tbuckley/cabot-search huggingface dataset:
Comparison of two induction chemotherapy regimens in combination with radiotherapy in patients with advanced nasopharyngeal carcinoma
Authors: D. T. Chua, J. Ma, J. Sham, H. Mai, M. Hong, T. Lu, H. Ming
Journal: Journal of Clinical Oncology (2006)

5535 Background: Prospective randomized trials failed to show any survival benefits associated with the use of induction chemotherapy in nasopharyngeal carcinoma (NPC). Although cisplatin-based regimens were commonly used in these trials, the impact of cisplatin dose was not clear. Methods: Individual patient data of two published phase III trials using different cisplatin-based induction chemotherapy regimens were pooled together for analysis. A total of 365 patients with stage II-IV NPC received either cisplatin &amp; epirubicin (EP, n = 144) or cisplatin, bleomycin &amp; fluorouracil (PBF, n = 221) followed by radiotherapy between September 1989 and July 1994. The mean total cisplatin dose received by patients ranged from 162 mg/m 2 in EP group to 232 mg/m 2 in PBF group. Median follow-up time was 59 months. Results: The response rates at the end of induction chemotherapy were 86% in PBF group and 84% in EP group. No significant differences in tumor control and survival were observed between the two groups. Five-year overall survival rates were 63% in PBF group and 62.5% in EP group. Five-year loco-regional failure-free rates were 74% in PBF group and 65% in EP group, the difference being not significant after adjusting for stage grouping. Conclusions: No significant difference in treatment outcome was observed in patients using different cisplatin-based induction chemotherapy. The absence of survival benefits in chemotherapy arms was probably not related to the dose-intensity of cisplatin used, and escalating the total cisplatin dose alone in induction chemotherapy is not likely to improve survival. No significant financial relationships to disclose.
A randomized phase 1b/2 study evaluating the safety and efficacy of doxorubicin (dox) with or without olaratumab (IMC-3G3), a human anti–platelet-derived growth factor &amp;agr; (pdgfr&amp;agr;) monoclonal antibody, in advanced soft tissue sarcoma (sts)
Authors: W. Tap, R.L. Jones, B. Chmielowski, A.D. Elias, D. Adkins, B.A. Van Tine, M. Agulnik, M. Cooney, M.B. Livingston, G. Pennock, A. Qin, A. Shahir, R. Ilaria, I. Conti, G. Schwartz
Journal: Annals of Oncology (2016)
404O The natural history and patterns of metastases from mucosal melanoma: an analysis of 706 prospectively-followed patients from china
Authors: B. Lian, C. Cui, L. Zhou, X. Song, X. Zhang, D. Wu, L. Si, Z. Chi, X. Sheng, C.M. Balch, J. Guo
Journal: Annals of Oncology (2016)
220O Claudin 18.2 - a novel treatment target in the multicenter, randomized, phase II FAST study, a trial of epirubicin, oxaliplatin, and capecitabine (EOX) with or without the anti-CLDN18.2 antibody IMAB362 as 1st line therapy in advanced gastric and gastroesophageal junction (GEJ) cancer
Authors: F. Lordick, M. Schuler, S.-E. Al-Batran, Z. Zvirbule, G. Manikhas, A. Rusyn, Y. Vinnyk, I. Vynnychenko, N. Fadeeva, M. Nechaeva, A. Dudov, E. Gotovkin, A. Pecheniy, I. Bazin, I. Bondarenko, B. Melichar, C. Huber, U. Sahin, O. Tu¨ reci
Journal: Annals of Oncology (2016)
Epratuzumab (Humanized Anti-CD22 MAb) Conjugated with SN-38, a New Antibody-Drug Conjugate (ADC) for the Treatment of Hematologic Tumors: Preclinical Studies Alone and In Combination with Veltuzumab, a Humanized Anti-CD20 MAb
Authors: David M Goldenberg, Serengulam Govindan, Tom M Cardillo, Robert M Sharkey
Journal: Blood (2010)
Role of Mesenchymal Stem Cell Galectin 3 in the AML Tumor Microenvironment
Authors: Peter Ruvolo, Yihua Qiu, Vivian Ruvolo, Rui-Yu Wang, Zhihong Zeng, Jared Burks, Rongqing Pan, Numsen Hail, Teresa McQueen, Suk-Young Yoo, Steven M. Kornblau, Michael Andreeff
Journal: Blood (2015)
A phase II study of perioperative therapy for patients with resectable and borderline-resectable pancreatic adenocarcinoma.
Authors: Andrew L. Coveler, Venu Gopal Pillarisetty, Grace Gyurkey, Wui-Jin Koh, Melissa Upton, Carlos Cuevas, Theodore Gooley, E. Gabriela Chiorean, Veena Shankaran, William Proctor Harris, James Oh Park, Gary N. Mann, David R. Byrd, Stacey Balas, Samuel H. Whiting
Journal: Journal of Clinical Oncology (2014)

4120 Background: Most patients (pts) who undergo surgical resection (SR) for pancreatic ductal adenocarcinoma (PDA) relapse and die. Adjuvant chemotherapy (CT) improves survival compared to observation in randomized trials, but median disease-free survival (DFS) and overall survival (OS) are only 13.4m and 22.1m, respectively. Multiagent CT in the metastatic setting improves DFS and OS compared to gemcitabine (G) alone. Neoadjuvant (NA) treatment of resectable PDA is a rational though unproven strategy to improve standard results. We hypothesized NA multiagent CT and chemoradiotherapy (CRT) paired with SR and adjuvant CT would be manageable and improve the OS of pts with borderline (BR)/resectable (R) PDA. Methods: This was a prospective, single arm, single institution phase II trial. Eligibility included confirmed PDA, R/BR disease, ECOG ≤ 2, and adequate organ function. NA CT (3 cycles of GTX (G 750mg/m2 over 75 minutes and docetaxel 30mg/m2 days (d) 4 and 11, capecitabine (C) 750mg/m2 BID d1-14)) followed by CRT (IMRT 3 Gy/fraction on days 1-5 and 8-12 (30 Gy total) with C 650mg/m2 BID d1-14 and oxaliplatin (O) 60mg/m2 d1 and 8. Adjuvant CT was 2m of GemOx (G 1000mg/m2 and O 85mg/m2 d1 every 14d) and 2m of standard G. The primary objective was to estimate the OS of pts treated in this fashion. Secondary objectives included DFS, Response Rate (RR), pathologic RR, SR completion and safety. Results: 35 pts were enrolled, 16 had BR disease and 16 were clinically node positive. One pt had progression during NA CT and 32 (91%) completed NA CRT. 31 (89%) pts went to surgery, 6 had occult metastases, 2 were locally advanced and 23 had SR (74% R0 and 26% R1). Pathology demonstrated 1 pCR and 87% N0. Among 35 pts enrolled, 21 (60%) are alive with a median follow-up of 23.6m. Median OS of all 35 patients is 31.1m and mDFS is 27.6m. Of 23 pts who underwent SR, 18 remain alive with a median follow-up of 25.7m. Estimated mDFS is 35.1m with a lower 95% confidence limit of 18.9m and mOS is not reached to date. Conclusions: In this phase II study, peri-operative multiagent CT and CRT was feasible and resulted in promising DFS and OS outcomes relative to historical controls. The current results are encouraging and warrant further evaluation. Clinical trial information: NCT00609336.
Role of Endogenous Protease Inhibitor in Airway Epithelial Cells in the Pathogenesis of Eoshinophilic Chronic Rhinosinusitis
Authors: Hideaki Kouzaki, Ichiro Tojima, Tomohisa Kato, Koji Matsumoto, Shino Shimizu, Takeshi Shimizu, Hirohito Kita
Journal: Journal of Allergy and Clinical Immunology (2017)
Bradykinin B2 Receptor KO Mice Are Protected From Thrombosis by A Platelet Spreading Defect
Authors: Chao Fang, Alec Schmaier, Evi Stavrou, Gregory Adams, Marvin T. Nieman, Gretchen LaRusch, Andrew Chen, Yihua Zhou, Matthew Bilodeau, Fakhri Mahdi, Mark Warnock, Alvin H. Schmaier
Journal: Blood (2010)
Peripherally Inserted Central Catheter: it is really time for intracavitary electrocardiography
Authors: S. Bontini, P. Mordenti, F. Oleari, S. Carini, S. Castellani, C. Gozzo, O. Grassi, M. Muroni, M.R. Cordani, G. Cremona, L. Cavanna
Journal: Annals of Oncology (2016)
Dermatofibrosarcoma protuberans (DFSP) in six patients with ADA-SCID
Authors: C. Kesserwan, R. Sokolic, E. Cowen, E. Garabedian, S. Pittaluga, K. Baird, D. López-Terrada, A. Issekutz, J. Bridge, A. Wayne, F. Candotti
Journal: Journal of Clinical Oncology (2009)

10570 Background: DFSP is a rare malignant skin tumor associated with a characteristic chromosomal translocation (t(17;22)(q22;q13)), resulting in the COL1A1-PDGFB fusion gene. We originally diagnosed DFSP in two patients affected with a rare form of severe combined immunodeficiency due to adenosine deaminase deficiency (ADA-SCID). The association of these two rare conditions has been described in two other cases, which prompted us to screen for DFSP systematically in patients with ADA-SCID. Methods: Eight ADA-SCID patients were evaluated with complete dermatological exam and skin biopsy. Molecular analysis (FISH and/or RT-PCR) and karyotype were performed when possible. Results: Six patients (age 2, 2, 5, 9, 12 and 22 years) were found to have DFSP. Five patients had between 4 and 12 multicentric lesions over the trunk and extremities. One patient had a single lesion. Most lesions appeared as 2–15 mm tan atrophic plaques. Nodular lesions were present in 3 patients. All lesions showed a spindle cell proliferation of the dermis, extending into the subcutaneous fat. A storiform pattern was only noticed in one adult patient. In all cases, CD34 expression was diffusely positive and FXIIIa was negative. Karyotype showed t(17;22)(q22;q13) in the 2 patients in whom it was performed. FISH was positive for COL1A1-PDGFB in 2 of 4 patients studied. RT-PCR showed the COL1A1-PDGFB fusion transcript in one case in which FISH was inconclusive.FISH and RT-PCR analyses are being conducted in 2 and 5 remaining cases, respectively. Conclusions: We describe a previously unrecognized association between multicentric DFSP and ADA-SCID. Multicentricity of DFSP to this extent has not previously been reported . We hypothesize that t(17;22)(q22;q13) may arise due to the known DNA repair defect in ADA-SCID and that the known dermal overexpression of PDGFB in this condition may favor the development of fibrotic tumors, as opposed to other skin cancers. Our observations can provide further insight into the pathogenesis of DFSP and should facilitate early diagnosis of DFSP in ADA-SCID. No significant financial relationships to disclose.
Drug resistance induced by paclitaxel and carboplatin plasmatic concentrations in lung cancer cell lines.
Authors: Raquel Luque, Aranzazu González Vicente, Jesús Soberino, Jose Carlos Prados, Consolación Melguizo, Cynthia S. González Rivas, Julia Ruiz Vozmediano, Veronica Conde, Javier Garcia Garcia, Antonia Aránega
Journal: Journal of Clinical Oncology (2012)

97 Background: Multidrug resistance (MDR) phenotype is the major cause of chemotherapy failure. It has been related to several proteins expression: P-glycoprotein (PgP), MRP family, LRP, and BCRP. We study the resistance pattern induced after paclitaxel and carboplatin in non-small cell lung cancer (NSCLC). Methods: We used 5 different cell lines. A549 and A427 cell lines were derived from lung epithelial carcinoma. NODO line was obtained from lung carcinoma metastases, and 3 cell lines derived from other tumours: gastric cancer (GAS), seminoma (SEM), breast cancer (MCF7). The cell lines were exposed to paclitaxel, carboplatin, and the combination of both drugs. The concentrations we used were similar to the plasma concentrations observed in patients treated previously. Results: A549 cell line did not show basal expression of MDR1, but a weak basal expression of MRP3 was observed. After chemotherapy, we observed that paclitaxel induced MDR1 and carboplatin induced MRP3. The combination of both drugs induced MDR1 and MRP3 expression, however, when paclitaxel is associated to carboplatin, MRP3 expression did not increase significantly. A427 cell line did not show basal expression of MDR1 and MRP3. Paclitaxel induced MDR1 and carboplatin induced MRP3. The association of both drugs increased significantly the expression of MDR1, and very few the expression of MRP3. NODO cell line did not show any basal expression. Paclitaxel induced MDR1 and carboplatin induced MRP3. Cell lines derived from other tumours not show any basal expression. Paclitaxel induced MDR1 in all cell lines. Carboplatin did not induce MDR1, nor MRP3 in GAS cell line. Conclusions: Plasma concentrations of paclitaxel induced MDR1 expression but not MRP3 in lung cancer and other tumours derived cell lines. Carboplatin produced overexpression of MRP3 but not MDR1 in the same cell lines. The combination of both drugs at plasma concentrations was not able to activate a new resistance mechanism in the studied cell lines, but improve the resistance mechanism induced by each one of the drugs individually.
Tumor response criteria and biomarkers associated with increased survival following adenoviral p53 gene therapy (ADVEXIN) in patients with recurrent squamous cell carcinoma of the head and neck (SCCHN)
Authors: J. J. Nemunaitis, G. Clayman, J. Hamm, C. Bier-Laning, H. Minn, D. Van Echo, G. Yoo, K. Menander, R. E. Sobol, W. J. Goodwin
Journal: Journal of Clinical Oncology (2007)

6057 Background: There is a growing body of data indicating that conventional WHO and RECIST criteria do not optimally identify tumor responses associated with increased survival. Methods: We compared several response criteria to assess the efficacy of intratumoral adenoviral p53 gene therapy (Advexin) in a Phase 2 trial of 106 patients with recurrent SCCHN. Results: The percentage of patients with tumor responses defined by reductions in bi-dimensional tumor area by CT scans of 50%, 30%, 25%, 10% or stable disease of &gt; 3 months were 8%, 10%, 11%, 16% and 20% respectively. The median survival for the entire population was 5.9 months while the responder populations defined by tumor decreases of 50%, 30%, 25%, 10% or stable disease &gt; 3 months had median survivals of 40.8, 17.0, 13.7, 12.3 and 11.4 months respectively. There was a statistically significant increase in median survival for each of the responder populations compared to non-responders (p &lt; 0.0009 for each comparison by logrank test). Statistical significance was maintained for the response definitions in landmark analyses excluding patients with survivals less than 3 and 6 months respectively. Locoregional disease control (CR + PR + SD &gt; 3 months) was a stronger predictor of survival by Cox Proportional Hazard analysis (p = 0.0002) than conventional &gt; 50% tumor reduction CR + PR response criteria (p = 0.005). With respect to abnormal p53 detected by immunohistochemistry (≥20% positive cells), 75% of patients (12/16) with p53 + tumors demonstrated locoregional disease control compared to only 18% (2/11) with p53 − tumors p=0.0063 Fisher’s Exact Test. In addition, the median survival of patients with abnormal p53 was 11.6 months compared to only 3.5 months in patients with normal p53 (p=0.0007 Logrank Test). Conclusions: Our findings indicate that abnormal p53 is a predictive biomarker that identifies a subset of patients most likely to benefit from p53 gene therapy and that recurrent SCCHN tumor response definitions based upon smaller reductions in tumor size or the absence of progression (stable disease &gt; 3 months) more accurately identified Advexin treated patients with increased survival than conventional response criteria. [Table: see text]
A phase II trial of gefitinib in patients (pts) with progressive metastatic neuroendocrine tumors (NET): A Phase II Consortium (P2C) study
Authors: T. J. Hobday, K. Holen, R. Donehower, J. Camoriano, G. Kim, J. Picus, P. Philip, R. Lloyd, M. Mahoney, C. Erlichman
Journal: Journal of Clinical Oncology (2006)

4043 Background: Systemic treatment options for progressive metastatic NET, including islet cell carcinoma (ICC) and carcinoid tumor (CT), are limited. These tumors frequently express the epidermal growth factor receptor (EGFR). Gefitinib, a small-molecule inhibitor of the EGFR tyrosine kinase, has been shown to inhibit the growth of NET cell lines. Methods: Eligibility criteria included: radiographic progression by RECIST criteria, ECOG PS ≤ 2, ≤ 1 prior chemotherapy, and good organ function. Prior interferon and prior or concurrent octreotide (if disease progression documented on stable dose) were allowed. Pts received gefitinib 250 mg po daily. We evaluated 6 month (mos) progression-free survival (PFS) in two cohorts (ie, CT and ICC) using separate 2-stage phase II designs. 6 mos PFS rates of 30% (CT) and 10% (ICC) were considered promising. Results: 96 pts were enrolled: (57 CT, 39 ICC). For pts evaluable for the primary endpoint, 23 of 38 (61%) CT pts and 9 of 29 (31%) pts with ICC were progression-free at 6 mos. 1 PR and one minor response (MR = 20–29% decrease in sum of target lesion diameters) were observed in 40 CT pts; 2 PR and 1 MR in 31 ICC pts. In addition, 32% (12/38) of CT and 14% (4/29) of ICC pts had stable disease on study for a duration that exceeded by at least 4 months the time to progression documented prior to study entry. Grade 3–4 toxicity was infrequent with fatigue (6%), diarrhea (5%) and rash (3%) most common. Evaluation of markers of the EGFR pathway on tumor tissue will be presented. Conclusions: Gefitinib is well-tolerated and results in prolonged disease stabilization in pts with prior documented objective progression of CT and ICC, with rare objective responses. Supported by NOI CM17104. No significant financial relationships to disclose.
Preliminary results of a biomarker discovery project for treatment-related brain injury (TRBI) in malignant glioma.
Authors: Susannah G. Yovino, Matthias Holdhoff, William J. Savage, Pratima Dulloor, Stuart A. Grossman, Allen Everett
Journal: Journal of Clinical Oncology (2012)

94 Background: Patients with malignant glioma often develop increased enhancement in the tumor bed after chemoradiation (CRT). Current imaging techniques cannot distinguish if these changes are due to recurrent disease or treatment-related brain injury (TRBI). Serum biomarkers could help noninvasively make this distinction. Brain-specific proteins have been used as markers of the severity of other brain injuries including stroke, hypoxia, and traumatic brain injury. We hypothesized that similar changes could be observed following brain CRT and could provide preliminary data supporting biomarker development for TRBI. Methods: Patients receiving concurrent radiation and temozolomide (TMZ) for malignant glioma were eligible. The study was approved by the institutional review board. Informed consent was obtained from all patients. Serum is sampled before CRT, in the last week of CRT, and at 1 month, 6 mos, and 1 year after CRT. Neurologic exams, cognitive testing, and imaging are performed at the same intervals. Serum samples were tested for glial fibrillary acidic protein (GFAP), neurogranin, ICAM-5, B-syn-nuclein, and brain-derived neurotrophic factor (BDNF). Samples were measured in duplicate using an electrochemiluminescent immunoassay. Results: Data are available for the first 7 patients enrolled in this study. All of the tested markers except GFAP were measurable at baseline and all other time points. None of the markers were consistently elevated during the last week of CRT or at any other time point during follow-up. Three patients had resection of suspected recurrent disease. Two had recurrent tumor and 1 had no evidence of disease. No correlation was apparent with the findings at surgery and serum levels of GFAP, neurogranin, ICAM-5, B-synuclein, or BDNF. Conclusions: This study describes a mechanism for identifying a serum protein marker of TRBI. Preliminary results did not identify elevations in any of the selected markers immediately after CRT when signs of TRBI should be apparent or at other points in the clinical course. Testing of additional serum markers is needed to identify a biomarker of TRBI which would provide valuable information for managing high-grade glioma patients.
Crucial Role of Langerhans Cells in Allergen Uptake and Regulatory T Cell Induction in Epicutaneous Immunotherapy
Authors: Vincent Dioszeghy, Lucie Mondoulet, Veronique Dhelft, Melanie Ligouis, Camille Plaquet, Christophe M. Dupont, Hugh A. Sampson, Pierre-Henri Benhamou
Journal: Journal of Allergy and Clinical Immunology (2017)
Advanced practice providers and survivorship care plans.
Authors: Sabrina Q. Mikan, Patricia Carter, Debra A. Patt
Journal: Journal of Clinical Oncology (2016)

70 Background: The American College of Surgeons mandate in 2012 challenged organizations to create and develop quality survivorship care programs. The NCCN and Commission on Cancer set the standard for quality psychosocial care recognizing distress as part of the cancer continuum. In order to meet this challenge, community cancer care organizations are incorporating delivery of survivorship and psychosocial care into the Advanced Practice Provider (APP) role. APPs include Physician Assistants (PAs) and Advanced Practice Nurses (APNs). We describe the development and feasibility testing of an APP-led survivorship program in a large network of community oncology practices. Methods: A descriptive study design was used with ten practices participating in the implementation of a structured APP-led survivorship program. The goals of each survivorship visit were to: review recommendations for care and healthy lifestyle behaviors, review surveillance recommendations, and to reconnect patients with their primary care providers. Nineteen APPs in the study site practices offered survivorship management between October 2012 and May 2015 to female breast and colon cancers at all stages. Results: Study sites used structured process maps to identify and refer patients to survivorship visits. Evaluations of additional referral strategies are ongoing. Participating APPs reported high self-efficacy in delivering survivorship care plans and high patient satisfaction following visits. All female breast or colon cancer patients, regardless of stage at diagnosis, attended the appointment and received a complete care plan based upon the ASCO Survivorship Care Plan. Surveillance education was provided specific to diagnosis utilizing the NCCN guidelines delivering person-centered care. Visits lasted an average of 60 minutes and were billable as counseling and coordination. Conclusions: Patients diagnosed with breast or colon cancer make up the largest majority of cancer survivors. This project reveals that an APP-led survivorship program is feasible and can help to meet the ASCO and NCCN challenge of providing survivorship care to this large population.
Targeting Bruton tyrosine kinase with ibrutinib in relapsed/refractory marginal zone lymphoma
Authors: Ariela Noy, Sven de Vos, Catherine Thieblemont, Peter Martin, Christopher R. Flowers, Franck Morschhauser, Graham P. Collins, Shuo Ma, Morton Coleman, Shachar Peles, Stephen Smith, Jacqueline C. Barrientos, Alina Smith, Brian Munneke, Isaiah Dimery, Darrin M. Beaupre, Robert Chen
Journal: Blood (2017)
A Monoclonal Antibody Specifically Targeting CD44 Inhibits B-Cell Chronic Lymphocytic Leukemia Cell Survival In Vitro and In Vivo
Authors: Suping Zhang, Christina C.N. Wu, Jessie-Farah Fecteau, Bing Cui, Rongrong Wu, Laura Z. Rassenti, Fitzgerald S. Lao, Rommel Tawatao, Stefan Weigland, Charles Prussak, Dennis A. Carson, Thomas J. Kipps
Journal: Blood (2011)