tbuckley/cabot-search huggingface dataset:
Randomized phase 2 trial of nab-paclitaxel plus gemcitabine, ± capecitabine, cisplatin (PAXG regimen) in unresectable or borderline resectable pancreatic adenocarcinoma
Authors: M. Reni, S. Zanon, G. Balzano, P. Passoni, A. Costantino, C. Pircher, M. Chiaravalli, R. Nicoletti, P.G. Arcidiacono, G. Pepe, S. Crippa, C. Doglioni, C. Fugazza, D. Ceraulo, M. Falconi, L. Gianni
Journal: Annals of Oncology (2016)
IMST-25. CD70—A NOVEL TARGET OF CAR-T-CELL THERAPY FOR GLIOMAS
Authors: Linchun Jin, Haitao Ge, Changlin Yang, Yu Long, Yifan Chang, Luyan Mu, Elias Sayour, Gabriel De Leon, Qiong Wang, James Yang, Jeffrey Drake, Paul Kubilis, Hongbo Bao, Songsong Xia, Dunyue Lu, Yingjun Kong, Li Hu, Yibo Yin, Yujiao Shang, Chencheng Jiang, Jing Nie, Shimin Li, Jiping Qi, Yunhe Gu, Jiahang Sun, Zhiguo Lin, Duane Mitchell, Jianping Huang
Journal: Neuro-Oncology (2016)

Gliomas are the most common primary malignant brain tumor and are uniformly lethal. Cancer immunotherapy has the potential to target gliomas; however, its antitumor effects are restricted by limitations in clinically useful tumor specific targets. Chimeric antigen receptor modified T-cell (CAR-T) therapy is a highly promising option for cancer treatment, due to its combination of precision antibody recognition and T-cell tumor-specific killing. CD70 is an antigen expressed by limited subsets of normal lymphocytes and dendritic cells but is aberrantly overexpressed by glioma cells, which makes it an outstanding glioma-antigen target. The gene and protein expression of CD70 were evaluated to identify its potential as a glioma target. Human and mouse versions of CD70-specific CAR-T cells were generated, and human primary GBM lines as well as murine lines (GL-261, KR-158B) were used as human and mouse tumor targets, respectively. The antitumor effect of the human and mouse CD70-sepecific CARs were tested in vitro and in an orthotopic murine syngeneic model in vivo. CD70 is only overexpressed by tumor cells in a subset of low-grade gliomas and GBM. The elevated gene and protein expression are associated with increased tumor grade and poor patient survival. Co-culturing CD70-specific CAR-T cells with CD70-positive glioma cells resulted in potent secretion of IFN-gamma and tumor-specific killing in a CD70-dependent manner. Irradiation enhances CD70 expression on glioma cells and thus increases CAR T-cell recognition. Adoptive transferring of the CD70 CAR-T cells resulted in total regression of gliomas in the brain of immunocompetent mice. CD70 can be an excellent tumor target for gliomas, and CD70-specific CAR-T cells have potent antitumor activity against CD70-positive gliomas both in vitro and in vivo. Our study provides crucial preclinical evidence to support the future clinical application of CD70 CAR-T cells to treat gliomas.
A Phase I Trial of the Small Molecule Pan-Bcl-2 Family Inhibitor Obatoclax Mesylate (GX15-070) Administered by Continuous Infusion for up to Four Days to Patients with Hematological Malignancies.
Authors: Aaron D. Schimmer, Joseph Brandwein, Susan M. O’Brien, Hagop Kantarjian, Bruce D. Cheson, Mark D. Minden, Karen Yee, Andre Schuh, Vikas Gupta, Jean Viallet, Gautam Borthakur
Journal: Blood (2007)
TMOD-12. A NOVEL PATIENT-DERIVED XENOGRAFT MODEL OF BRAIN METASTASIS
Authors: Amin Kassam, Amber Lacrosse
Journal: Neuro-Oncology (2016)

The establishment of a disease model that adequately reflects the characteristics of metastatic brain tumors is crucial to the development of novel therapeutics. Patient-derived xenograft (PDX) models have a high clinical relevance, offering the potential for individualized patient treatment. Previous research demonstrated that successful PDX modeling can be achieved by direct intracranial implantation of metastatic cells or tissue into the lateral ventricle and frontal cortex, or through the use of a subarachnoid catheter placed into the cisterna magna. However, it is not known if one method is superior. Since injection of metastatic cells into the cerebrospinal fluid (CSF) increases the probability of cancer cell dissemination, we hypothesized that CSF injection of metastatic cells would yield a higher success rate of tumor development compared to animals that were injected in the frontal cortex. Patient-derived brain metastases obtained at surgery were immediately processed into single cell suspension and adaptively cultured as spheres in progenitor cell-enriching condition. After passage 2-6, 5 X 104 – 1 X 105 cells were injected into the frontal cortex, lateral ventricle, or cerebral aqueduct of female athymic nude mice at 6 – 10 weeks of age. The brains of neurologically symptomatic mice were histologically examined using 5-micron paraffin sections. We found that mice injected at the cerebral aqueduct displayed higher rate of tumorigenicity and shorter time to tumor development than those injected at the frontal cortex or lateral ventricle. (Figure 1) To the best of our knowledge this is the first report in which the cerebral aqueduct has been targeted for metastatic PDX modeling. Our data indicate that intracranial injection of metastatic cells into the cerebral aqueduct is a reproducible model to study both local growth of metastases and leptomeningeal disease.
Phase 3 study of quizartinib (AC220) monotherapy vs salvage chemotherapy (SC) in patients (pts) with FLT3-ITD+ acute myeloid leukemia (AML) refractory to or relapsed (R/R) after 1st-line treatment with or without hematopoietic stem cell transplant (HSCT) consolidation: the QuANTUM-R study
Authors: J. Cortes, G. Gammon, S. Khaled, G. Martinelli, A. Kramer, B. Steffen, D. Hogge, B.A. Jonas, H. Dombret, A. Perl
Journal: Annals of Oncology (2016)
Estimation of glomerular filtration rate in patients with abnormal body composition and relation with carboplatin toxicity
Authors: M. Bretagne, A. Jouinot, J.-P. Durand, C. Tlemsani, J. Arrondeau, O. Huillard, P. Boudou Rouquette, F. Goldwasser, J. Alexandre
Journal: Annals of Oncology (2016)
P08.18 LC-MS-based genome-wide profiling of glioblastoma multiforme reveals distinct metabolism within the invasive region
Authors: J. Wood, D. Kim, S. Smith, A. Lourdusamy, J. Ward, D. Barrett, R. Grundy, R. Rahman
Journal: Neuro-Oncology (2016)

subtypes showed that M1 was enriched with neural subtype-specific genes.Using the gene expression data from four fetal neuronal stem cell lines and 15 GBM-derived neural stem (GNS) cell lines, we found that M1 was also enriched for genes that are up regulated in GNS.CONCLUSIONS: These results provide empirical support for a unique gene network influencing GBM invasive margins and illustrate how systemslevel analyses can reveal relationships between invasion-associated genes in GBM. P08.
Nivolumab for previously treated unresectable metastatic anal cancer (NCI9673): a multicentre, single-arm, phase 2 study
Authors: Van K Morris, Mohamed E Salem, Halla Nimeiri, Syma Iqbal, Preet Singh, Kristen Ciombor, Blase Polite, Dustin Deming, Emily Chan, James L Wade, Lianchun Xiao, Tanios Bekaii-Saab, Luis Vence, Jorge Blando, Armeen Mahvash, Wai Chin Foo, Chimela Ohaji, Manolo Pasia, Gail Bland, Aki Ohinata, Jane Rogers, Amir Mehdizadeh, Kimberly Banks, Richard Lanman, Robert A Wolff, Howard Streicher, James Allison, Padmanee Sharma, Cathy Eng
Journal: The Lancet Oncology (2017)
Osteomyelosclerosis, Anemia and Extramedullary Hematopoiesis in Mice Deficient for the Transcription Factor NFAT (Nuclear Factor of Activated T Cells) c2
Authors: Satu Kyttälä, Wolfgang Bauer, Michael Haase, Ivonne Habermann, Gerhard Ehninger, Alexander Kiani
Journal: Blood (2008)
Bariatric surgery cuts hyperglycaemia in diabetes more than drugs alone, study finds
Authors: Susan Mayor
Journal: BMJ (2017)

Bariatric surgery plus intensive medical therapy is more effective than drug treatment alone in reducing or even resolving hyperglycaemia in overweight and obese patients with type 2 diabetes, five year results from a randomised trial have shown.1

Researchers randomly assigned 150 patients with type 2 diabetes (mean glycated haemoglobin 9.2%+1.5%) and a body mass index of 27-43 to treatment with intensive medical therapy alone or to bariatric surgery plus drug treatment. Surgery involved either Roux en Y gastric bypass or sleeve gastrectomy.

Five year results, reported in the New England Journal of Medicine ,1 …
EPID-02. SURVIVAL IN ELDERLY PATIENTS WITH GLIOBLASTOMA IN THE USA: BEVACIZUMAB-CONTAINING VERSUS NON-BEVACIZUMAB-CONTAINING REGIMENS
Authors: Jessica Davies, Irmarie Reyes-Rivera, Thirupathi Pattipaka, Stephen Skirboll, Beatrice Ugiliweneza, Shiao Woo, Maxwell Boakye, Josep Garcia, Eric Burton
Journal: Neuro-Oncology (2016)

Limited information on systemic treatment and outcome in elderly patients with glioblastoma is available. Since the 2009 accelerated FDA approval of bevacizumab as a single-agent therapy for adult patients with recurrent glioblastoma, bevacizumab-based regimens have become the standard of care in this setting. The objective of this analysis was to evaluate the effect of bevacizumab use on survival in elderly patients with glioblastoma, using a population-based database. We analyzed the Surveillance, Epidemiology, and End Results (SEER) Medicare database for patients aged >65 years diagnosed with primary glioblastoma between 01 Jan 2006 and 31 Dec 2011 who received anti-systemic cancer treatment (n=2,603). Patients who received bevacizumab-containing treatment at any time were included in the BEV group (n=597); all other patients were included in the non-bevacizumab (NBEV) group (n=2,006). To account for survival bias and time prior to bevacizumab treatment, a time-dependent multivariate Cox model was used to evaluate the association of BEV compared with NBEV on overall survival, adjusting for potential confounders: age, gender, Charlson comorbidity index, region, race, radiotherapy after initial surgery, and diagnosis of coronary artery disease. A higher proportion of patients in the BEV arm were female and/or white; BEV patients were younger and had fewer co-morbid conditions, more initial resections, and received more cycles of temozolomide than patients in the NBEV group. The mean time to initiation of bevacizumab from diagnosis was 10 months (25th–75th percentile: 4.8–12.8 months). The multivariate Cox model with bevacizumab exposure as a time-dependent variable showed that the BEV group was associated with a lower risk of death, compared with the NBEV group (hazard ratio 0.81 [95% confidence interval 0.72–0.90]). Exposure to bevacizumab-containing treatment was associated with a lower risk of death in elderly patients with glioblastoma in the USA.
Interim results from the completed first-in-human phase I dose escalation study evaluating MP0250, a multi-DARPin® blocking HGF and VEGF, in patients with advanced solid tumors
Authors: M.R. Middleton, A. Azaro, S. Kumar, P. Niedermann, J. Rodón, K.H. Herbschleb, J. Steiner, C. Zitt, D. Feurstein, S. Schreiner, D. Turner, K. Dawson, K. Tadjalli-Mehr, Evom Baur, M. Stumpp, A. Harstrick, R. Baird, A. Omlin
Journal: Annals of Oncology (2016)
Low dose computed tomography scan (LDCT) screening versus empiric surveillance in asbestos exposed subjects: an update from the ATOM002 study
Authors: G. Fasola, A. Follador, F. Barbiero, V. Rosolen, O. Belvedere, F. Grossi, C. Rossetto, S. Rizzato, M. Giavarra, L. Gerratana, F. Barbone
Journal: Annals of Oncology (2016)
Poor Mobilizers in an Autologous Hematopoietic Stem Cell Transplantation Setting: Matched Pair Analysis Profiling G-CSF and Plerixafor-Mobilized Stem Cells
Authors: Line Nederby, Lea Bjerre Hokland, Katrine Nielsen, Erik Kay Segel, Peter Hokland, Anne Stidsholt Roug
Journal: Blood (2012)
Efficacy, safety, and health-related quality of life (HRQoL) of regorafenib in patients with hepatocellular carcinoma (HCC) progressing on sorafenib: Results of the international, double-blind phase 3 RESORCE trial
Authors: J. Bruix, P. Merle, A. Granito, Y.-H. Huang, G. Bodoky, O. Yokosuka, O. Rosmorduc, V. Breder, R. Gerolami, G. Masi, P.J. Ross, S. Qin, T. Song, J.-P. Bronowicki, I. Ollivier-Hourmand, M. Kudo, M.-A. LeBerre, A. Baumhauer, G. Meinhardt, G. Han
Journal: Annals of Oncology (2016)
Biomarker Profiling Differentiates Sepsis from Cytokine Release Syndrome in Chimeric Antigen Receptor T-Cell Therapy for Acute Lymphoblastic Leukemia (ALL)
Authors: Simon F. Lacey, Pamela A Shaw, David T Teachey, Scott L. Weiss, Fang Chen, Vanessa E Gonzalez, Noelle Frey, David L Porter, Shannon L Maude, Stephan A Grupp, Edward Pequignot, Carl H June, Jan J. Melenhorst
Journal: Blood (2016)
Efficacy and safety of targeted agents for treatment of gastroenteropancreatic (GEP) neuroendocrine tumor (NET)
Authors: H. Chae, C. Yoo, K.-P. Kim, H.-M. Chang, T.W. Kim, Y.S. Hong, S.-M. Hong, S.C. Kim, B.-Y. Ryoo
Journal: Annals of Oncology (2016)
NIMG-45. THE ROLE OF MR SPECTROSCOPY AND DIFFUSION WEIGHTED MR IMAGING IN THE DIAGNOSIS OF GLIOBLASTOMA RELAPSE AFTER COMPLEX ONCOLOGY TREATMENT: FINAL RESULTS
Authors: Radim Jancalek, Tomas Kazda, Martin Bulik
Journal: Neuro-Oncology (2016)

The accurate identification of glioblastoma progression remains an unmet clinical need. The aim of this prospective single-institutional study is to determine and validate thresholds for the main metabolite concentrations obtained by MR spectroscopy (MRS) and the values of the apparent diffusion coefficient (ADC) to enable distinguishing tumor recurrence from pseudoprogression. Thirty-nine patients after the standard treatment of a glioblastoma underwent advanced imaging by MRS and ADC at the time of suspected recurrence - median time to progression was 6.7 months. The highest significant sensitivity and specificity to call the glioblastoma recurrence was observed for the total choline (tCho) to total N-acetylaspartate (tNAA) concentration ratio with the threshold ≥1.3 (sensitivity 100.0% and specificity 94.7%). The ADCmean value higher than 1313 × 10-6 mm2/s was associated with the pseudoprogression (sensitivity 98.3%, specificity 100.0%). The combination of MRS focused on the tCho/tNAA concentration ratio and the ADCmean value represents imaging methods applicable to early non-invasive differentiation between a glioblastoma recurrence and a pseudoprogression. However, the institutional definition and validation of thresholds for differential diagnostics is needed for elimination of setup errors before implementation of these multimodal imaging techniques into clinical practice, as well as into clinical trials.
Clonal Evolution and Lack of BCR-ABL1 Mutations in Pediatric Ph+ ALL Patients Resistant/Refractory to Imatinib Treatment
Authors: Valeria Cazzaniga, Paola De Lorenzo, Federica Mottadelli, Grazia Fazio, Tiziana Villa, Vincenzo Rossi, Martina Pigazzi, Marcela B. Mansur, Marco Zecca, Elena Barisone, Franco Locatelli, Giuseppe Basso, Maria Grazia Valsecchi, Mel Greaves, Andrea Biondi, Anthony M Ford, Giovanni Cazzaniga
Journal: Blood (2015)
A phase 1/2 trial of a monoclonal antibody targeting fucosyl GM1 in relapsed/refractory small cell lung cancer (SCLC): Safety and preliminary efficacy
Authors: Q.S.-C. Chu, B. Markman, N. Leighl, L. Krug, C. Rudin, D. Lathers, P. Basciano, P.M. Fracasso, G. Kollia, P. Phillips, G. Kolaitis, D. Williams, J. Jackson, N. Ready
Journal: Annals of Oncology (2016)
BCR-ABL Regulates Death Receptor Expression for TNF-Related Apoptosis-Inducing Ligand (TRAIL) in Philadelphia Chromosome-Positive Leukemia
Authors: Itaru Kuroda, Takeshi Inukai, Xiaochun Zhang, Jiro Kikuchi, Yusuke Furukawa, Atsushi Nemoto, Koshi Akahane, Kinuko Hirose, Hiroko Honna- Oshiro, Kumiko Goi, Keiko Kagami, Hideo Yagita, Tetsuzo Tauchi, Yasuhiro Maeda, Kanji Sugita
Journal: Blood (2011)
Final Results of A Phase 1 Study Investigating the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Quizartinib (AC220) Administered Daily to Patients with Relapsed or Refractory Acute Myeloid Leukemia Irrespective of FLT3-ITD Status
Authors: Jorge E. Cortes, Hagop M. Kantarjian, James M. Foran, Darejan Ghirdaladze, Mamia Zodelava, Gautam Borthakur, Guy Gammon, Denise Trone, Robert C Armstrong, Joyce James, Mark J. Levis
Journal: Blood (2012)
Reproducibility of colon tumor grade and relationship to recurrence in the context of clinical, pathologic, and genomic tumor features in 504 patients with stage II colon cancer treated with surgery alone at the Cleveland Clinic.
Authors: I. C. Lavery, F. L. Baehner, M. Lopatin, G. Iezza, C. Millward, K. Clark-Langone, M. Lee
Journal: Journal of Clinical Oncology (2011)

526 Background: High tumor grade is included in practice guidelines as a marker of higher recurrence risk in stage II colon cancer. Multiple systems for tumor grading exist, without a standardized approach. We characterize agreement of 2 methods for tumor grading and association with recurrence in the context of clinical, pathologic, and genomic tumor features including mismatch repair (MMR) and the 12-gene recurrence score (RS). Methods: Colon tumors were graded independently by 2 academic GI pathologists (P1, P2). Grade was defined by % tumor with gland-like structures: well (&gt; 95%), moderately (50-95%) and poorly (&lt; 50%) differentiated. P1 used this 3-tier system while P2 used 2-tier scheme with well and moderately differentiated tumors defined as low grade and poorly differentiated as high grade. All mucinous tumors were high-grade by P2 but not P1. Relationship to recurrence-free interval (RFI) was assessed by Cox regression. Results: Primary tumors from 504 stage II colon cancer treated with surgery alone were included. 18% (P1) and 31% (P2) were high grade. High grade tumors were more likely right-sided (≥ 60%) and MMR deficient (≥ 35%) for P1 and P2 (all p &lt; 0.001). Proportion of mucinous tumors was similar for high and low grade by P1 (25% vs. 21%, p = 0.39). P2 high grade trended to lower recurrence (HR = 0.63, p = 0.10) while P1 grade was not associated w/ RFI (p = 0.46). In multivariate analyses including grade and RS, P2 high grade was associated with lower recurrence (p = 0.007) but P1 grade was not associated w/ RFI (p = 0.30). Neither grade was associated w/ RFI (p &gt; 0.30) after controlling for RS, MMR, tumor location and mucinous histology. Using the two-tier scheme, agreement b/w the 2 pathologists was low (kappa = 0.30, 95% CI 0.21-0.39) in all pts and moderate if mucinous tumors were excluded (kappa = 0.52, 95% CI 0.40-0.64). Conclusions: High tumor grade was not found to be a marker of higher recurrence risk in stage II colon cancer. Other markers validated in stage II colon cancer, such as MMR and RS, should be considered. Interpathologist agreement on colon tumor grade is modest, even with central expert review. [Table: see text]
ANGI-01. TRANSFORMATION OF TUMOR ENDOTHELIAL CELLS TO MESENCHYMAL STEM CELL-LIKE CELLS INDUCES THERAPY RESISTANCE IN GLIOBLASTOMA
Authors: Menggui Huang
Journal: Neuro-Oncology (2016)

Newly formed tumor blood vessels deliver oxygen and nutrients and produce paracrine factors to tumor microenvironment, fueling tumor growth, progression and metastasis. Likewise, targeting vascular endothelial cells (ECs) has emerged as a fundamental strategy for cancer treatment. However, inefficient eradication and insufficient functional inhibition of tumor-associated ECs remains a major barrier for current anti-vascular therapies. As such, current anti-angiogenic therapies that mainly target vascular endothelial growth factor (VEGF) have encountered difficulties and failure in most types of malignant cancers. Our recent work has identified endothelial mesenchymal transformation in glioblastoma (GBM), which leads to the suppression of VEGF signaling in GBM-associated ECs and renders intrinsic EC resistance to anti-VEGF treatment (Huang et al, JCI 2016). Here, we reveal cell plasticity in ECs drives their resistance to chemotherapy. Our data show that tumor ECs derived from human GBM patients are resistant to chemotherapy, and the resistance correlates with the mesenchymalization in ECs. Utilizing EC lineage tracing in a genetic murine GBM model, we show that mesenchymal transformation induces EC resistance to temozolomide (TMZ) chemotherapy. Interestingly, transcriptome analysis by RNA deep sequencing reveals that ECs undergo transformation to mesenchymal stem cell (MSC)-like cells after expose to GBM microenvironment. ECs acquire MSC signature genes and stemness-associated transcriptional activation, leading to chemoresistance. Our further mechanistic study identifies a c-Met-mediated axis that induces canonical activation of Wnt signaling. Finally, genetic ablation and pharmacological inhibition of c-Met reduce EC transformation and overcome chemoresistance in ECs. These findings illustrate a cell transformation-based mechanism that controls chemoresistance in tumor ECs, and suggest that targeting c-Met may sensitize ECs to chemotherapy and improve anti-vascular treatment for cancers.
High incidence of metastases detected on 18F-FDG PET-CT in patients with gall bladder cancer incidentally discovered after laparoscopic cholecystectomy
Authors: A. Bhattacharya, R. Kumar, S.K. Vadi, A.K.R. Gorla, A. Sood, B.R. Mittal
Journal: Annals of Oncology (2016)
TP53 germline mutation testing in early onset breast cancer
Authors: B. Conte, L. Varesco, G. Iacono, F. Poggio, E. Blondeaux, A. Levaggi, A. D'Alonzo, C. Bighin, S. Giraudi, M. Vaglica, P. Pronzato, L. Del Mastro
Journal: Annals of Oncology (2016)
Updated safety and efficacy of durvalumab (MEDI4736), an anti-PD-L 1 antibody, in patients from a squamous cell carcinoma of the head and neck (SCCHN) expansion cohort
Authors: N.H. Segal, S.-H.I. Ou, A.S. Balmanoukian, E. Massarelli, J.R. Brahmer, J. Weiss, P. Schoffski, S.J. Antonia, C. Massard, D.P. Zandberg, C. Maher, S. Khleif, X. Jin, M. Rebelatto, K. Steele, J. Antal, A. Gupta, A. Spreafico
Journal: Annals of Oncology (2016)
Association of circulating cytokine and angiogenic factors (CAFs) with outcomes to second-line FOLFOX plus bevacizumab or cediranib in metastatic colorectal cancer.
Authors: S. Kopetz, H. T. Tran, D. Cunningham, B. Mookerjee, L. Pike, J. Jurgensmeier, J. Heymach
Journal: Journal of Clinical Oncology (2011)

406 Background: Chemotherapy combined with inhibitors of VEGF signaling is associated with improved outcomes, but biomarkers of therapeutic benefit have been elusive. Cediranib (Ced) is an oral VEGFR tyrosine kinase inhibitor that has been investigated as a treatment for metastatic colorectal cancer (mCRC). Methods: 215 patients with progressive disease and no prior VEGF inhibitor therapy were enrolled in a randomized phase II study of FOLFOX + Ced 20mg/d, Ced 30mg/d or bevacizumab (Bev) 10mg/kg (Cunningham D, et al. J Clin Oncol 26: 2008 (May 20 suppl; abstr 4028). 36 CAFs were analyzed at 3 time points (baseline, wk 4, wk 8). Groups were dichotomized by median CAF value. Hazard ratios (HRs) were estimated from a Cox model with a single term. Results: Data were available for &gt; 85% patients for each CAF. When pooled across all arms, several baseline CAFs including VEGF, interleukin (IL)-2Rα, IL-8 and PDGF were associated with improved PFS (Table). Low and high baseline CAF subgroups were evaluated for potential predictive CAFs. Pts with elevated baseline IL-8 did better with Ced 30mg/d than Bev (HR 0.6 for PFS, CI 0.3-1.0) while low IL-8 was associated with greater benefit from Bev than Ced (HR 2.1, CI 1.0 to 4.2). For Ced 20mg/d, PFS HRs were 0.9 (CI 0.5, 1.6) and 1.7 (CI 0.9, 3.2) for elevated and low baseline IL-8 respectively. Hepatocyte-growth factor (HGF) demonstrated a similar relationship, while a trend for the inverse association was seen with IP-10. Distinct patterns of cytokine modulation were seen between Ced and Bev during the 8 wks, including decreases of sVEGFR2, IL-13 and increases in osteopontin. Conclusions: Several potential prognostic factors for second-line mCRC therapy were identified including VEGF and IL-8. Further work in larger placebo-controlled studies is required to further evaluate predictive markers for VEGF signaling inhibitors. [Table: see text] [Table: see text]