Alexander Patricio Conway

All Publications

• Management of tenosynovial giant cell tumor: approved and investigational therapies. Expert review of anticancer therapy Conway, A. P., Lim, A., Schulte, B. C., Agulnik, M. 2026; 26 (7): 881-889

  Abstract

  Tenosynovial giant cell tumor (TGCT) is a rare, benign neoplasm driven by overexpression of colony-stimulating factor 1 (CSF-1), which recruits CSF-1 receptor (CSF-1 R)-bearing macrophages and other inflammatory cells to promote tumor formation. While surgery remains the first-line treatment for TGCT, many patients experience unresectable or recurrent disease with high morbidity, highlighting the need for effective systemic treatments.This review summarizes the molecular pathogenesis, diagnostic approach, and evolving systemic treatment landscape for TGCT, with a focus on treatments directed at CSF-1/CSF-1 R inhibition. Relevant literature published between 2005 and 2025 was identified through PubMed searches and manual review of reference lists. Clinical efficacy and safety data for approved and investigational CSF-1/CSF-1 R inhibitors, including pexidartinib, vimseltinib, and emerging agents, are discussed.Pexidartinib and vimseltinib demonstrate comparable efficacy in TGCT with objective response rates (ORR) of 39% and 40%, respectively, at week 25 of treatment; however, vimseltinib offers improved hepatic safety and tolerability, supporting its use as the preferred first-line systemic therapy. Emerging agents, including pimicotinib and emactuzumab, show potential for higher response rates and favorable safety profiles and may further reshape the TGCT treatment paradigm pending phase 3 trial results.

  View details for DOI 10.1080/14737140.2026.2620510

  View details for PubMedID 41557367

• Semaglutide improves metabolic dysfunction-associated steatohepatitis: A 10-year retrospective study. JGH open : an open access journal of gastroenterology and hepatology Shah, P., White, M., Sievert, A., Conway, A., Kneepkens, A., Sayuk, G., Lisker-Melman, M., Elwing, J. 2024; 8 (2): e13037

  Abstract

  Semaglutide has been studied in patients with metabolic dysfunction-associated steatohepatitis (MASH) due to potential benefit from weight loss on liver inflammation. However, preclinical studies suggest that MASH improvement may be independent of weight loss. We aim to assess the impact of semaglutide on MASH in relation to weight loss.This retrospective study included 420 patients with diabetes on semaglutide for at least 12 months between 2011 and 2022. Exclusion criteria were liver disease other than MASH, decompensated cirrhosis, malignancy, and bariatric surgery. Primary endpoints were clinically significant improvements in AST or ALT (mean difference > 6.3 U/L and > 10.6 U/L respectively). Statistical analysis included Student's t-test/ANOVA, Wilcoxon signed-rank test/Friedman test as appropriate, and binary logistic regression.Median duration of semaglutide was 22.5 months and 80% of patients received 1 mg/week. BMI improved by a mean (SD) of 1.9 points (2.8), weight by 13.3 lbs. (19.1), AST by 4.1 U/L (11.5), and ALT by 5.3 U/L (14.2). In 28% and 22% of patients respectively, AST and ALT had a clinically significant improvement. MASH scores (NFS, FIB4, APRI) improved after semaglutide (p < 0.001). No statistically significant differences in AST or ALT improvement were found when patients were stratified by BMI prior to semaglutide or when stratified by percentage of weight loss. On logistic regression, the duration of semaglutide and pretreatment APRI score increased the odds of clinically significant improvements of AST and ALT.Semaglutide treatment was associated with improvement in transaminases and MASH scores. Higher odds of positive semaglutide effects were observed with longer treatment duration and were independent of weight loss.

  View details for DOI 10.1002/jgh3.13037

  View details for PubMedID 38389719

  View details for PubMedCentralID PMC10883239

• Complications and risk factors after digital subtraction angiography: 1-year single-center study. Journal of cerebrovascular and endovascular neurosurgery Lauzier, D. C., Conway, A. P. 2023; 25 (4): 473-474

  View details for DOI 10.7461/jcen.2023.E2023.04.008

  View details for PubMedID 37423719

  View details for PubMedCentralID PMC10774678

• Screening for Pancreatic Ductal Adenocarcinoma: Are We Asking the Impossible? Cancer prevention research (Philadelphia, Pa.) Caldwell, K. E., Conway, A. P., Hammill, C. W. 2021; 14 (3): 373-382

  Abstract

  Pancreatic cancer is projected to become the second leading cause of cancer-related death in the United States by 2020. Because of this, significant interest and research funding has been devoted to development of a screening test to identify individuals during a prolonged asymptomatic period; however, to date, no such test has been developed. We evaluated current NIH spending and clinical trials to determine the focus of research on pancreatic cancer screening as compared with other cancer subtypes. Using statistical methodology, we determined the effects of population-based pancreatic cancer screening on overall population morbidity and mortality. Population-based pancreatic cancer screening would result in significant harm to non-diseased individuals, even in cases where a near-perfect test was developed. Despite this mathematical improbability, NIH funding for pancreatic cancer demonstrates bias toward screening test development not seen in other cancer subtypes. Focusing research energy on development of pancreatic screening tests is unlikely to result in overall survival benefits. Efforts to increase the number of patients who are candidates for surgery and improving surgical outcomes would result in greater population benefit.Prevention Relevance: For patients with pancreatic cancer, early stage detection offers the greatest survival benefit. However, the incidence of pancreatic cancer and associated mortality of pancreatic resections make development of a screening test a difficult, if not impossible, challenge.

  View details for DOI 10.1158/1940-6207.CAPR-20-0426

  View details for PubMedID 33148677

  View details for PubMedCentralID PMC8089111

• LRRK2 mutation alters behavioral, synaptic, and nonsynaptic adaptations to acute social stress. Journal of neurophysiology Guevara, C. A., Matikainen-Ankney, B. A., Kezunovic, N., LeClair, K., Conway, A. P., Menard, C., Flanigan, M. E., Pfau, M., Russo, S. J., Benson, D. L., Huntley, G. W. 2020; 123 (6): 2382-2389

  Abstract

  Parkinson's disease (PD) risk is increased by stress and certain gene mutations, including the most prevalent PD-linked mutation LRRK2-G2019S. Both PD and stress increase risk for psychiatric symptoms, yet it is unclear how PD-risk genes alter neural circuitry in response to stress that may promote psychopathology. Here we show significant differences between adult G2019S knockin and wild-type (wt) mice in stress-induced behaviors, with an unexpected uncoupling of depression-like and hedonia-like responses in G2019S mice. Moreover, mutant spiny projection neurons in nucleus accumbens (NAc) lack an adaptive, stress-induced change in excitability displayed by wt neurons, and instead show stress-induced changes in synaptic properties that wt neurons lack. Some synaptic alterations in NAc are already evident early in postnatal life. Thus G2019S alters the magnitude and direction of behavioral responses to stress that may reflect unique modifications of adaptive plasticity in cells and circuits implicated in psychopathology in humans.NEW & NOTEWORTHY Depression is associated with Parkinson's disease (PD), and environmental stress is a risk factor for both. We investigated how LRRK2-G2019S PD mutation affects depression-like behaviors, synaptic function, and intrinsic neuronal excitability following stress. In response to stress, the mutation drives abnormal synaptic changes, prevents adaptive changes in intrinsic excitability, and leads to aberrant behaviors, thus defining new ways in which PD mutations derail adaptive plasticity in response to stress that may contribute to disease onset.

  View details for DOI 10.1152/jn.00137.2020

  View details for PubMedID 32374202

  View details for PubMedCentralID PMC7311730