tbuckley/cabot-search huggingface dataset:
ACTR-53. INTERIM ANALYSIS OF PHASE 1B/2 COMBINATION STUDY OF THE IDO PATHWAY INHIBITOR INDOXIMOD WITH TEMOZOLOMIDE FOR ADULT PATIENTS WITH TEMOZOLOMIDE-REFRACTORY PRIMARY MALIGNANT BRAIN TUMORS
Authors: Yousef Zakharia, David Munn, Charles Link, Nicholas Vahanian, Eugene Kennedy
Journal: Neuro-Oncology (2016)

Indoleamine 2, 3-dioxygenase (IDO) is a key immune-modulatory enzyme within the IDO Pathway that inhibits CD8+ T cells and enhances the suppressor activity of Tregs. IDO is expressed in a large proportion of solid tumors including 50 to 90% of glioblastoma (GBM). IDO high expression is correlated with poor prognosis in GBM. IDO pathway inhibitors such as indoximod can improve anti-tumor T cell response slowing the tumor growth in vivo. We have demonstrated a synergistic effect of indoximod when combined with temozolomide (TMZ) and radiation in a syngeneic orthotopic brain tumor model. The purpose of this phase 1b/2 study is to determine the safety and preliminary efficacy of indoximod in combination with TMZ in recurrent refractory malignant brain tumors. After progression on TMZ, patients are eligible for enrollment in this study of indoximod (1200 mg twice daily orally) combined with a standard fixed dose of TMZ (150mg/m2 x 5 days). In the phase 2 expansion, patients are enrolled into 3 cohorts: 2a: indoximod with TMZ (for patients refractory to TMZ), 2b: indoximod with TMZ and bevacizumab (for patients who have progressed on bevacizumab), 2c: indoximod with TMZ in conjunction with stereotactic radiosurgery in select patients. Indoximod is administered for all 28 days of each treatment cycle.
Retrospective Analysis of Fractionated High-Dose Melphalan (F-MEL) and Bortezomib-Thalidomide-Dexamethasone (VTD) with Autotransplant (AT) Support for Advanced and Refractory Multiple Myeloma (AR-MM).
Authors: Mauricio Pineda-Roman, Michelle H. Fox, Klaus A. Hollmig, Elias J. Anaissie, Frits van Rhee, Guido Tricot, Maurizio Zangari, Abid Mohiuddin, Bart Barlogie
Journal: Blood (2006)
MPTH-55. RESULTS OF MOLECULAR PROFILING FOR RECURRENT MALIGNANT GLIOMAS REVEAL SIGNIFICANT CHANGES IN BIOMARKERS COMPARED TO MOSTLY TREATMENT NAÏVE TUMORS THAT COULD IMPACT TREATMENT DECISION
Authors: Lyndon Kim, Joanne Xiu, Kevin Judy, James Evans, David Andrews, Christopher Farrell
Journal: Neuro-Oncology (2016)

Studies in systemic malignancies investigating differences in molecular profiling in newly-diagnosed versus recurrence revealed changes in biomarkers, potentially impacting treatment. The difference between treatment naïve and recurrent malignant gliomas profiling is not well-known. 10 pts with paired samples were identified retrospectively with tumor profiling on multiple specimens. Tests included IHC, NGS, ISH and fragment-analysis. Total: 10 pts. M:F 8:2 Age: 22-69 yrs Median Age: 42 yo. 2 pts: AA, 1 pt: AO, 7 pts: GBM. 8/10 pts: tests performed at first surgery and first recurrence. 2 pts: first test at recurrence, 1 (GBM) and 8 (AO) yrs from diagnosis and second test after third and second surgery, 3 and 1 year after, respectively. Average time between two tests/time of recurrences: 33.1 mo for AA/AO and 21.2 mo for GBM, respectively. Decreased expression of TLE3, RRM1, EGFR, PTEN, ERCC1 and PD-L1 were seen over time in 4/6(67%), 2/5(40%), 2/6(33%), 3/9(33%), 2/7(29%) and 2/8(25%), respectively, while no increase of expression were seen. EGFRvIII and 1p19q co-deletion were lost over time in 1/5(20%) and 1/6(17%), respectively. In contrast, cMET expression, amplification, and TUBB3 expression increased in 1/5(20%), 1/4(25%) and 2/10(20%) tumors while no decrease seen. Expression of PD-1, TOP2A, TOPO1 and TS showed both increase and decrease. 8 pairs had paired sequencing, acquisition of EGFR(V292L), FLT3(D324N), NOTCH1(G736R) and RB1 (E746fs) were seen in one case each. In 8 pairs of MGMT methylation, two samples showed decreased MGMT methylation. Although cohort is small, we show dynamic changes in recurrent malignant gliomas with high discordance rate of 29% compared to the first test. There was greater loss of targetable-biomarkers than gains over time which could impact the selection of treatment options (p=0.015). Reanalyzing the most current tissue prior to making a decision on the next line of treatment should be considered.
Missense Mutations in the ABCB6 Transporter Cause Dominant Familial Pseudohyperkalemia
Authors: Immacolata Andolfo, Seth Alper, Jean Delaunay, Carla Auriemma, Roberta Russo, Maria Rosaria Esposito, Alok K. Sharma, Boris E Shmukler, David H Vandorpe, Carlo Brugnara, Lucia De Franceschi, Achille Iolascon
Journal: Blood (2012)
ANGI-10. GENETIC DOWN REGULATION OF CXCR4 IN GLIOMA CELLS REDUCES INVASION, REDUCES TUMOR PROGRESSION, AND INCREASES SENSITIVITY TO RADIATION
Authors: Viveka Nand Yadav, Daniel Zamler, Sebastien Motsch, Maria G. Castro, Pedro R Lowenstein
Journal: Neuro-Oncology (2016)

Glioblastoma multiforme (GBM) is a lethal brain tumor. Radiation therapy has been an essential part of treatment for glioma patients. Despite high radiation therapy along with anticancer drugs, GBMs invariably recur. Glioma Stem Cells (GSCs) resistant to chemo and radiation therapies are mainly responsible for GBM recurrence. Therefore, increase sensitivity of GBM cells to radiation and/chemo therapies could be of therapeutic value. We have recently described that GBM derived glioma stem cells grow along blood vessels (Baker et al, 2014). In this study we observed that different primary human glioma stem cell lines, HF2303, MSP-12, IN859 and IN2045, and a mouse glioma Gl26-cit cell line, showed significant directional migration towards human and mouse brain-derived endothelial (MBVE) cells. To uncover the mechanism of GBM cell migration, we tested the role of various chemokines and inhibitors utilizing in vitromigration assays. Notably, migration of Gl26-cit and HF2303 towards MBVE was significantly inhibited by AMD3100 (CXCR4 inhibitor). We further confirmed these findings by knocking down of CXCR4 in GL26-cit cells using shRNA. The migration of CXCR4 knock-down in GL26-cit-shCXCR4 cells towards MBVE was significantly reduced compared to control shRNA treated Gl26-cit cells (Gl26-cit-NT). We next established an orthotopic brain tumor in mice using GL26-cit-shCXCR4 and Gl26-cit-NT cells. Mice implanted with down regulated CXCR4 GL26-cit-shCXCR4 cells exhibited prolonged survival compared to Gl26-cit-NT mice. Brain section analysis showed that GL26-cit-shCXCR4 cells are less invasive. Lastly, we tested the effect of radiation on mice implanted with GL26-cit-shCXCR4 or Gl26-cit-NTcells. Mice implanted with GL26-cit-shCXCR4 cells showed further improvement in survival compared to Gl26-cit-NT tumor-bearing mice upon radiation. In summary, CXCR4-CXCL12 signaling is critical for the perivascular invasion of GBM cells and targeting this axis makes tumors less invasive and more sensitive to radiation therapy. Targeting CXCR4-CXCL12 signaling could be a potential therapeutic strategy for treatment of GBM.
Interim estimates of 2016/17 vaccine effectiveness against influenza A(H3N2), Canada, January 2017
Authors: Danuta M Skowronski, Catharine Chambers, Suzana Sabaiduc, James A Dickinson, Anne-Luise Winter, Gaston De Serres, Steven J Drews, Agatha Jassem, Jonathan B Gubbay, Hugues Charest, Robert Balshaw, Nathalie Bastien, Yan Li, Mel Krajden
Journal: Eurosurveillance (2017)

Using a test-negative design, the Canadian Sentinel Practitioner Surveillance Network (SPSN) assessed interim 2016/17 influenza vaccine effectiveness (VE) against dominant influenza A(H3N2) viruses considered antigenically matched to the clade 3C.2a vaccine strain. Sequence analysis revealed substantial heterogeneity in emerging 3C.2a1 variants by province and over time. Adjusted VE was 42% (95% confidence interval: 18–59%) overall, with variation by province. Interim virological and VE findings reported here warrant further investigation to inform potential vaccine reformulation.
Elevated sphingosine-1-phosphate promotes sickling and sickle cell disease progression
Authors: Yujin Zhang, Vladimir Berka, Anren Song, Kaiqi Sun, Wei Wang, Weiru Zhang, Chen Ning, Chonghua Li, Qibo Zhang, Mikhail Bogdanov, Danny C. Alexander, Michael V. Milburn, Mostafa H. Ahmed, Han Lin, Modupe Idowu, Jun Zhang, Gregory J. Kato, Osheiza Y. Abdulmalik, Wenzheng Zhang, William Dowhan, Rodney E. Kellems, Pumin Zhang, Jianping Jin, Martin Safo, Ah-Lim Tsai, Harinder S. Juneja, Yang Xia
Journal: Journal of Clinical Investigation (2014)
Development as Anti-Leukemic Agents, a Novel Synthesis of Phospha Sugar Derivatives in Therapy for Leukemias, and Analysis of Their Characterizations.
Authors: Satoki Nakamura, Keiji Okinaka, Isao Hirano, Takaaki Ono, Kazuyuki Shigeno, Kaori Shinjo, Michio Fujie, Yukiko Iguchi, Taishi Niimi, Satoru Ito, Takuya Suyama, Kazuhide Asai, Mitsuji Yamashita, Kazunori Ohnishi
Journal: Blood (2007)
Intrathoracic Accessory Lobe of Liver Masquerading as a Paraesophageal Mass
Authors: Christopher Ball, Jason Wayne Wachsmann
Journal: Clinical Nuclear Medicine (2017)

Heterotopic liver tissue is a relatively rare finding, which has historically been discovered incidentally during surgery or at autopsy. However, we present a 28-year-old woman who presented to the emergency department with shortness of breath and stabbing chest pain. An emergent CT angiogram of the chest was performed, which incidentally revealed a mediastinal paraesophageal mass. Subsequent endoscopic ultrasound showed a hypoechoic area that appeared to connect to the liver. A liver/spleen scan with SPECT/CT with Tc sulfur colloid demonstrated that the mass was paraesophageal heterotopic liver tissue with a connection to the orthotropic liver by a small stalk.
Phase I/II trial of X-396 in patients (pts) with ALK+ non-small cell lung cancer (NSCLC): Correlation with plasma and tissue genotyping and response to therapy (tx)
Authors: L. Horn, H. Wakelee, G. Blumenschein, K. Reckamp, S. Waqar, C.A. Carter, B.J. Gitlitz, J.R. Infante, R.E. Sanborn, J. Neal, J.P. Gockerman, G. Dukart, K. Harrow, C. Liang, J.J. Gibbons, J. Hernandez, T. Newman-Eerkes, L. Lim, C. Lovly
Journal: Annals of Oncology (2016)
Platelet-Targeted Pro-Urokinase as a Novel Thromboprophylaxis Fibrinolytic Strategy
Authors: Rudy Fuentes, M. Anna Kowalska, Samira Tliba, Daniel W. Bougie, Richard H. Aster, Douglas B. Cines, Vladimir R. Muzykantov, Mortimer Poncz, Sergei Zaitsev
Journal: Blood (2010)
Circulating Platelet-Monocyte Aggregates Predict Venous Thromboembolism in Older Adults Undergoing Major Orthopedic Surgery
Authors: Lauren C. Shih, David Kaplan, Larry W. Kraiss, T. Charles Casper, Robert C. Pendleton, Christopher L. Peters, Mark A. Supiano, Guy A. Zimmerman, Andrew S. Weyrich, Matthew T. Rondina
Journal: Blood (2015)
Lysosomal Enzymes in Pericellular Environment: A Factor in Tumor Regression?: Reply
Authors: Pietro M. Gullino
Journal: JNCI Journal of the National Cancer Institute (1973)

Journal Article Lysosomal Enzymes in Pericellular Environment: A Factor in Tumor Regression?: Reply Get access Pietro M. Gullino Pietro M. Gullino Laboratory of Pathophysiology National Cancer Institute, Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 51, Issue 1, July 1973, Pages 314–315, https://doi.org/10.1093/jnci/51.1.314 Published: 01 July 1973
A phase II study of cabozantinib in patients (pts) with relapsed/refractory metastatic urothelial carcinoma (mUC)
Authors: R. Nadal, H.L. Parnes, D.C. Francis, L.M. Cordes, M. Berninger, R. Costello, L. Folio, M. Linderberg, L. Machado, S.M. Steinberg, J.J. Wright, Y.M. Ning, D.P. Bottaro, W.L. Dahut, A.B. Apolo
Journal: Annals of Oncology (2016)
Young women with metastatic breast cancer (mbc): a restrospective single institution analysis of clinical-pathological characteristics and outcomes
Authors: A. Fontana, L. Diodati, I. Bertolini, C. De Angelis, I. Ferrarini, B. Salvadori, A. Michelotti, E. Landucci, E. Pfanner, P. Ferrari, M. Lo Russo, L. Fustagno, E. Rossetti, M. Ghilli, M. Roncella, A. Falcone
Journal: Annals of Oncology (2016)
A single centre pilot study aiming to determine the recommended dose (RD) of metronomic oral vinorelbine in combination with oral cyclophosphamide and bevacizumab in advanced breast cancer (ABC) patients
Authors: G. Sanna, A.R. Mislang, M. Pestrin, C. Biagioni, E. Risi, S. Cappadona, E. Moretti, S. Gabellini, A. Di Leo, L. Biganzoli
Journal: Annals of Oncology (2016)
Clonal Hematopoiesis Associated with Adverse Outcomes Following Autologous Stem Cell Transplantation for Non-Hodgkin Lymphoma
Authors: Christopher J. Gibson, R. Coleman Lindsley, Vatche Tchekmedyian, Jiantao Shi, Brenton G. Mar, Siddhartha Jaiswal, Alysia Bosworth, Liton F. Francisco, Jianbo He, Elizabeth A. Morgan, Ann S. LaCasce, John Koreth, Vincent T. Ho, Jerome Ritz, Sarah Nikiforow, Joseph H. Antin, Robert J. Soiffer, Stephen J. Forman, Franziska Michor, Donna S. Neuberg, Smita Bhatia, Ravi Bhatia, Benjamin L. Ebert
Journal: Blood (2016)
Finding of Kinase Domain Mutations at Diagnosis IN PATIENTS with Chronic PHASE Chronic Myeloid Leukemia (CP-CML) MAY Identify Those at High RISK of Disease Progression.
Authors: Angelo Michele Carella, Gabriella Cirmena, Gioacchino Catania, Gianmatteo Pica, Germana Beltrami, Alberto Ballestrero, Franco Patrone, Anna Garuti
Journal: Blood (2009)
P07.06 Does IDH1 R132H Mutation alter phospholipid metabolism in glioma? A 31 P-MRS in vivo study
Authors: K. J. Wenger-Alakmeh, U. Pilatus, O. R. Bähr
Journal: Neuro-Oncology (2016)

1/23, tuberculosis 1/23), and a histiocytosis was found in 1/23].MRI findings revealed 15 patients with diffuse lesions vs 8 focal lesions respectively and 21 patients with enhancing lesions vs 2 patients with nonenhancing brainstem lesions.CONCLUSION: Despite its retrospective nature, our study underlines the risk of misdiagnosis and therapeutic mistakes in the evaluation of infiltrating mass suggesting brainstem glioma.It illustrates the need to promote a more systematic "check-list" based approach of brainstem lesions, including biopsies when needed, as recently shown in the pediatric population. P07.
The clinical value of patient-derived glioblastoma tumorspheres in predicting treatment response
Authors: Quintino Giorgio D’Alessandris, Mauro Biffoni, Maurizio Martini, Daniele Runci, Mariachiara Buccarelli, Tonia Cenci, Michele Signore, Louis Stancato, Alessandro Olivi, Ruggero De Maria, Luigi M. Larocca, Lucia Ricci-Vitiani, Roberto Pallini
Journal: Neuro-Oncology (2016)

Advances from glioma stemlike cell (GSC) research, though increasing our knowledge of glioblastoma (GBM) biology, do not influence clinical decisions yet. We explored the translational power of GSC-enriched cultures from patient-derived tumorspheres (TS) in predicting treatment response.The relationship between TS growth and clinical outcome was investigated in 52 GBMs treated with surgical resection followed by radiotherapy and temozolomide (TMZ). The effect on TS of radiation (6 to 60 Gy) and of TMZ (3.9 μM to 1 mM) was related with patients' survival.Generation of TS was an independent factor for poor overall survival (OS) and poor progression-free survival (PFS) (P < .0001 and P = .0010, respectively). Growth rate and clonogenicity of TS predicted poor OS. In general, TS were highly resistant to both radiation and TMZ. Resistance to TMZ was stronger in TS with high clonogenicity and fast growth (P < .02). Shorter PFS was associated with radiation LD50 (lethal dose required to kill 50% of TS cells) >12 Gy of matched TS (P = .0484). A direct relationship was found between sensitivity of TS to TMZ and patients' survival (P = .0167 and P = .0436 for OS and PFS, respectively). Importantly, values for TMZ half-maximal inhibitory concentration <50 μM, which are in the range of plasma levels achieved in vivo, identified cases with longer OS and PFS (P = .0020 and P = .0016, respectively).Analysis of TS holds translational relevance by predicting the response of parent tumors to radiation and, particularly, to TMZ. Dissecting the clonogenic population from proliferating progeny in TS can guide therapeutic strategies to a more effective drug selection and treatment duration.
Chimeric Antigen Receptor Modified T Cells Directed Against CD19 (CTL019) in Patients with Poor Prognosis, Relapsed or Refractory CD19+ Follicular Lymphoma: Prolonged Remissions Relative to Antecedent Therapy
Authors: Elise A. Chong, Jakub Svoboda, Sunita Dwivedy Nasta, David L. Porter, Nicole Winchell, Daniel J. Landsburg, Anthony R. Mato, Simon F. Lacey, Jan J. Melenhorst, Anne Chew, Jens Hasskarl, Katherine T. Marcucci, Bruce L Levine, Carl H June, Stephen J. Schuster
Journal: Blood (2016)
Disparity in governmental cancer resource allocation between East and West Texas.
Authors: C. P. Reynolds, D. G. Stallings, A. K. Knight, K. A. Hargrave, B. U. Philips
Journal: Journal of Clinical Oncology (2011)

e16604 Background: Disparities in outcome have been documented for medically underserved populations, including those in the rural United States. Federal programs seeking to improve care and outcomes for some underserved populations may not meet the needs of rural cancer patients. We compared demographics and cancer funding in West (rural) vs East (urban) areas of Texas. Methods: We compiled data that might reflect rural/urban disparities using geographic health services regions in Texas and reliable publically available databases. Results: Data show a disparity between East Texas (which contains several large urban areas) and the mostly frontier-designated West Texas in terms of oncology physicians, NCI-designated Cancer Centers, and cancer grant funding. The distribution of funding is not directly proportional to population density, cancer incidence, or geographic sources of revenue to governments. Conclusions: These data suggest rural West Texas populations are underserved when it comes to cancer research and ready access to cutting-edge clinical trials. We propose that creation of government programs seeking to eliminate these disparities by funding academic cancer infrastructure, i.e., NCI-designated Cancer Center(s) in West Texas, will improve outcomes and decrease the many burdens of cancer for West Texans. Category West TX (n) % East TX (n) % Area in sq mi 131,839 49.1 136,742 50.9 Total population 2,671,198 11.2 21,167,544 88.8 Adult cancer pts/yr 11,404 12.1 82,918 87.9 Peds cancer pts/yr 116 9.1 1,167 90.9 Adult cancer mortality/yr 4,625 13.1 30,665 86.9 Peds cancer mortality/yr 28 14.6 164 85.4 Total oncology physicians 110 8.6 1175 91.4 Adult hem/onc 76 8.7 799 91.3 Gyn onc 5 7.2 65 92.8 Peds onc 7 4.2 159 95.8 Radiation onc 22 4.2 153 95.8 Medical schools 2 22 7 78 NCI cancer centers 0 0 4 100 NCI funding $2,869,948 1 $334,010,296 99 DOD funding $616,810 0.4 $160,801,262 99.6 CPRIT funding $5,598,810 2.1 $260,200,733 97.9 Total grant funding $9,085,249 1.2 $751,525,533 98.8 Total funding per person $3.40 $35.50 Total personal income $87,591,368,000 9.5 $918,921,246,000 90.5 TX oil tax income $828,660,340 82 $180,004,017 18 TX natural gas tax income $169,235,607 26 $433,748,893 74 TX sales tax income $1,598,308,877 8.1 $18,137,366,362 91.9
Radium-223 re-treatment from an international, prospective, open-label study in patients with castration-resistant prostate cancer and bone metastases
Authors: O. Sartor, D. Heinrich, N. Mariados, M.J. Méndez Vidal, D. Keizman, C. Thellenberg Karlsson, A. Peer, G. Procopio, S.J. Frank, K.J. Pulkkanen, E. Rosenbaum, S. Severi, J.M. Trigo Perez, V. Wagner, J. Garcia-Vargas, R. Li, L.T. Nordquist
Journal: Annals of Oncology (2016)
Langerhans-Cell Histiocytosis
Authors: Carl E. Allen, Miriam Merad, Kenneth L. McClain
Journal: New England Journal of Medicine (2018)

A spectrum of diseases formerly known as histiocytosis X and now called Langerhans-cell histiocytosis is characterized by ERK pathway activation (including BRAF V600E mutations) and diverse clinical manifestations involving bone, skin, lung, and pituitary.
Sodium Channel Subunit SCNN1B Suppresses Gastric Cancer Growth and Metastasis via GRP78 Degradation
Authors: Yun Qian, Chi Chun Wong, Jiaying Xu, Huarong Chen, Yanquan Zhang, Wei Kang, Hua Wang, Li Zhang, Weilin Li, Eagle S.H. Chu, Minnie Y.Y. Go, Philip W.Y. Chiu, Enders K.W. Ng, Francis K.L. Chan, Joseph J.Y. Sung, Jianmin Si, Jun Yu
Journal: Cancer Research (2017)

There remains a paucity of functional biomarkers in gastric cancer. Here, we report the identification of the sodium channel subunit SCNN1B as a candidate biomarker in gastric cancer. SCNN1B mRNA expression was silenced commonly by promoter hypermethylation in gastric cancer cell lines and primary tumor tissues. Tissue microarray analysis revealed that high expression of SCNN1B was an independent prognostic factor for longer survival in gastric cancer patients, especially those with late-stage disease. Functional studies demonstrated that SCNN1B overexpression was sufficient to suppress multiple features of cancer cell pathophysiology in vitro and in vivo Mechanistic investigations revealed that SCNN1B interacted with the endoplasmic reticulum chaperone, GRP78, and induced its degradation via polyubiquitination, triggering the unfolded protein response (UPR) via activation of PERK, ATF4, XBP1s, and C/EBP homologous protein and leading in turn to caspase-dependent apoptosis. Accordingly, SCNN1B sensitized gastric cancer cells to the UPR-inducing drug tunicamycin. GRP78 overexpression abolished the inhibitory effect of SCNN1B on cell growth and migration, whereas GRP78 silencing aggravated growth inhibition by SCNN1B. In summary, our results identify SCNN1B as a tumor-suppressive function that triggers UPR in gastric cancer cells, with implications for its potential clinical applications as a survival biomarker in gastric cancer patients. Cancer Res; 77(8); 1968-82. ©2017 AACR.