tbuckley/cabot-search huggingface dataset:
NIMG-61. PATTERNS OF GLIOBLASTOMA RECURRENCE IN LOW FIELD INTENSITY REGIONS DURING TTFIELDS TREATMENT
Authors: James Battiste, Suriya Jeyapalan, Edward Pan, Josie Sewell, Denise Damek, Daniela Bota, John Villano
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) is an aggressive neoplasm that invariably recurs despite recent advances in therapy. Here, we describe a series of patients treated with Tumor Treating Fields (TTFields) who developed brain stem recurrence post TTFields therapy. TTFields is an FDA-approved therapeutic option for recurrent supratentorial GBM, as a monotherapy after surgical and radiation options have been exhausted, and recently in combination with maintenance temozolomide (TMZ) for treatment of newly diagnosed adult GBM patients. TTFields is a non-invasive, regional antimitotic treatment modality, alternating electric fields to tumors, through transducer arrays placed on the scalp of GBM patients. TTFields disrupts normal cell division processes, selectively targeting proliferating cancer cells. Some mechanisms of escape have been described (eg, out of field recurrence). It is known that the brainstem dose not receive high intensity TTFields due to anatomic limitations of the treatment delivery. Six cases were obtained by retrospective chart review from multiple providers that have experience with prescribing and planning treatment with TTFields. Clinical and radiographic reviews were performed after de-identification of patient records. Cases were compared according to demographics, tumor location and molecular genetics. Patients were a median age of 60 years old (range 52-69), who underwent standard therapy including surgery radiation, adjuvant TMZ, and subsequently received TTFields. There were various tumor locations at baseline presentation. Median duration of TTFields prior to development of brainstem recurrence was 3.5 months, range 2-5 months. Most patients discontinued treatment on TTFields after recurrence. Treatment options for patients with GBM are limited, however TTFields have been shown to improve OS when added to TMZ. TTFields can only be delivered in therapeutic intensities to the supratentorial brain. These out-of-field recurrences are of concern, given the stable primary supratentorial tumor. Further investigation is warranted to improve treatment of the entire nervous system with TTFields.
Prognostic Value of Chromosome 1 Abnormalities in Myelodysplastic Syndrome
Authors: Paloma Ibarrondo, Andres Insunza, Sonia González de Villambrosia, María José Calasanz, Ana Belén Valencia, Valeria Santini, Francesca Torricelli, Teresa González, Miriam Fernández, Elisa Luño, Carmen Sanzo, Rosa Collado, Blanca Espinet, Alberto Valiente, Benet Nomdedeu, María Díez, Consuelo Cañizo, Vera Adema, Mar Mallo, Margarita Ortega, Julia Montoro, Javier De la Serna, Maite Ardanaz, Victor Marco, Javier Grau, Jose Cervera, Guillermo F. Sanz, Teresa Vallespi, David Valcárcel, Francesc Solé, Ana Batlle-López
Journal: Blood (2014)
PTEN loss as a predictive biomarker for the Akt inhibitor ipatasertib combined with abiraterone acetate in patients with metastatic castration-resistant prostate cancer (mCRPC)
Authors: J.S. de Bono, U. De Giorgi, C. Massard, S. Bracarda, D. Nava Rodrigues, I. Kocak, A. Font, J. Arranz Arija, K. Shih, G.D. Radavoi, W. Yu, W. Chan, S. Gendreau, L. Zhang, R. Riisnaes, M.J. Wongchenko, D. Maslyar, V. Jinga
Journal: Annals of Oncology (2016)
Secondary resectability rates observed in a multicenter randomized phase II study of modified capecitabine/irinotecan (mXELIRI) plus bevacizumab (bev) followed by capecitabine/oxaliplatin (XELOX) plus bev or the reverse sequence in patients with metastatic colorectal cancer (mCRC)
Authors: W. Scheithauer, G. Prager, R. Greil, B. Mlineritsch, R. Schaberl-Moser, A. Gerger, F. Längle, I. Viragos-Toth, J. Andel, A. Pichler, M. Pecherstorfer, A. Kretschmer, A. Seebacher, B. Jagdt, W. Eisterer, P. Krippl
Journal: Annals of Oncology (2016)
Cereblon (CRBN) Splice Isoform Lacking Exon 10 Attenuates Lenalidomide-Mediated Degradation of Aiolos and Is Upregulated in Immunomodulatory Drugs (IMiDs) Resistant Myeloma (MM) Patients
Authors: Ranjan Maity, Paola E. Neri, Ines Tagoug, Li Ren, Jiri Slaby, Victor H Jimenez-Zepeda, Peter Duggan, Justin Simms, Nizar J Bahlis
Journal: Blood (2014)
Total Therapy 3 (TT 3) for Newly Diagnosed Myeloma, Incorporating Velcade into Remission Induction with DT PACE: Early Results Regarding Efficacy, PBSC Mobilization and Toxicities.
Authors: Bart Barlogie, Klaus Hollmig, Maurizio Zangari, Julie Stover, Lisa Jackson, Teresa Milner, Athanasios Fassas, Guido Tricot
Journal: Blood (2004)
Thymic Stromal Lymphopoietin Stimulation of Pediatric Acute Lymphoblastic Leukemias with CRLF2 Alterations Induces JAK/STAT and PI3K Phosphosignaling
Authors: Sarah K Tasian, Michelle Y Doral, Brent L Wood, Michael J Borowitz, J. Racquel Collins-Underwood, Richard C Harvey, Kathleen M Sakamoto, Cheryl L. Willman, Stephen P Hunger, Charles G Mullighan, Mignon L Loh
Journal: Blood (2010)
PALL-03. THE IMPACT OF MOLECULAR DIAGNOSTICS ON FUNCTION AND SYMPTOM BURDEN IN GLIOMA PATIENTS
Authors: Terri Armstrong, Samuel Payen, Elizabeth Vera, Alvina Acquaye, Kristin Alfaro-Munoz, Douglas Nielsen, Marta Penas-Prado, Shiao-Pei Weathers, Barbara O’Brien, John de Groot
Journal: Neuro-Oncology (2016)

IDH mutation status and 1p19q loss have been shown to be predictors of survival and are incorporated into the 2016 WHO diagnostic criteria. The impact of molecular subgroups on function and symptom outcomes have not been explored. A cross-sectional sample of ninety patients participating in the MDACC PROACTIVE study completed the M.D. Anderson Symptom Inventory-Brain Tumor. Functional status (KPS), demographic and clinical factors (disease grade, treatment status, recurrence, and surgery extent) were also collected. Group means and associations were compared with Mann-Whitney tests and chi-square tests. A two-way ANOVA evaluated the interaction of IDH status and performance on symptom burden. The sample was primarily male (65%) GBM (43%) patients, with a median age of 46 (range 20-84) with 41% having had a recurrence. Sixty-three percent of patients (n=44) were IDH wild type (IDHw), 42 IDH mutated (IDHm) with the majority of these also exhibiting TP53mutation (23%), and 13% with 1p19q loss. Two-thirds of patients with poor KPS had IDHw tumors. Patients with poor KPS reported worse overall (U=295.5,p<0.01), neurologic (U=241.0,p<0.01), and treatment-related (U=359.0,p<0.01) symptom burden and overall (U=174.0,p<0.01), activity-related (U=155.5,p<0.01), and mood-related (U=347.5,p<0.01)) interference scores. While symptom burden/interference did not differ based on molecular status, there was a significant interaction between IDH status and KPS, with patients with IDHm and poor KPS (n=8) reporting higher symptom burden (F(1,81)=7.21,p<0.01) compared to all other molecular subgroups. Patients with IDHw tumors were more likely to have lower KPS. Symptom burden did not differ based on IDH status, in itself. Rather, it was in conjunction with KPS that differences were seen in symptom severity, with patients with IDHm tumors with poor KPS experiencing the most severe symptom burden. This potentially is a consequence of IDHm tumor’s infiltrative nature. Future studies exploring associated imaging characteristics are warranted.
Donor cell leukemia arising from preleukemic clones with a novel germline DDX41 mutation after allogenic hematopoietic stem cell transplantation
Authors: S Kobayashi, A Kobayashi, Y Osawa, S Nagao, K Takano, Y Okada, N Tachi, M Teramoto, T Kawamura, T Horiuchi, S Kato, T Maekawa, T Yamamura, J Watanabe, Y Harada, H Harada, K Sato, F Kimura
Journal: Leukemia (2017)
NCI Community Cancer Center Program (NCCCP): Understanding why hormonal therapy for breast cancer was considered but not administered.
Authors: Pamela Spain, Stephanie Teixeira-Poit, Michael T. Halpern, Kathleen Castro, Irene Prabhu Das, Brenda A. Adjei, Steven Clauser
Journal: Journal of Clinical Oncology (2016)

74 Background: The National Cancer Institute Community Cancer Centers Program (NCCCP) was designed to improve the quality of cancer care and reduce disparities at hospital-based community cancer centers. This study examined when guideline-concordant therapy was considered but not administered, who made the decision to not receive treatment. Methods: A retrospective analysis of patients diagnosed and receiving all or part of their initial cancer treatment at one of 12 NCCCP sites was conducted. We examined patients who were guideline-concordant with the hormonal therapy (HT) for breast cancer quality measure, but for whom treatment was considered but not administered. We compared patients diagnosed in the pre-NCCCP period (2006 – 2007) and during the NCCCP period (2008-2013). Results: Overall, a low proportion of cases had HT considered but not administered (4% in pre-NCCCP period; 5% in NCCCP period – difference not significant). In the pre-NCCCP period, white patients were twice as likely as Black patients to have HT considered but not administered, while there were no racial differences during the NCCCP period. In both time periods, older patients and Medicare patients were more likely to have HT considered but not administered. The most common reason for considering but not administering HT was refusal by the patient or patient’s family and this more likely for White patients, patients in the middle age groups (50-59 and 60 to 69), and Medicare patients. The second most common reason was that the physician determined it to be contraindicated due to patient risk factors. This was more likely to be a reason for Black and Medicaid patients. Conclusions: Results show that a large proportion of cases that had treatment considered but not administered did not receive treatment because of patient/family refusal or it was contraindicated due to other patient risk factors, both before and during the NCCCP period. Additional studies could inform the long-term outcomes of patients with comorbid conditions who were considered for guideline-concordant treatment but did not receive it (but the data were not available for this study).
GENT-45. HETEROGENEITY OF SWI-SNF COMPONENTS IN MALIGNANT RHABDOID TUMORS
Authors: Pooja Panwalkar, Daniel Martinez, Jill Bayliss, Sameer Khatri, Alexander Judkins, Sriram Venneti
Journal: Neuro-Oncology (2016)

Malignant Rhabdoid Tumors (MRT’s) are highly aggressive and often fatal pediatric tumors that can occur in the central nervous system (CNS) or outside the CNS. When they occur in the CNS, they are called atypical teratoid rhabdoid tumors (AT/RT) and are most common in children younger than 3 years of age. The loss of the tumor suppressor SMARCB1 on chromosome 22 as a result of homozygous deletions, truncating non-sense mutations or frameshift mutations is the common driver event in all MRT’s. SMARCB1 is a core component of the SWI/SNF chromatin-remodeling complex that regulates gene expression by reorganizing chromatin in an ATP dependent manner. Histopathologically, MRT’s are characterized by polyphenotypic differentiation. Since the SWI/SNF complex closely regulates differentiation, we examined the composition of the SWI/SNF complex in MRT’s derived from different locations using immunohistochemistry in a cohort of 43 rhabdoid tumors. Further, the expression of these SWI/SNF components during brain development was analyzed using gene expression data from the Allen Brain Atlas. We found that the expression of SMARCB1 was highest in the cerebellum throughout development. Global levels of other members of the SWI/SNF complex did not vary significantly during brain development. In MRTs, the expression of the core SWI/SNF members (SMARCC1, SMARCC2) remained relatively stable across tumors from different locations. Surprisingly, other SWI/SNF components including ARID1A, ARID1B and BRD7 show heterogeneity in expression depending on the location of tumors within the CNS. Other SWI/SNF members such as ACTL6A, ACTL6B, SMARCD1 and PBRM1 showed differences between the CNS and non-CNS tumors. These data have implications to understand the complex biology of MRTs.
Pancreatic neuroendocrine tumour (pNET) profiles in the NETwork! programme: clinic–enabled genomics for genomic-enabled clinical decisions
Authors: B. Lawrence, C. Blenkiron, K. Parker, S. Fitzgerald, P. Shields, P. Tsai, S. James, N. Poonawala, M.L. Yeong, N. Kramer, B. Robinson, S. Connor, R. Ramsaroop, M. Yozu, M. Elston, C. Jackson, R. Carroll, D. Harris, M. Findlay, C. Print
Journal: Annals of Oncology (2016)
ACTR-01. THE ROLE OF CLINICAL CHARACTERISTICS IN LOW GRADE GLIOMAS PATIENTS IN THE ERA OF MOLECULAR BIOMARKERS: A STUDY FROM GRUPPO ITALIANO COOPERATIVO DI NEURO-ONCOLOGIA (GICNO)
Authors: Enrico Franceschi, Dario De Biase, Annalisa Pession, Alexandro Paccapelo, Michele Reni, Anna Mandrioli, Daniela Danieli, Stefania Bartolini, Gianluca Marucci, Laura Lombardo, Benedetta Urbini, Maria Michiara, Alicia Tosoni, Giovanni Tallini, Claudia Biasini, Alba Ariela Brandes
Journal: Neuro-Oncology (2016)

Outcome of low-grade gliomas (LGG) is highly variable and depends on clinical factors, molecular features, and treatments. Molecular characterization of LGG has improved in recent years and is now essential for diagnosis and treatment of these diseases. Clinical factors, such as age and the extent of surgery, were considered prognostic for decades, but now their role is less clear. We retrospectively evaluated all adult LGG patients from our data warehouse who received surgery and had sufficient tissue to assess biomarkers characterization. IDH1/2 mutation, MGMT methylation and 1p/19 codeletion were assessed on formalin-fixed paraffin-embedded samples. 204 consecutive LGG were included. Median follow up was 78.6 months. The mean age was 40 (range:18–72), 111 patients (54.4%) were <40 years of age; 27 patients (13.2%) underwent biopsy, 123 patients (60.3%) partial resection, 54 patients (26.5%) complete resection. Twenty-eight patients (13.7%) were considered low risk according to RTOG (<40 years with complete resection). IDH mutation was found in 82.8% of patients. 1p/19q codeletion was found in 46.4% of patients, MGMT methylation in 65.2% of patients. Median survival was 211.0 months (95%CI:190.4–231.6) in low risk patients, and 145.3 months (95%CI: 135.1–155.6) in high risk patients (P=0.010). Median survival for patients with IDH 1/2 mutation was 164.0 months (95%CI:112.1–215.9) and 77.1 months in patients IDH 1/2 wild type (95%CI:15.4–138.9, P<0.001). Multivariate analysis showed that low risk according to RTOG (P=0.006), IDH 1/2 mutation (P<0.001) and 1p/19q codeletion (P=0.035) were significantly correlated with overall survival. MGMT methylation was not significant. The management of LGG is complex. Both molecular profiling and clinical risk assessment are necessary for the decision making process in these rare tumors.
Cost-effectiveness of the 2014 U.S. Preventive Services Task Force (USPSTF) Recommendations for Intensive Behavioral Counseling Interventions for Adults With Cardiovascular Risk Factors
Authors: Ji Lin, Xiaohui Zhuo, Barbara Bardenheier, Deborah B. Rolka, W. Edward Gregg, Yuling Hong, Guijing Wang, Ann Albright, Ping Zhang
Journal: Diabetes Care (2017)

In 2014, the U.S. Preventive Services Task Force (USPSTF) recommended behavioral counseling interventions for overweight or obese adults with the following known cardiovascular disease risk factors: impaired fasting glucose (IFG), hypertension, dyslipidemia, or metabolic syndrome. We assessed the long-term cost-effectiveness (CE) of implementing the recommended interventions in the U.S.We used a disease progression model to simulate the 25-year CE of the USPSTF recommendation for eligible U.S. adults and subgroups defined by a combination of the risk factors. The baseline population was estimated using 2005-2012 National Health and Nutrition Examination Survey (NHANES). The cost and effectiveness of the intervention were obtained from systematic reviews. Incremental CE ratios (ICERs), measured in cost/quality-adjusted life-year (QALY), were used to assess the CE of the intervention compared with no intervention. Future QALYs and costs (reported in 2014 U.S. dollars) were discounted at 3%.We estimated that ∼98 million U.S. adults (44%) would be eligible for the recommended intervention. Compared with no intervention, the ICER of the intervention would be $13,900/QALY. CE varied widely among subgroups, ranging from a cost saving of $302 per capita for those who were obese with IFG, hypertension, and dyslipidemia to a cost of $103,200/QALY in overweight people without these conditions.The recommended intervention is cost effective based on the conventional CE threshold. Considerable variation in CE across the recommended subpopulations suggests that prioritization based on risk level would yield larger total health gains per dollar spent.
Reduced Binding of C/EBPα to Myeloid Specific Promoters with Altered Gene Expression in the Presence of PML/RARα.
Authors: Katharina Wagner, Jürgen Krauter, Kerstin Görlich, Bettina Drescher, Lisa M. Johansen, Hanna S. Radomska, Estelle Duprez, Arnold Ganser, Daniel G. Tenen
Journal: Blood (2005)
Should the Definition of Health Include a Measure of Tolerance?
Authors: Robert H. Brook
Journal: JAMA (2017)

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Rituxiamb Did Not Improve Clinical Outcomes In AIDS-Related Burkitt Lymphoma
Authors: Hideyuki Yamamoto, Shotaro Hagiwara, Yuki Kojima, Asako Uehira, Atsushi Ajisawa, Akira Kitanaka, Junko Tanuma, Seiji Okada, Hirokazu Nagai
Journal: Blood (2011)
89Zr-labeled CEA-targeted IL-2 variant immunocytokine in patients with solid tumors: CEA-mediated tumor accumulation in a dose-dependent manner and role of IL-2 receptor-binding
Authors: C.W. Menke-van der Houven van Oordt, E. van Brummelen, T. Nayak, M. Huisman, L. de Wit- van der Veen, E. Mulder, O. Hoekstra, M. Stokkel, G.A. van Dongen, H.M. Verheul, M. Feilke, C. Guizani, E. Guarin, S. Evers, J. Saro, J.H.M. Schellens
Journal: Annals of Oncology (2016)
SIGNIFICANCE of ABSOLUTE LYMPHOCYTE COUNT at RELAPSE as a PROGNOSTIC FACTOR in PATIENTS with T-CELL NON-HODGKIN'S LYMPHOMA.
Authors: Dae Ro Choi, Dok Hyun Yoon, Heui June Ahn, Yoojin Cho, Eun Kyoung Kim, Shin Kim, Jooryung Huh, Dae Ho Lee, Sang We Kim, Jung Shin Lee, Cheolwon Suh
Journal: Blood (2009)
Multifocal Osteosarcoma
Authors: Somali Gavane, Anita P. Price, Heather Magnan, Sonia Mahajan, Neeta Pandit-Taskar
Journal: Clinical Nuclear Medicine (2017)

Multifocal osteosarcoma is usually defined as the occurrence of a tumor at 2 or more sites in a patient without pulmonary metastases and may be synchronous with more than one lesion seen at presentation or metachronous with new tumors developing after the initial treatment. It is difficult to determine whether these represent synchronous multiple primary lesions or metastases. We present a rare case of widespread synchronous multifocal osteosarcoma and a brief review of the literature.
Different Roles of Two Autotaxin Isoforms in Proliferation, Migration and Adhesion in the Non-Mutational Tyrosine Kinase Inhibitor Resistant Acute Lymphoblastic Leukemia Cell Line SupB15.
Authors: Aline Schmidt-Tanguy, Annette Romanski, Mathilde Hunault-Berger, Oliver G. Ottmann
Journal: Blood (2008)
Clonal Origin of Circulating Endothelial Progenitor Cells in Patients with Myelofibrosis with Myeloid Metaplasia.
Authors: Gaetano Bergamaschi, Tiziano Pramparo, Vittorio Rosti, Isabella Ramajoli, Giuliana Gregato, Margherita Massa, Monia Marchetti, Orsetta Zuffardi, Mario Cazzola, Giovanni Barosi
Journal: Blood (2004)
Down-Regulation of NF-κB and STAT3 Signaling Pathways Upon Protein Kinase CK2 Inhibition Empowers Bortezomib-Induced Multiple Myeloma Cell-Death
Authors: Sabrina Manni, Alessandra Brancalion, Quotti Tubi Laura, Anna Cabrelle, Livio Trentin, Renato Zambello, Fausto Adami, Gianpietro Semenzato, Francesco Piazza
Journal: Blood (2011)
IMST-49. MECHANISM AND THERAPEUTIC TARGETING OF OSTEOPONTIN-MEDIATED IMMUNE SUPPRESSION IN GBM
Authors: Jun Wei, Anantha Marisetty, Ling-Yuan Kong, Konrad Gabrusiewicz, Yuuri Hashimoto, Xiaoyang Ling, Shouhao Zhou, Gregory Fuller, Amy Heimberger
Journal: Neuro-Oncology (2016)

Osteopontin has been shown to have an oncogenic role in a variety of cancers and may have immune modulatory effects on T cells and macrophages. Quantitative PCR, immune blotting, and ELISA were used to determine osteopontin expression, including within specific tumor-infiltrating cell subsets. Knock down of osteopontin was achieved in innate immune cells and glioblastoma stem cells (GSCs) using complementary siRNA, shRNA and CRISPR/CAS9 techniques followed by a series of in vitrofunctional migration, invasion, phagocytosis and immunological assays. Osteopontin gene deficient mice were used to examine the roles of non-tumor derived osteopontin on survival of mice harboring intracranial gliomas. High levels of osteopontin expression in GBM patients is a negative prognosticator for survival. Comparative expression profiling revealed that osteopontin was the number one elevated gene in human GBM-infiltrating innate immune cells relative to peripheral blood monocytes. Both GBM-infiltrating innate immune cells and GSCs secrete large amounts of osteopontin. Immunofluorescence analysis of GBM tissues from patients and murine clonotypic GL26 and Ntv-a-RCAS models demonstrated that osteopontin is mainly expressed in the cytosol and co-localizes with Iba1+ innate immune cells as well as OLIG2+/SOX2+ GSCs. Migration assays indicated osteopontin was a potent chemokine for macrophages and its blockade significantly impaired the ability of GSCs to recruit monocytes/macrophages. In addition, non-tumor derived osteopontin was critical for glioma development as gene deficient mice with intracranial GL261 tumor had a significantly extended survival. Osteopontin is an important chemokine to recruit peripheral monocytes to the GBM microenvironment and is essential in mediating crosstalk between tumor cells and the innate immune system.
Single Nucleotide Polymorphisms (SNPs) and Recurrent Mutations in the Hyaluronan Synthase 1 (HAS1) Gene May Predispose to Multiple Myeloma (MM) and Waldenstrom’s Macroglobulinemia (WM).
Authors: Sophia Adamia, Steve Treon, Daniel Santos, Zachary Hunter, Michael J. Mant, Tony Reiman, Andrew R. Belch, Linda M. Pilarski
Journal: Blood (2005)