-amyloid (Aβ) biomarker in participants with RHI exposure at risk for CTE, and explore concordance with CTE neuropathology in a postmortem subsample. Design, Setting, and Participants This longitudinal, multicenter, case-control study used data from the Diagnostics, Imaging, and Genetics Network for the Objective Study and Evaluation of CTE (DIAGNOSE CTE) Research Project, collected from September 2016 to October 2023. Participants were former American football players (case participants) and asymptomatic men unexposed to RHI (control participants). A subsample had available neuropathologic data. Exposures RHI, traumatic encephalopathy syndrome (TES) diagnoses, and levels of CTE certainty. Main Outcomes and Measures Plasma p-tau217 (classified as positive [≥0.63 pg/mL], intermediate [0.40-0.62 pg/mL], and negative [&amp;lt;0.40 pg/mL]), Aβ–positron emission tomography (PET; 18 F-florbetapir; with Aβ-positive defined as a standardized uptake value ratio [SUVR] ≥1.10), and tau-PET ( 18 F-flortaucipir). TES diagnoses were assigned by multidisciplinary consensus conference. Analyses of postmortem brains controlled for age, race, and APOE ε4 status. Results Among 231 participants (mean [SD] age, 57.75 [8.25] years), 177 were former football players (117 professional and 60 college) and 54 were unexposed participants. Former football players had higher baseline mean (SD) p-tau217 concentrations than unexposed participants (0.35 [0.26] pg/mL vs 0.27 [0.14] pg/mL; P = .008), although this was driven by a higher proportion of Aβ-PET–positive participants among former players. Plasma p-tau217 increased over time across the sample (B = 0.207 [95% CI, 0.117-0.298]; P &amp;lt; .001), with no significant time × exposure group interactions. Among football players, p-tau217 showed no time × group interactions with TES diagnosis, TES-CTE certainty, or RHI metrics. Higher p-tau217 concentration correlated with higher global Aβ-PET SUVR (B = 0.058 [95% CI, 0.053-3.501; P = .01), with a few discordant cases (5 participants were p-tau217–negative and Aβ-PET–positive; 7 participants were p-tau217–positive and Aβ-PET–negative). P-tau217 had similar areas under the curve for projecting Aβ-PET positivity as cerebrospinal fluid (CSF) p-tau181/Aβ42 and CSF Aβ40/42 measures (p-tau217: AUC, 0.88 [95% CI, 0.80-0.96]; CSF p-tau181/Aβ42: AUC, 0.89 [95% CI, 0.79-1.00]; CSF Aβ40/42: AUC, 0.85 [95% CI, 0.72-0.98]). Among 9 brain donors, 6 had CTE (stages II-IV; none with Alzheimer disease). Seven had negative or intermediate p-tau217, concordant with Aβ-PET. Two p-tau217 outliers with stage III CTE had normal concentrations upon additional testing. Conclusions and Relevance The findings of this study suggest that plasma p-tau217 concentration is unlikely to be useful for the detection of CTE, but it does show utility for ruling out Aβ pathology in participants at risk for CTE.
Expanding Microgel Parameters to Model the Tumor Microenvironment and Examine Temozolomide Resistance in Glioblastoma
Payan, Brittany A. , Kattoor, Joel, Leon, Annika Carrillo Diaz De, Thompson, Gunnar, Molley, Tom, Sarkaria, Jann N., Harley, Brendan A.C. , Harley, Brendan A C , Thompson, Gunnar B. , Kilian, Kristopher Alan , Sarkaria, Jann N.

No container title available | July 9, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.64898/2026.07.08.737105 | PMID 42465419 Get It

ABSTRACT Glioblastoma (GBM) is a highly aggressive brain tumor with a five-year survival rate of less than 5%. The current standard of care established 20 years ago includes maximal surgical resection and administration of alkylating agent temozolomide (TMZ). GBM is highly invasive, and GBM cells that evade surgical resection can become resistant to TMZ and develop new aggressive secondary tumors. Post-relapse there are few treatment options available to patients. Tissue engineering approaches suggest the opportunity to develop in vitro models of the GBM tumor microenvironment that may accelerate the discovery of novel therapies for GBM. Here, we report the adaptation of hydrogel microdroplets (microgels) to encapsulate GBM cells in a tailorable 3D matrix to assess patters of growth and to screen TMZ drug response using patient-derived xenograft (PDX) specimens. We exploit a unique aspect of the microgel system to account for the cellular heterogeneity within the tumor microenvironment (TME). We combine cell-laden microgels generated from TMZ-resistant and TMZ responsive variants of the same PDX specimens to create heterogeneous populations with varying levels of drug sensitivity. We demonstrate a range of drug resistance phenotypes as a function of the ratio of TMZ-responsive to resistance cells and identify the population required for TMZ-resistance to overtake take the response. We then investigate the influence of tumor mimetic shifts in hyaluronic acid bioavailability and hypoxia on patterns of TMZ resistance. We show exposure to matrix-bound hyaluronan increases TMZ resistance and the glioma stem cell population in both cell variants. Lastly, we report an increase in TMZ sensitivity but divergent changes in the GSC subfraction for TMZ resistant vs responsive GBM in the presence of hypoxia. Together, we demonstrate the versatility of cell-laden microgel approach to replicate heterogenous tumor populations, model shifts in the tumor microenvironment, and rapidly screen therapeutic response.
Association of a Polygenic Risk Score with Diagnosis and Outcomes in Idiopathic Pulmonary Fibrosis
Kalra, S. , Grilli, Christopher, Coombes, Brandon J. , Armasu, Sebastian M. , Upjohn, D, Egan, Jan B. , Chen, Qingwen , Tern, Courtney , Zhang, Chengyue, Rose, Jonathan A. , Putman, Rachel, McDermott, Greg, Hsieh, Yuli Lily , Bublitz, Michele L., Carmona, Eva M. , Klee, Eric W, Lazaridis, K, Peljto, Anna L. , Schwartz, D A, Silverman, Edwin K. , Olson, Janet, Walker, T, Zamora, Ana C., Zein, Joe , Ortega, V E, Cohort, Tapestry, McDermott, Gregory C , Kalra, Sean S , Grilli, Christopher B , Armasu, Sebastian , Upjohn, David P , Hsieh, Yuli L , Lasky-Su, Jessica , Silverman, Edwin K , Allen, Richard J , Walker, T'Nita, Wain, Louise V , Zamora, Ana, Zein, Joe G, Hunninghake, Gary M , Moll, Matthew , Cho, Michael H , Carmona, Eva M , McDermott, Gregory , Coombes, Brandon J , Putman, Rachel K. , Kn, Lazaridis, Lasky‐Su, Jessica , Dudbridge, Frank , Allen, Richard J. , Olson, JA, Hunninghake, Gary M. , Ali, Ahmad Hafiz , Sekulić, Aleksandar , Athreya, Arjun P. , Clermont, Blake J, N, Brittany, Burnap, Graddy, Courtney B., Cahn, Elliot, Klee, Eric W. , Sicotte, Hugues , Ekpoh, Idara U., Frank, Jacob A., Bruflat, Jamie K., Kemppainen, Jennifer L., Samadder, Jewel, Presutti, John J, Leitzke, Jon W, Lazaridis, Konstantinos N. , Tree, Kristine M, Jones, Leila A, Bandel, Lorelei A. , Karow, Mary E., Peterson, Melanie M., Bublitz, Michelle L. , Morales-Rosado, Joel, Erwin, Nate P., Larson, Nicholas B. , Olson, Rory, Vierkant, Robert A., Pignolo, Robert J. , Safgren, Stephanie, Bagaria, Sanjay P. , Tian, Shulan , Kaggal, Suneetha, Walker, T'Nita S., Wilson, Tammy A., McAllister, Tammy M., Tan-Arroyo, Jennifer, Luehrs, Tony, Ortega, Victor E. , Chen, Wenan , Cho, Michael H.

American Journal of Respiratory and Critical Care Medicine | July 2, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.1093/ajrccm/aamag271 | PMID 42391602 Get It

Abstract Rationale Idiopathic Pulmonary Fibrosis (IPF) is characterized by chronic progressive pulmonary fibrosis and high mortality. Genetic markers, summarized into a polygenic risk score (PRS), associate with IPF in well-phenotyped research cohorts. Objectives To evaluate the performance of the PRS using real-world data from routinely captured electronic healthcare records. Methods We conducted an observational study evaluating the association of a PRS for IPF with electronic healthcare record diagnosis of IPF as well as lung transplant-free survival in four independent cohorts; the Mass General Brigham Biobank (MGBB), Mayo Clinic Biobank (MCBB), Mayo Clinic Tapestry Cohort (Tapestry), and U.K. Biobank (UKBB). We used multivariable logistic regression and multivariable Cox proportional hazards models adjusting for age, gender, and principal components of ancestry. The cohorts then underwent fixed and random effects meta-analysis. Measurements and Main Results Of 37,709; 44,195; 43,202; and 447,422 participants from MGBB, MCBB, Tapestry and UKBB respectively, 1,015 (2.7%) 2,879 (6.5%), 1,310 (3.0%), and 2,742 (0.6%) participants had an IPF diagnosis. Meta-analysis demonstrated a high-risk PRS associated with IPF diagnosis, OR 2.88 (95%CI 2.41-3.44) compared to all other individuals. A high-risk PRS also associated with the composite endpoint of mortality or lung transplant among those with an IPF diagnosis, HR 1.23(95%CI 1.11-1.35) compared to all other individuals. Conclusions A PRS can identify those at risk for an IPF diagnosis and mortality in biobank-scale data, which may have implications for clinical decisions. Further work is necessary to evaluate the utility of adding genetics in clinical settings.