tbuckley/cabot-search huggingface dataset:
SURG-20. CRANIOTOMY AND SURVIVAL FOR PRIMARY CENTRAL NERVOUS SYSTEM LYMPHOMA
Authors: Ali Rae, Amol Mehta, Michael Cloney, Connor Kinslow, Tony Wang, Govind Bhagat, Peter Canoll, George Zanazzi, Michael Sisti, Sameer Sheth, E Sander Connolly, Guy McKhann, Jeffrey Bruce, Fabio Iwamoto, Adam M Sonabend
Journal: Neuro-Oncology (2017)

Cytoreductive surgery is considered controversial and high-risk for primary central nervous system lymphoma (PCNSL). We investigated survival following craniotomy or biopsy for PCNSL. The National Cancer Database-Participant User File (NCDB, n=8,936), Surveillance, Epidemiology, and End Results Program (SEER, n=5,615), and an institutional series (IS, n=132) were used. We investigated the relationship among craniotomy, prognostic factors, and survival for PCNSL. In NCDB, craniotomy was associated with increased median survival over biopsy (19.5 vs. 11.0 months), independent of subsequent radiation and chemotherapy (HR 0.83, p<0.001). We found a similar trend with survival for craniotomy vs. biopsy in the IS (HR 0.68, p = 0.15). In SEER, gross total resection (GTR) was associated with increased median survival over biopsy (29 vs. 10 months, HR 0.68, p<0.001). The survival benefit associated with craniotomy was greater within Recursive Partitioning Analysis (RPA) class 1 group in NCDB (95.1 v. 29.1 months, HR 0.66, p<0.001), but was smaller for RPA 2-3 (14.9 vs. 10.0 months, HR 0.86, p<0.001). A surgical risk category (RC) considering lesion location and number, age, and frailty was developed. Craniotomy was associated with increased survival versus biopsy for patients with low-RC (133.4 vs. 41.0 months, HR 0.33, p=0.01), but not high-RC in the IS. Craniotomy is associated with increased survival over biopsy for PCNSL in three datasets. Prospective studies are necessary to adequately evaluate this relationship. Such studies should focus on patients most likely to benefit from cytoreductive surgery; i.e. those with favorable RPA and RC.
P2.02-054 Thymidylate Synthase Promotes Epithelial-To-Mesenchymal Transition and Aggressiveness in NSCLC
Authors: P. Ceppi, A. Siddiqui, M.E. Vazakidou, A. Schwab, F. Napoli, I. Rapa, M. Volante, T. Brabletz
Journal: Journal of Thoracic Oncology (2017)
MA 08.10 Favorable Clinical Status Predicts Benefit From Early-Palliative Cares &amp; OS Improvement in NSCLC: A Randomized Clinical Study
Authors: O. Arrieta, L. Ramirez-Tirado, D. Michel-Tello, J. Turcott, J. Martinez-Hernandez, A. Beck-Magaña, E. Montes-Servin, E. Verastegui, S. Allende-Perez
Journal: Journal of Thoracic Oncology (2017)
CSIG-40. PHOSPHOGLYCERATE MUTASE 1 (PGAM1) ACTIVATES DNA DAMAGE REPAIR VIA REGULATION OF WIP1 ACTIVITY
Authors: Joydeep Mukherjee, Shigeo Ohba, Tor-Christian Aase Johannessen, Chatla Kamalakar, Russell O Pieper
Journal: Neuro-Oncology (2017)

In normal cells, phosphoglycerate mutase 1(PGAM1) converts 3-phospho glycerate to 2-phospho glycerate. PGAM1, however is overexpressed in different forms of cancer and has been suggested to have additional functions beyond its role in metabolism. We here report that PGAM1 is overexpressed in GBMs and by indirectly increasing the efficiency of DNA damage repair, increases resistance to radiation (IR) and temozolomide (TMZ) treatment. Specifically, suppression of PGAM1 in multiple GBM cell lines decreased gH2AX foci, increased apoptosis and decreased clonagenicity relative to control cells following exposure to radiation and TMZ. In control GBM cells PGAM1 co-immunoprecipitated with WIP1, a phosphatase reported to bind and dephosphorylate ATM, Chk1, and Chk2. Binding of PGAM1 biochemically inactivated the phosphatase activity of WIP1 leaving ATM and its downstream substrates phosphorylated and active in DNA repair. In contrast, in isogenic PGAM1 knockdown cells, WIP1 bound and dephosphorylated ATM at s1981, further limiting the downstream phosphorylation of Chk1, Chk2 and cdc25C (s216). Furthermore, genetic or pharmacological ablation of WIP1 in PGAM1 knockdown cells rescued ATM, Chk1 and Chk2 phosphorylation, downstream signaling, and IR/TMZ sensitivity. Consistent with these observations, mice intracranially implanted with PGAM1 knockdown GBM cells and treated with TMZ and IR had longer survival than similarly treated mice implanted with matched control cells. These results therefore define the metabolic enzyme PGAM1 as an activator of DNA damage repair pathway and a therapeutically targetable regulator of drug response in GBM.
Sidedness influences prognosis in colon cancer patients receiving an adjuvant therapy. A GISCAD analysis from three randomized trials including 5234 patients
Authors: F. Gelsomino, V. Torri, A. Zaniboni, R. Labianca, A. Sobrero, D. Poli, L. Frontini, S. Cascinu
Journal: Annals of Oncology (2017)
CSIG-36. DECREASED CAPICUA (CIC) ENHANCES ONCOGENIC ETV4 SIGNALING IN A MOUSE MODEL OF ASTROCYTOMA AND GLIOMA STEM CELLS
Authors: Annmarie Ramkissoon, Amanda Smith, Alexander Merk, Ralph Salloum, Ying-Wooi Wan, Mutsuko Minata, Ichiro Nakano, Christine Fuller, Zhandong Liu, Lionel M L Chow
Journal: Neuro-Oncology (2017)

High grade astrocytomas are brain tumors that currently have no cure. Understanding mechanisms that sustain and help them to resist therapy are urgently necessary. The capicua (CIC) transcriptional repressor is a target of receptor tyrosine kinase (RTK) signaling. Upon phosphorylation by RTK signaling, CIC loses its repressor activity. We hypothesize that loss of CIC activity and the subsequent activation of the genes it normally represses plays an important role in astrocytoma biology. In humans, CIC inactivating mutations are found in a subset of gliomas, specifically oligodendrogliomas associated with 1p/19q chromosomal losses. In astrocytoma and oligodendroglioma without 1p/19q loss, CIC mutations are rare. Given the genetic heterogeneity of gliomas, it is conceivable that subpopulations within astrocytomas may utilize different mechanisms to ablate CIC activity, for example through RTK signaling. Using a novel mouse model of astrocytoma with enhanced RTK signaling, we identified that CIC expression was decreased by 50–70% compared to normal cortex and correlated with significant increased RNA and protein levels of known oncogenic signals including E-twenty six transformation specific (ETS)-related transcription factor 4 (ETV4) and matrix metalloproteinase 2 (MMP2). Mouse astrocytoma tumor spheres also had lower CIC protein levels and higher protein levels of ETV4 and MMP2 compared to normal neurospheres. Low CIC-expressing human astrocytoma stem cells were also highly expressing ETV4 and MMP2. Functional effects of CIC knockdown in mouse astrocytoma tumor spheres included enhanced self-renewal and invasiveness which also correlated with increased ETV4 and MMP2. Intracranial tumors generated from injection of control or CIC knockdown glioma stem cells into mouse brain led to no difference in Kaplan-Meier survival curves however, histological analysis suggested that the CIC knockdown tumors displayed evidence of enhanced pleomorphism, spindle shaped cells and staghorn vasculature. These studies highlight that even when not mutated, CIC activity may be dynamically regulated to modulate astrocytoma biology.
18F-FDG PET/CT of Generalized Arteritis
Authors: Anna Margherita Maffione, Lucia Rampin, Gaia Grassetto, Maria Cristina Marzola, Sotirios Chondrogiannis, Domenico Rubello, Patrick M Colletti
Journal: Clinical Nuclear Medicine (2017)

A 75-year-old man presented with significant weight loss, persistent cough, single episode of frontotemporal pulsatile headache, and leg weakness. A paraneoplastic syndrome was suspected, and F-FDG PET/CT was performed. Diffuse, moderate-to-intense tracer symmetrical uptake of many large and medium arteries was unexpectedly noted. The peculiarity of this case is the extensive involvement of both large and medium head and neck and extremity vessels, whereas the aorta was relatively spared.
“Weekend effect” is not reduced by clinical standards designed to tackle it, study finds
Authors: Abi Rimmer
Journal: BMJ (2017)

Clinical standards designed to reduce mortality at the weekend have not made any overall difference, researchers have found.

In a paper published in the Emergency Medicine Journal , researchers from the University of Manchester said that four NHS priority standards for emergency care have not reduced excess deaths on Saturdays and Sundays.1

The four standards were originally developed in 2013 by the NHS Services, Seven Days a Week Forum. They were introduced in 2015 and form part of the government’s aim to reduce the “weekend effect”—when patients admitted to hospital at a weekend have greater mortality than patients admitted on weekdays—through increased …
RARE-09. MINIMALLY TOXIC MULTIMODAL AND POLYPHARMACOLOGICAL THERAPY IN TREATMENT OF DIFFUSE MIDLINE GLIOMA
Authors: Michael Salacz, Marc-Eric Halatsch, Georg Karpel-Massler, Richard Kast
Journal: Neuro-Oncology (2017)

Malignant gliomas are among the most deadly human cancers. One subtype, diffuse midline glioma (DMG), WHO Grade IV, is characterized by the H3 K27M histone mutation which is mutually exclusive with the favorable MGMT promoter methylation, IDH 1/2 mutation and EGFR amplification. DMGs have limited treatment options: surgery is typically subtotal or biopsy-only given their midline location; radiotherapy is not curative, and chemotherapy has a limited role. To report a novel anti-cancer treatment utilizing non-cytotoxic, repurposed drugs (modified CUSP/MTZ) along with the Nativis Voyager® System in a patient with H3 K27M mutated DMG. A young patient presented with a rapidly progressing right thalamic enhancing mass with extension to the right frontal lobe and midbrain; initial biopsy demonstrated glioblastoma. Subsequent H3 K27M mutation positivity defined this as a DMG. Initial treatment included laser thermotherapy to the right thalamic tumor followed by standard concurrent radiotherapy and temozolomide. Post-radiation imaging revealed several new foci of enhancement in the right frontal portion of the tumor, progressing despite adjuvant Temozolomide on subsequent imaging and associated with clinical decline. Biopsy demonstrated persistent/recurrent glioma. Salvage therapy included repurposed non-cytotoxic drugs (modified CUSP/MTZ: alendronate, aprepitant, auranofin, celebrex, minocycline, pantoprazole, quetiapine, sertraline, telmisartan and valproic acid) dosed in a metronomic fashion with the Nativis Voyager® system. Over the following six months, serial MRIs demonstrated a near complete remission of the enhancing tumor. Steady clinical improvement and no significant toxicity to treatment were observed. We believe this to be the first report of (initial) successful treatment of a patient with H3 K27M mutated DMG utilizing modified CUSP/MTZ along with the Nativis Voyager® system. We are in the planning stages for a pilot study with this approach for patients with H3 K27M mutated tumors which includes pediatric diffuse pontine gliomas.
P1.03-005 Phase 2 Study of Ceritinib in Patients with ALK+ NSCLC with Prior Alectinib Treatment in Japan: ASCEND-9
Authors: H. Horinouchi, M. Maemondo, T. Hida, M. Takeda, K. Hotta, F. Hirai, Y. Kim, S. Matsumoto, T. Mitsudomi, T. Seto, S. Moizumi, K. Tokushige, B. Hatano, M. Nishio
Journal: Journal of Thoracic Oncology (2017)
A doença dos legionários associada a viagens na Europa: 2002
Authors: K D Ricketts, C Joseph
Journal: Eurosurveillance (2004)

Vinte e sete paises notificaram 676 casos de doenca dos legionarios associada a viagens a rede de vigilância EWGLINET e 94 clusters foram detectados. O teste da antigenuria na urina permitiu diagnosticar 80,5% de todos os casos. 
O periodo medio entre o inicio da doenca e a notificacao de casos foi de 20,5 dias, em 2002,comparado com os 51,5 dias registados em 1993. 
Desde a introducao das recomendacoes do EWGLI, em 1 de Julho 2002, ate ao fim desse ano, 37 relatorios finais de investigacao foram mandados atempadamente (ate seis semanas) e considerados satisfatorios pelos respectivos centros coordenadores de vigilância. Em 2002 foram investigadas 274 possiveis fontes de infeccao. 
As actividades turisticas dos principais notificadores a rede EWGLINET influenciaram o periodo de pico de actividade e permitiram definir os paises que efectuaram maior numero de investigacoes.
Metastatic duodenal germ cell tumor diagnosed with endoscopic ultrasound
Authors: Nayana George, Abhilash Perisetti, Saikiran Raghavapuram, Debdeep Banerjee, Enoch Kuo, Benjamin Tharian
Journal: Endoscopy (2017)

Testicular tumors are the most common solid tumors reported in young males aged 15 – 35 years [1] [2]. These tumors frequently metastasize to retroperitoneal lymph nodes, but only 5 % of these tumors seed the gastrointestinal (GI) tract [3] [4], with the duodenum being the least common site (1.4 %) [4]. Local extension from the retroperitoneal lymph node into the GI tract is the common method of spread.
IMMU-49. TARGETING CCR2 SIGNALING IN PEDIATRIC MEDULLOBLASTOMA
Authors: Amy-Lee Bredlau, Ramin Eskandari, Fraser Henderson, Libby Kosnik Infinger, Daniel G McDonald, Kenneth N Vanek, Sunil J Patel, Samuel H Cheshier, Stephen Lowe, David Cachia, Arabinda Das
Journal: Neuro-Oncology (2017)

As chemokines are important mediators of cell–cell communication, we sought to identify commonly expressed chemokines in mouse and human medulloblastoma (MB) lines as surrogates to microglia/MB tumor cell interactions. We found CCL2 (chemokine (C-C motif) ligand 2) messenger RNA to be expressed by medulloblastoma lines. However, these lines did not express the CCL2 receptor, CCR2, which was found on microglia. The MP-1 medulloblastoma cell line is known to have low basal levels of CCL2. Hence, we overexpressed CCL2 plasmid with GFP tagging in the MP-1 medulloblastoma line to investigate the hypothesis that medulloblastoma-secreted CCL2 interacts with microglia to affect medulloblastoma growth and invasion. In medulloblastoma–microglia co-culture models, we observed an increase in the proliferation of CCL2-overexpressing clones. ELISA protein analyses revealed that interleukin-6 (IL-6) was consistently increased in the co-culture. Recombinant IL-6 enhanced the invasion of medulloblastoma cells when these were cultured alone, whereas a neutralizing antibody to IL-6 attenuated the microglia-stimulated invasion. This study has uncovered a mechanism by which medulloblastoma cells exploit microglia (M2-phenotype) for increased invasion. Specifically, medulloblastoma-derived CCL2 acts upon CCR2-bearing tumor-associated microglias (TAMs), which produce IL-6 to stimulate medulloblastoma cells, in a CCL2/CCR2/IL-6 loop. We targeted this loop by combining radiation therapy with 4-1BB (CD-137) monoclonal antibody (mAb), as CD-137 is involved in regulation of immune cell proliferation and survival. We re-educated microglia cells toward a cytotoxic M1-like phenotype and amplified effective anti-tumor immune responses in in vitro co-culture models. ELISA spot shows treatment with 50 ng of 4-1BB (CD137) + 1Gy X-ray radiation converted the microglia from M2 to M1 phenotype via a decrease in CCR2. This treatment induces the M1 phenotype microglia to induce MP-1 cell death. Based on our results, the use of 4-1BB mAb plus low-dose single fraction radiation may prove to be beneficial for the treatment of medulloblastoma.
OA 09.07 Clonality of c-MET Copy Number Gain as a Determinant of Primary TKI Resistance in EGFR-Mutant NSCLC
Authors: G. Lai, R. Nahar, T. Lim, X. Kwang, P. Liew, J. Lim, Z.W. Aung, A. Takano, W. Lim, D. Lau, W.L. Tan, M. Ang, C.K. Toh, B.S. Tan, A. Devanand, C.W. Too, A. Gogna, B.H. Ong, T. Koh, R. Kanesvaran, Q.S. Ng, A. Jain, J. Yuan, T. Lim, A. Lim, A. Hillmer, W. Zhai, G. Iyer, E.H. Tan, W. Tam, D. Tan
Journal: Journal of Thoracic Oncology (2017)
PL 02.06 The IASLC Lung Cancer Staging Project: Analysis of Resection Margin Status and Proposals for R Status Descriptors for Non-Small Cell Lung Cancer
Authors: J. Edwards, K. Chansky, L. Shemanski, P. Van Schil, H. Asamura, R. Rami-Porta
Journal: Journal of Thoracic Oncology (2017)
Incorrect Absolute Risk Values
Authors: John Santelli, Ronald Bayer, Robert Klitzman
Journal: JAMA (2015)

Michael H. Criqui, MD, MPH; Julie O. Denenberg, MA; Joachim H. Ix, MD, MAS; Robyn L. McClelland, PhD; Christina L. Wassel, PhD; Dena E. Rifkin, MD, MS; Jeffrey J. Carr, MD, MS; Matthew J. Budoff, MD; Matthew A. Allison, MD, MPH
P1.01-053 Italian Nivolumab Expanded Access Programme (EAP): Data from Patients with Advanced Non-Squamous NSCLC and Brain Metastases
Authors: L. Crinò, P. Bidoli, P. Ulivi, E. Minenza, E. Cortesi, M. Garassino, F. Cappuzzo, F. Grossi, G. Tonini, M.G. Sarobba, G. Pinotti, G. Numico, R. Samaritani, L. Ciuffreda, A. Frassoldati, M.B. Bregni, A. Santo, F. Piantedosi, A. Illiano, F. De Marinis, A. Delmonte
Journal: Journal of Thoracic Oncology (2017)
Use of scalp-cooling device to prevent alopecia for breast cancer patients receiving chemotherapy: a single-Institution prospective study
Authors: T. Giarratano, M.V. Dieci, V. Guarneri, D. Grosso, M. Zanocco, G. Faggioni, C. Falci, C. Ghiotto, C.A. Giorgi, G. Griguolo, E. Mioranza, G. Pernice, G. Vernaci, P. Conte
Journal: Annals of Oncology (2017)
MA 19.06 Multiple Mechanisms Contribute to Downregulation of Tumor Suppressor microRNAs in Malignant Pleural Mesothelioma
Authors: M. Williams, M. Kirschner, Y.Y. Cheng, K. Sarun, B. Mccaughan, S. Kao, N. Van Zandwijk, G. Reid
Journal: Journal of Thoracic Oncology (2017)
TMOD-45. DEFINING THE ROLE OF MUTANT IDH IN GLIOMA INITIATION
Authors: Beatrice Philip, Mark Silvis, Diana Yu, Clifford Shin, James Robinson, Joshua Sonnen, Adam Welker, Matthew VanBrocklin, Howard Colman, Sheri Holmen
Journal: Neuro-Oncology (2017)

Gliomas are the most common primary central nervous system tumor but the molecular mechanisms responsible for their development and progression are not completely understood. Genomic analyses identified a mutation at codon 132 in the isocitrate dehydrogenase 1 (IDH1) gene in ~80% of grade II-III gliomas. In patient tumors, IDH1R132H mutations co-exist with TP53 mutations and inactivating alterations of alpha thalassemia/mental retardation syndrome X-linked (ATRX). Some of these tumors also have amplification of loci encoding platelet-derived growth factor receptor A (PDGFRA), cyclin dependent kinase 4 (CDK4), and MYC. Loss of the chromosomal region surrounding phosphatase and tensin homolog deleted on chromosome ten (PTEN) is associated with the progression of low grade glioma to grade IV glioblastoma. The functional requirement of these alterations for glioma initiation has previously been hampered by difficulties in generating autochthonous mouse models harboring mutant IDH. In this study, we used the RCAS/TVA glioma mouse model to evaluate the effect of these clinically-relevant genetic alterations on the growth of astrocytes in vitro and glioma development in vivo. In the context of mutant IDH1 expression, increased proliferation and anchorage-independent growth was observed in astrocytes derived from these mice, relative to wild type IDH-expressing cells. Similar to patient tumors, mutant IDH elevated intracellular (R)-2-hydroxyglutarate (2-HG) levels and reduced NADPH, which results from the conversion of α-KG to 2-HG. Postnatal delivery of IDH1R132H to Nestin-expressing cells in vivo initiated neoplasms that resembled human gliomas harboring mutant IDH1, both genetically and histologically. These results functionally validate the genomic alterations observed in the human disease and suggest that mutant IDH is a bona fide glioma oncogene. This model will aid in furthering our understanding of the biology of mutant IDH1-driven gliomas and is ideally suited for assessing rational therapeutic strategies designed to combat this deadly disease.
Epidemia de hepatitis A en Puglia, Italia, 1996
Authors: P Malfait, P L Lopalco, S Salmaso, C A Germinario, G Salamina, M Quarto, S Barbuti, R Cipriani, A Mundo, G Pesole
Journal: Eurosurveillance (1996)

En la region de Puglia, al sudeste de Italia (poblacion: 4 millones), el numero de notificaciones de infecciones por virus de la hepatitis A (VHA) aumenta en ciclos bianuales. En 1992 se observo un gran brote, pero no se llevo a cabo ninguna investigacion epidemiologica. La mayoria de los casos se notifican al comenzar el ano (figura 1). A finales de 1995, Puglia se unio al proyecto nacional de informatizacion del sistema de vigilancia de enfermedades infecciosas (Sistema Informatizzato sulle Malattie Infettive, SIMI). La informatizacion empezo a funcionar en Puglia el 1 de enero de 1996, facilitando el intercambio y analisis puntual de la informacion.
La prévention de la rubéole congénitale : un défi pour chaque pays d'Europe
Authors: N Crowcroft, R G Pebody
Journal: Eurosurveillance (2004)

Ce numero d'Eurosurveillance porte sur l'epidemiologie et le controle du syndrome de rubeole congenitale (SRC) en Europe. Il montre qu'en depit de l'existence depuis plusieurs annees d'un vaccin sur et efficace, le SRC - consequence d'une rubeole en cours de grossesse - reste un probleme de sante publique important tant dans l'Union Europeenne que dans la region Europe de l'OMS. Les articles presentes montrent les defis que represente la mise en place des programmes de vaccination nationaux en Europe. Ils illustrent les variations en termes de morbidite et en termes d'acces aux soins preventifs a l'interieur de chaque pays et d'un pays a l'autre.
NIMG-80. SHAPE ATTRIBUTES OF ENHANCING LESION BOUNDARIES CAN DIFFERENTIATE TUMOR RECURRENCE FROM PSEUDO-PROGRESSION ON ROUTINE BRAIN MRI SCANS: PRELIMINARY FINDINGS
Authors: Marwa Isamail, Prateek Prasanna, Raymond Huang, Gagandeep Singh, Rajat Thawani, Anant Madabhushi, Manmeet Ahluwalia, Pallavi Tiwari
Journal: Neuro-Oncology (2017)

A significant challenge in post-chemo-radiation response assessment in brain tumors is distinguishing pseudo-progression (PsP), a temporary radiation-induced treatment effect, from tumor recurrence (TR). PsP closely mimics TR appearance on MRI, making their visual identification challenging. This work targets analyzing enhancing lesion shape of TR and PsP. Studies show that tumors may alter white-matter structure due to infiltration leading to uneven lesion boundaries. The hypothesis is that shape analysis of lesion could reveal morphometric differences across PsP and TR, thus distinguishing them on MRI. 32 MRI studies were acquired from an IRB approved study from Brigham and Women’s hospital (10 PsP, 22 TR cases). Co-registration and bias correction followed by expert delineation of lesion were performed. Three shape features were computed; Curvedness (C), describes how highly curved a point is, Sharpness (S), measures sharpness of curvature, and Shape Index (SI), captures areas with low curvature, were computed from lesion regions for all subjects. The mean, standard deviation, median, and kurtosis were computed per feature. Finally, a KNN classifier and leave-one-out-approach were employed to identify the top 10 significant features between PsP and TR, to be used to classify cases from an independent study obtained from Cleveland Clinic (8 PsP, and 5 TR cases). The most significant features were identified as Mean of C (0.7 +/- 0.3 TR, 0.4 +/- 0.1 PsP), mean of S (1.5 +/- 1.6 TR, 0.6 +/- 0.4 PsP), and median of SI (0.4 +/- 0.1 TR, 0.06 +/- 0.6 PsP) of lesion, and resulted in correctly classifying 26 out of 32 subjects. These features, when used with subjects from the independent study, classified 10 out of 13 subjects. Shape features of enhancing lesion can classify PsP and TR on MRI. CLINICAL IMPLICATION: Distinction of PsP from TR helps early identify patients with TR, while avoiding overtreatment in PsP.