tbuckley/cabot-search huggingface dataset:
The “Quality Minute”—A New, Brief, and Structured Technique for Quality Improvement Education During the Morbidity and Mortality Conference
Authors: Rebecca L. Hoffman, Jon B. Morris, Rachel R. Kelz
Journal: JAMA Surgery (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Surgery journal
Patients with new-onset rheumatoid arthritis had increased risk for ischemic and nonischemic heart failure
Authors: Ami Schattner
Journal: Annals of Internal Medicine (2017)

Source Citation Mantel A, Holmqvist M, Andersson DC, Lund LH, Askling J. Association between rheumatoid arthritis and risk of ischemic and nonischemic heart failure. J Am Coll Cardiol. 2017;69:1275-85. 28279294
Neutropenia in Patients With Multiple Sclerosis Treated With Alemtuzumab
Authors: María Inés Gaitán, María Célica Ysrraelit, Jorge Correale
Journal: JAMA Neurology (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Circulating tumor cells (CTCs) and endothelial cells (CECs) in primary lung cancer
Authors: F. Tanaka, K. Yoneda, M. Hashimoto, T. Takuwa, S. Matsumoto, Y. Okumura, N. Kondo, S. Hasegawa, K. Fukuoka, T. Nakano
Journal: Journal of Clinical Oncology (2009)

11066 Background: Circulating tumor cell (CTC), a surrogate of distant metastasis, and circulating endothelia cell (CEC), a surrogate of angiogenesis, are potentially useful in the diagnosis of malignant tumors, but clinical significance of CTC/CEC in primary lung cancer (LC) remains unclear. Methods: A total of 342 cases who presented at our institute from August 2007 through December 2008 were included in the study. CTC/CEC in the peripheral blood (7.5mL/4.0mL) were captured and quantitatively evaluated with the “CellSearch” system without knowledge of clinical characteristics of each case. Results: In 42 (30.7%) of 137 LC cases, CTC in the peripheral blood was positive (CTC-count, more than 1 cell/7.5mL), and the maximum CTC-count was 62 cells. In 11 (18.3%) of 145 cases with non-malignant (NM) diseases, CTC was also positive; however, in NM cases, CTC-count was 1 (cell/7.5mL) in most CTC-positive cases and the maximun CTC-count was 2. Among LC cases, the incidence of case with CTC-positive (CTC-count, 1 or more) was highest in small cell carcinoma cases (7/10, 70.0%), followed by squamous cell carcinoma (9/22, 40.9%) and adenocarcinoma (23/94, 24.5%) cases; the incidence of CTC-positive case was significantly higher in stage IV cases (68.6%; p&lt;0.001), but it should be noted that CTC was positive in 17.4% of stage I cases and 15.4% of stage II cases. The mean CEC number (/4.0mL) was significantly higher in LC cases than in NM cases (97.5 versus 52.5, respectively; p=0.023), Among LC cases, the mean CEC significantly increased along with tumor progression (mean CEC for stage I, II, III, and IV cases: 58.7, 57.9, 83.4, and 178.4, respectively; p=0.002). Conclusions: CTC and CEC are useful clinical markers in LC, and its clinical value should be validated in future clinical trials. [Table: see text] No significant financial relationships to disclose.
Germinal centres in diagnostic labial gland biopsies of patients with primary Sjögren’s syndrome are not predictive for parotid MALT lymphoma development
Authors: Erlin A Haacke, Bert van der Vegt, Arjan Vissink, Fred K L Spijkervet, Hendrika Bootsma, Frans G M Kroese
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Objective</h3> Patients with primary Sjögren's syndrome (pSS) have an increased risk of developing non-Hodgkin's lymphoma (NHL), particularly parotid gland mucosa-associated lymphoid tissue (MALT) lymphomas. Presence of germinal centres (GCs) in labial gland biopsies has been suggested as predictive factor for NHL. We assessed whether presence of GCs is increased in labial gland biopsies from patients with pSS who developed parotid MALT lymphoma, the dominant NHL-subtype in pSS, compared with patients with pSS who did not develop lymphoma. <h3>Methods</h3> Eleven labial gland biopsies from patients with pSS that were taken prior to parotid MALT lymphoma development were compared with biopsies of 22 matched pSS controls (1:2) who did not develop lymphoma. Biopsies were evaluated for GCs (H&amp;E and Bcl6). <h3>Results</h3> Labial gland biopsies of pSS MALT lymphoma patients, revealed GCs in 2/11 (18%) H&amp;E sections and 3/11 (27%) Bcl6 stained sections. In controls, GCs were present in 4/22 (18%) of H&amp;E sections and 5/22 (23%) of Bcl6 stained sections. <h3>Conclusion</h3> Presence of GCs in labial gland biopsies does not differ between patients with pSS that develop parotid MALT lymphoma and patients with pSS who do not develop lymphoma. The presence of GCs in labial gland biopsies is therefore not a predictive factor for pSS-associated parotid MALT lymphomas.
Endothelin-1 Stimulates Vasoconstriction Through Rab11A Serine 177 Phosphorylation
Authors: Xue Zhai, M. Dennis Leo, Jonathan H. Jaggar
Journal: Circulation Research (2017)

Large-conductance calcium-activated potassium channels (BK) are composed of pore-forming BKα and auxiliary β1 subunits in arterial smooth muscle cells (myocytes). Vasoconstrictors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contraction, but mechanisms involved are unclear. Recent evidence indicates that BKα is primarily plasma membrane localized, whereas the cellular location of β1 can be rapidly altered by Rab11A-positive recycling endosomes. Whether vasoconstrictors regulate the multisubunit composition of surface BK channels to stimulate contraction is unclear.Test the hypothesis that ET-1 inhibits BK channels by altering BKα and β1 surface trafficking in myocytes, identify mechanisms involved, and determine functional significance in myocytes of small cerebral arteries.ET-1, through activation of PKC (protein kinase C), reduced surface β1 abundance and the proximity of β1 to surface BKα in myocytes. In contrast, ET-1 did not alter surface BKα, total β1, or total BKα proteins. ET-1 stimulated Rab11A phosphorylation, which reduced Rab11A activity. Rab11A serine 177 was identified as a high-probability PKC phosphorylation site. Expression of a phosphorylation-incapable Rab11A construct (Rab11A S177A) blocked the ET-1-induced Rab11A phosphorylation, reduction in Rab11A activity, and decrease in surface β1 protein. ET-1 inhibited single BK channels and transient BK currents in myocytes and stimulated vasoconstriction via a PKC-dependent mechanism that required Rab11A S177. In contrast, NO-induced Rab11A activation, surface trafficking of β1 subunits, BK channel and transient BK current activation, and vasodilation did not involve Rab11A S177.ET-1 stimulates PKC-mediated phosphorylation of Rab11A at serine 177, which inhibits Rab11A and Rab11A-dependent surface trafficking of β1 subunits. The decrease in surface β1 subunits leads to a reduction in BK channel calcium-sensitivity, inhibition of transient BK currents, and vasoconstriction. We describe a unique mechanism by which a vasoconstrictor inhibits BK channels and identify Rab11A serine 177 as a modulator of arterial contractility.
A Unique Program to Incorporate Volunteers Into a Nationwide Emergency Medical System
Authors: Eli Jaffe, Evan Avraham Alpert, Ari M. Lipsky
Journal: JAMA Surgery (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Surgery journal
MicroRNA-92a Mediates Endothelial Dysfunction in CKD
Authors: Fenqing Shang, Shen-Chih Wang, Chien-Yi Hsu, Yifei Miao, Marcy Martin, Yanjun Yin, Chih-Cheng Wu, Yun-Ting Wang, Gaihong Wu, Shu Chien, Hsien-Da Huang, Der-Cherng Tarng, Yan-Ting Shiu, Alfred K. Cheung, Po-Hsun Huang, Zhen Chen, John Y.-J. Shyy
Journal: Journal of the American Society of Nephrology (2017)

CKD is an independent risk factor for cardiovascular disease (CVD). The accumulation of uremic toxins in CKD induces oxidative stress and endothelial dysfunction. MicroRNA-92a (miR-92a) is induced by oxidative stress in endothelial cells (ECs) and involved in angiogenesis and atherosclerosis. We investigated a role for oxidative stress-responsive miR-92a in CKD. Our study of patients at three clinical sites showed increased serum miR-92a level with decreased kidney function. In cultured ECs, human CKD serum or uremic toxins (such as indoxyl sulfate), compared with non-CKD serum, induced the levels of miR-92a and suppressed the expression of miR-92a targets, including key endothelial-protective molecules. The antioxidant N-acetylcysteine inhibited these vasculopathic properties. In rats, adenine-induced CKD associated with increased levels of miR-92a in aortas, serum, and CD144+ endothelial microparticles. Furthermore, CD144+ microparticles from human uremic serum contained more miR-92a than those from control serum. Additional analysis showed a positive correlation between serum levels of miR-92a and indoxyl sulfate in a cohort of patients with ESRD undergoing hemodialysis. Collectively, our findings suggest that the uremic toxins accumulated in CKD can upregulate miR-92a in ECs, which impairs EC function and predisposes patients to CVD.
Mature overall survival (OS) results from the LUME-Meso study of nintedanib (N) + pemetrexed/cisplatin (PEM/CIS) vs placebo (P) + PEM/CIS in chemo-naïve patients (pts) with malignant pleural mesothelioma (MPM).
Authors: Anna K. Nowak, Federica Grosso, Nicola Steele, Silvia Novello, Sanjay Popat, Laurent Greillier, Tom John, Natasha B. Leighl, Martin Reck, Nick Pavlakis, Jens Benn Soerensen, David Planchard, Giovanni Luca Ceresoli, Brett Gordon Maxwell Hughes, Julien Mazieres, Mark A. Socinski, Derek Velema, Ute von Wangenheim, Nassim Morsli, Giorgio V. Scagliotti
Journal: Journal of Clinical Oncology (2017)

8506 Background: LUME-Meso is a Phase (Ph) II/III, double-blind, randomized study. N targets MPM by inhibiting VEGFR 1–3, PDGFR α/β, FGFR 1–3, Src and Abl kinases. Primary analysis of the Ph II data demonstrated improved progression-free survival (PFS; hazard ratio [HR]=0.56; 95% confidence interval [CI] 0.34–0.91; p=0.017). Mature Ph 2 OS and updated PFS results are reported here. Methods: Pts with unresectable MPM (ECOG PS 0–1) were stratified by histology (epithelioid/biphasic) and randomized 1:1 to receive ≤6 cycles PEM (500 mg/m 2 )/CIS (75 mg/m 2 ) Day 1 + N or P (200 mg bid, Days 2–21), followed by N or P monotherapy until progression or toxicity. The primary endpoint was PFS. The primary OS analysis and updated PFS analysis were performed as predefined. Results: 87 pts were randomly assigned (N=44, P=43). OS benefit favored N over P treatment (HR=0.77; 95% CI 0.46–1.29; p=0.319; 62 [71%] OS events) and was greatest in epithelioid pts (HR=0.70; 95% CI 0.40–1.21; p=0.197) with a median (m) OS gain of 5.4 months (mOS [95% CI]: 20.6 [16.2–28.8] N vs 15.2 [12.2–23.6] P). Updated PFS results (HR=0.54; 95% CI 0.33–0.87; p=0.010) also showed greatest benefit for epithelioid pts (HR=0.49; 95% CI 0.30–0.82; p=0.006) with a mPFS gain of 4.0 months (mPFS [95% CI]: 9.7 [7.2–12.4] N vs 5.7 [5.5–7.0] P). Improved forced vital capacity, objective response rates and duration of response were also observed with N treatment. Drug-related adverse events (AEs) in N- vs P-treated pts were 97.7% vs 97.6%. Grade ≥3 AEs of note included neutropenia (27.3% vs 4.9%), ALT (11.4% vs 0) and GGT (6.8% vs 0) elevations, and diarrhea (6.8% vs 0). AEs led to trial discontinuation in only 3 (6.8%) N vs 7 (17.1%) P pts. Conclusions: Mature Ph II OS data show that adding N to standard 1 st -line treatment gives a strong signal towards improved OS. Updated PFS confirmed the primary analysis; AEs were manageable. The greatest clinical benefit was observed in pts with epithelioid histology. Median survival of 20.6 months in epithelioid pts treated with N is unprecedented in advanced MPM trials. Ph III is actively recruiting in this pt population. Clinical trial information: NCT01907100.
ASCEND-8: A Randomized Phase 1 Study of Ceritinib, 450 mg or 600 mg, Taken with a Low-Fat Meal versus 750 mg in Fasted State in Patients with Anaplastic Lymphoma Kinase (ALK)-Rearranged Metastatic Non–Small Cell Lung Cancer (NSCLC)
Authors: Byoung Chul Cho, Dong-Wan Kim, Alessandra Bearz, Scott A. Laurie, Mark McKeage, Gloria Borra, Keunchil Park, Sang-We Kim, Marwan Ghosn, Andrea Ardizzoni, Evaristo Maiello, Alastair Greystoke, Richard Yu, Karen Osborne, Wen Gu, Jeffrey W. Scott, Vanessa Q. Passos, Yvonne Y. Lau, Anna Wrona
Journal: Journal of Thoracic Oncology (2017)
Characterization and in vitro release studies of oral microbeads containing thiolated pectin–doxorubicin conjugates for colorectal cancer treatment
Authors: Kamonrak Cheewatanakornkool, Sathit Niratisai, Somkamol Manchun, Crispin R. Dass, Pornsak Sriamornsak
Journal: Asian Journal of Pharmaceutical Sciences (2017)

Novel oral microbeads were developed based on a biopolymer-drug conjugate of doxorubicin (DOX) conjugated with thiolated pectin via reducible disulfide bonds. The microbeads were fabricated by ionotropic gelation with cations such as Al
Detection of Lung Cancer and EGFR Mutation by Electronic Nose System
Authors: Dekel Shlomi, Manal Abud, Ori Liran, Jair Bar, Naomi Gai-Mor, Maya Ilouze, Amir Onn, Alon Ben-Nun, Hossam Haick, Nir Peled
Journal: Journal of Thoracic Oncology (2017)
Inhibition of survivin expression by small interfering RNA (siRNA) in brain tumor cell lines.
Authors: Hye Lim Jung, Jaewon Choi, Yoo Kyung Hwang, Dong Hyun Kim, Keon Hee Yoo, Ki Woong Sung, Hong Hoe Koo
Journal: Cancer Research (2005)

63  Survivin, a member of inhibitor of apoptosis gene (IAP) family, has been proposed as a promising target for new anticancer interventions. Here we report an application of RNA interference with small interfering RNA (siRNA) of survivin to human brain tumor cell lines. The purposes of this study are to investigate the ability and biological effects of siRNA induced inhibition of survivin, and to determine the potentiality of survivin siRNA as a new therapeutic tool in brain tumors. The survivin mRNA expression was measured by real-time RT-PCR in 7 brain tumor cell lines (Daoy, T98G, U118MG, U87MG, A172, IMR32, SH-SY5Y), and one lung adenocarcinoma cell line A549 as a positive control. Three brain tumor cell lines including Daoy (medulloblastoma), U87MG (glioblastoma cell line with wild type p53) and A172 (glioblastoma cell line with mutant p53) were transfected with siRNA oligonucleotides of survivin. Survivin mRNA and protein expressions were measured by real-time RT-PCR and Western blot analysis after 24, 48 and 72 hours of treatment with survivin siRNA, and then compared to nonsense siRNA treated cells. The effects on cytotoxicity and induction of apoptosis were assessed with MTT assay and FACS analysis using Annexin V, before and after treatment with survivin siRNA. High survivin expression was detected in all 7 brain tumor cell lines normalized with A549. After 48 hours of treatment with siRNA of survivin, survivin mRNA level was reduced by 39, 65 and 77% in U87MG, A172 and Daoy cell line, respectively, and protein expression was reduced by 30% in all 3 cell lines. Knockdown of survivin by siRNA induced 32, 32 and 38% of cell death in U87MG, A172 and Daoy cell line, respectively, after 72 hrs of treatment with siRNA of survivin. Knockdown of survivin by siRNA induced 5% of apoptosis in U87MG after 24 hrs of transfection with siRNA of survivin. The effect of siRNA was independent of p53 gene mutation. Our findings suggest that survivin may play an important role in oncogenesis of brain tumors, and survivin-specific siRNA could be a selective therapeutic tool to kill medulloblastoma and glioblastoma cells regardless of the presence or absence of wild-type p53 genes.
Preventing Human Immunodeficiency Virus Acquisition in Youth—Generations at Risk
Authors: Lynne M. Mofenson
Journal: JAMA Pediatrics (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Re: Philipp Mandel, Felix Preisser, Markus Graefen, et al. High Chance of Late Recovery of Urinary and Erectile Function Beyond 12 Months After Radical Prostatectomy. Eur Urol 2017;71:848–50
Authors: Jae Heon Kim, Bora Lee, Benjamin I. Chung
Journal: European Urology (2017)
Abstract 17961: Conundrum of Sudden Death With a Psychiatric Diagnosis: Disease Process or Culprit Drug?
Authors: Audrey Uy-Evanado, Kyndaron Reinier, Carmen Teodorescu, Eloi Marijon, Kumar Narayanan, Harpriya Chugh, Gregory A Nichols, Karen Gunson, Jonathan Jui, Sumeet S Chugh
Journal: Circulation (2013)

Introduction: Mechanisms of sudden cardiac death (SCD) in patients with a psychiatric diagnosis could be related to clinical risk factors/comorbidities, QT interval-prolonging therapeutic drugs or ...
Phase III study of aldoxorubicin vs investigators' choice as treatment for relapsed/refractory soft tissue sarcomas.
Authors: Sant P. Chawla, Kristen N. Ganjoo, Scott Schuetze, Zsuzsanna Papai, Brian Andrew Van Tine, Edwin Choy, David A. Liebner, Mark Agulnik, Shanta Chawla, Scott Wieland, Daniel J. Levitt
Journal: Journal of Clinical Oncology (2017)

11000 Background: Aldoxorubicin (A) is a novel drug that binds covalently to albumin in the circulation, accumulates in tumors and releases doxorubicin in the acidic tumor environment. It has demonstrated enhanced antitumor activity in several murine models and in a phase IIb STS study when compared with doxorubicin. Trial Design: Phase III open-label study evaluating efficacy and safety of A compared to investigators' choice (IC) of treatment in subjects with soft tissue sarcomas (STS) who have relapsed or were refractory to prior chemotherapy. Objectives: (1) Primary: Efficacy of A vs IC: progression-free survival (PFS); (2) Secondary: Efficacy of A vs IC: tumor response (ORR), disease control rate (DCR; CR+PR+SD &gt; 4 months), overall survival (OS) and safety. Methods: A: 350 mg/m 2 (260 mg/m 2 dox. equiv.) iv q3 wks. IC drugs: dacarbazine, doxorubicin, pazopanib, ifosfamide, gemcitabine/docetaxel administered per package insert or study site's standard practice; provided, with G-CSF, by the sponsor. AEs, serum chemistries, CBCs, EKG and ECHOs obtained frequently. CT scans every 6 weeks for 30 weeks, then every 12 weeks; analyzed using RECIST 1.1 by Blinded Independent Central Review. Results: Randomized 433 subjects; 79 countries; 313 (72%) in North America (NA) and 121 (28%) in Rest of World (ROW). Leiomyosarcoma 42.5%, liposarcoma 15%, synovial sarcoma 9%, others 33.5%, L-sarcomas (lipo+leiomyo) 57.5%. Median PFS Total Pop. (months): A= 4.06; IC= 2.96; p = 0.12; HR = 0.82 (0.64-1.06). Median PFS NA (months): A= 4.21; IC= 2.96; p = 0.027; HR = 0.71 (0.53-0.97). Median PFS L-sarcomas (months): A= 5.32; IC= 2.96; p = 0.007; HR = 0.62 (0.44-0.88). DCR Total Pop.(%): A= 30.3; IC= 20.9; p = 0.028; DCR NA (%): A= 32.9; IC= 19.2; p = 0.007; DCR L-Sarcomas (%): A= 37.5; IC= 23.0; p = 0.018. ORR and OS will be reported. TEAEs gr 3 or 4 (%): A= 61.0; IC= 46.4. Trtmt Rel. SAEs (%): A= 27.0; IC= 14.0. TEAEs leading to Drug Discontinue (%): A= 4.2; IC= 6.3. Trtmt Related Deaths (#); A= 3; IC= 0; LVEF &lt; 50% expected (%): A= 2.8%;Dox = 12.8%. Conclusions: Aldox is an active, well-tolerated drug for treating relapsed or refractory STS and is significantly better than standard treatments for patients with L-sarcomas. Clinical trial information: NCT02049905.