tbuckley/cabot-search huggingface dataset:
ACTR-24. COMBINATION OF IFN’S PROLONGS THE SURVIVAL OF PATIENTS WITH HIGH GRADE GLIOMA AND IMPACT IN VITRO PROLIFERATION AND GENE EXPRESSION PATTERNS OF GENOMIC SUBTYPES
Authors: Iraldo Bello-Rivero, Agustin Arocha-Garcia, Rafael Dominguez-Pena, Margarita Rios-Cabrera, Lysy Rodriguez-Rodriguez, Norma Mora-Garcia, Idrian Garcia-Garcia, Dania Vazquez-Blomquist, Jamilet Miranda-Navarrro, Sieger Leenstra, Ivette Raices-Cruz, Reinier Hernandez-Rodriguez, Hector Santana-Milian
Journal: Neuro-Oncology (2016)

The interferons have demonstrated effectivity in the control of malignant glioma. The aim of this work is to evaluate the effect of the combination of IFNs alpha-2b and gamma in the treatment of high grade glioma (HGG) evaluating survival of patients and gene expression profiles of glioma genomic subtypes. Patients with HGG after signing an informed consent were treated with the combination of IFNs (HEBERFERON) 7.0 MIU, intravenously, 2–3 times a week for several months. Genomic subtypes of clones from malignant gliomas were treated in vitro with HEBERFERON and gene expression of IFN signaling pathway evaluated. Thirty six HGG patients at diagnosis (grade III: 15; grade IV: 21), with mean ages 46 ± 12 and 51 ± 13, respectively, were evaluated. Seventy two percent of patients received surgery and radiotherapy prior to HEBERFERON treatment. Median tumor resection was 80%. Eighty six and 57.1% of grade III and grade IV patients were alive at 12 months after surgery-RT and HEBEFERON administration. The schedule was well ­tolerated. In vitro combination of HEBERFERON with RT and TMZ showed a potentiation of anti-proliferative effect in some genomic clones, which is compatible with the radio-sensibilization of IFNs and the down regulation of gene expression of MGMT by HEBERFERON in several genomic clones (classic, proneural). No response to IFNs was associated to lower level of expression of components of IFN signaling in evaluated genomics subtypes. The prolongation of survival of patients with HGG and identification of the growth inhibitory response of malignant glioma subtypes to HEBERFERON and the molecular characterization of responders and nor responders will permit to design better treatment schedules in combination with other therapies to fight this devastating challenging form of cancer.
EXTH-16. THE KETONE BODY β-HYDROXYBUTYRATE INHIBITS HISTONE DEACETYLASE ACTIVITY AND ALTERS EXPRESSION OF DNA REPAIR PROTEINS IN MALIGNANT GLIOMA CELLS
Authors: Eric C. Woolf, Alex P. Rossi, Helena B. Silva-Nichols, Kara D. Gardner, Nelofer Syed, Adrienne C. Scheck
Journal: Neuro-Oncology (2016)

Several preclinical studies support the use of the therapeutic ketogenic diet (KD) as an adjuvant therapy for malignant glioma. These studies have demonstrated that this approach alters multiple hallmarks of cancer growth, and it may also enhance other therapeutic modalities. We have demonstrated that the KD greatly increases survival in a mouse model of malignant glioma when administered ad libitum in combination with radiation, yet the underlying mechanisms have not been fully elucidated. The KD causes a decrease in blood glucose and an increase in the blood ketones acetoacetate and β-hydroxybutyrate (βHB). It was recently demonstrated that βHB inhibits histone deacetylase (HDAC) activity in normal mouse tissue. Evidence suggests that many cancers exhibit increased HDAC activity which contributes to the epigenetic milieu found in tumors, alters DNA damage repair, and impacts radiosensitivity As the use of HDAC inhibitors for the treatment of brain tumors has generated great interest, we examined the effect of βHB on HDAC activity and radiosensitivity in the context of malignant glioma. We now report that βHB inhibits HDAC activity in a dose dependent manner in glioma cells and decreases expression of DNA damage repair proteins including RAD51, KU70, KU80, MRE11, and NBS1. We also found that βHB radiosensitizes mouse glioma cells, cells from human glioblastomas and human glioma stem-like cells in vitro. Further, cell cycle analysis demonstrated that βHB induces G2 arrest, providing an additional potential mechanism for the observed radiosensitivity. Western blot analyses show decreased expression of cyclin B1 and activation of cyclin-dependent kinase 2 (CDC2), two proteins that modulate G2 progression. Taken together this data opens up another avenue for understanding the mechanisms underlying the KD and its impact on radiation therapy, ultimately helping us better understand how to implement it for clinical use.
Dynamic presenilin 1 and synaptotagmin 1 interaction modulates exocytosis and amyloid β production
Authors: Katarzyna Marta Zoltowska, Masato Maesako, Iryna Lushnikova, Shuko Takeda, Laura J. Keller, Galina Skibo, Bradley T. Hyman, Oksana Berezovska
Journal: Molecular Neurodegeneration (2017)

Alzheimer's disease (AD)-linked protein, presenilin 1 (PS1), is present at the synapse, and the knock-out of presenilin in mice leads to synaptic dysfunction. On the other hand, synaptic activity was shown to influence PS1-dependent generation of distinct amyloid β (Aβ) species. However, the precise nature of these regulations remains unclear. The current study reveals novel role of PS1 at the synapse, and deciphers how PS1 and synaptic vesicle-associated protein, synaptotagmin 1 (Syt1) modulate each other functions in neurons via direct activity-triggered interaction. Additionally, the therapeutic potential of fostering PS1-Syt1 binding is investigated as a synapse-specific strategy for AD prevention. PS1-based cell-permeable peptide targeting PS1-Syt1 binding site was designed to inhibit PS1-Syt1 interaction in neurons. PS1 conformation, synaptic vesicle exocytosis and trafficking were assayed by fluorescence lifetime imaging microscopy (FLIM), glutamate release/synaptopHluorin assay, and fluorescence recovery after photobleaching, respectively. Syt1 level and interaction with PS1 in control and sporadic AD brains were determined by immunohistochemistry and FLIM. AAV-mediated delivery of Syt1 into mouse hippocampi was used to investigate the therapeutic potential of strengthening PS1-Syt1 binding in vivo. Statistical significance was determined using two-tailed unpaired Student's t-test, Mann-Whitney's U-test or two-way ANOVA followed by a Bonferroni's post-test. We demonstrate that targeted inhibition of the PS1-Syt1 binding in neurons, without changing the proteins' expression level, triggers "pathogenic" conformational shift of PS1, and consequent increase in the Aβ42/40 ratio. Moreover, our data indicate that PS1, by binding directly to Syt1, regulates synaptic vesicle trafficking and facilitates exocytosis and neurotransmitter release. Analysis of human brain tissue revealed that not only Syt1 levels but also interactions between remaining Syt1 and PS1 are diminished in sporadic AD. On the other hand, overexpression of Syt1 in mouse hippocampi was found to potentiate PS1-Syt1 binding and promote "protective" PS1 conformation. The study reports novel functions of PS1 and Syt1 at the synapse, and demonstrates the importance of PS1-Syt1 binding for exocytosis and safeguarding PS1 conformation. It suggests that reduction in the Syt1 level and PS1-Syt1 interactions in AD brain may present molecular underpinning of the pathogenic PS1 conformation, increased Aβ42/40 ratio, and impaired exocytosis.
Analysis of patient-reported outcomes by disease progression status in patients (pts) with BRAF V600–mutant metastatic melanoma in the COMBI-d and COMBI-v trials
Authors: C. Robert, D. Schadendorf, G.V. Long, D. Stroyakovskiy, E. Levchenko, V. Chiarion-Sileni, K. Flaherty, P. Nathan, A. Ribas, M. Davies, J. Zhang, L. Chen, B. Mookerjee, S. Redhu, J.J. Grob
Journal: Annals of Oncology (2016)
Michael John Aldridge
Authors: Stephen Aldridge
Journal: BMJ (2017)

As a medical student, Michael John Aldridge (“John”) spent his elective in Rhodesia (now Zimbabwe). When he returned there after his house jobs he met Eva, whom he later married, and discovered his passion for orthopaedics. He returned to Birmingham for his orthopaedic training and was appointed to Coventry and Warwickshire Hospital in 1977.

He was a pioneer in sports medicine at all levels. He worked closely with physiotherapists to develop an understanding of the …
HGS-ETR1, a fully human monoclonal antibody to the tumor necrosis factor-related apoptosis-inducing ligand death receptor 1 (TRAIL-R1) in patients with advanced solid cancer: Results of a phase 1 trial
Authors: S. J. Hotte, H. W. Hirte, E. X. Chen, L. H. Le, A. Corey, M. Maclean, A. Iacobucci, N. L. Fox, A. M. Oza
Journal: Journal of Clinical Oncology (2005)

3052 Introduction: HGS-ETR1 (TRM-1) is a fully human monoclonal antibody that is agonistic to the R1 (TRAIL-R1 or DR4) receptors for TRAIL that are expressed on the surface of multiple cancer cell types. A member of the TNF ligand superfamily, TRAIL has been shown to be an important mediator of apoptosis in cancer cell lines. Promising preclinical activity of HGS-ETR1 has been observed in multiple studies. Methods: This phase I, open-label, dose-escalation study assesses the tolerability and toxicity profile of ≥ 2 doses of HGS-ETR1 administered IV in patients (pts) with advanced solid tumors or NHL. Secondary objectives were to evaluate the pharmacokinetic (PK) profile and immunogenicity of HGS-ETR1. Pts received HGS-ETR1 every 28 days until progression or unacceptable toxicity and were evaluated weekly for toxicity. Tumor measurements were repeated after each second cycle. Results: The 6 planned escalation levels (in mg/kg) are: 0.01; 0.03; 0.3; 3.0; 10.0; and 20.0. To date, 24 pts, 14 of them female, with a median age of 56 yrs (range, 29–81 yrs) have been entered onto the first 4 cohorts. Twenty-two pts had PS of 0/1 and the commonest diagnoses were colorectal (9 pts) or ovarian cancer (5 pts). Pts received a median of 2 cycles (range, 1 - 14+) cycles. HGS-ETR1 has been very well tolerated with no clearly attributable toxicity other than 1 episode of gr 3 thrombocytopenia and one episode of transient grade 3 hypertension. Dose limiting toxicity has been not observed. Linear pharmacokinetics are observed for doses up to 0.3 mg/kg, consistent with a two compartment model with first order elimination from the central compartment. At doses of 3 and 10mg/kg, less than proportional increase in exposure is noted. No antibodies to HGS-ETR1 have yet been detected. No responses have yet been observed but 8 patients have stable disease for 2–14 cycles. Conclusions: HGS-ETR1 has been well tolerated. Dose escalation and accrual continues. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Human Genome Sciences Human Genome Sciences
Accelerated Proliferation and Limited Differentiation, Mediated through Jak2, Exacerbate Ineffective Erythropoiesis in β-Thalassemia.
Authors: Ella Guy, Ilaria Libani, Luca Melchiori, Thomas Scholzen, Raffaella Schiro, Pedro Ramos, Margrit Kernbach, Bettina Baron-Luehr, Laura Breda, Matteo Porotto, Maria de Sousa, Maria Domenica Cappellini, Patricia J. Giardina, Robert W. Grady, Johannes Gerdes, Stefano Rivella
Journal: Blood (2007)
Clinical Pharmacokinetics and FLT3 Phosphorylation of AC220, a Highly Potent and Selective Inhibitor of FLT3
Authors: Joyce James, Keith Pratz, Adam Stine, Julius L Apuy, Darren E Insko, Robert C Armstrong, Patrick P Zarrinkar, Donald Small, Wendell Wierenga, Mark J. Levis
Journal: Blood (2008)
Analysis of regional differences in the phase 3 METEOR study of cabozantinib (cabo) versus everolimus (eve) in advanced renal cell carcinoma (RCC)
Authors: N. Tannir, T. Powles, R.J. Motzer, F. Rolland, G. Gravis, M. Staehler, M. Rink, M. Retz, T. Csoszi, J. McCaffrey, U. De Giorgi, C. Caserta, S. Cheporov, E. Esteban Gonzalez, I. Duran, J.G. Larkin, W. Berg, D. Clary, B. Escudier, T.K. Choueiri
Journal: Annals of Oncology (2016)
Frequency, patterns and prognostic impact of distant metastases in a large mono-institutional series of malignant pleural mesothelioma (MPM): Not necessarily bad news
Authors: F. Grosso, A. Roveta, G. Gallizzi, A. Muzio, S. Zai, F. Ugo, A. Aurelio, R. Libener, M. Mancuso, G. Ferretti, P. Franzone, M. Pastormerlo, E. Piccolini, D. Degiovanni, G. Numico
Journal: Annals of Oncology (2016)
Phase 1b Study of TRU-016, an Anti-CD37 SMIP™ Protein, in Combination with Bendamustine Vs Bendamustine Alone in Relapsed Chronic Lymphocytic Leukemia
Authors: Farrukh Awan, Ulrich Jaeger, Robert Rifkin, Michael J Thirman, John C. Byrd, Michael Hallek, Scott Stromatt, John M. Pagel
Journal: Blood (2012)
BMET-24. LASER ABLATION AFTER STEREOTACTIC RADIOSURGERY (LAASR) – RESULTS OF A MULTI-CENTERED PROSPECTIVE STUDY
Authors: Veronica Chiang, Jorg Dietrich, Steven Tatter, Alireza Mohammadi, Eric Leuthardt, Roukoz Chamoun, Kevin Judy, Gene Barnett, Manmeet Ahluwalia
Journal: Neuro-Oncology (2016)

The Laser Ablation After Stereotactic Radiosurgery (LAASR) Study was performed to prospectively determine safety, efficacy and outcome of use of laser ablation in patients with progressive brain metastases following prior stereotactic radiosurgery. STUDY DESIGN: Patients were included if they had Karnofsky Performance Status (KPS) ≥60, age >18 years and ability to undergo surgery. Primary outcome was Progression Free Survival (PFS) as assessed by RANO criteria. Secondary outcomes were overall survival (OS), safety and tolerability, cognitive function as measured by HVLT-R and MMSE and quality of life (QoL) as measured using FACT-Br. 42 subjects were treated with laser ablation between October 2012 and December 2015. 19 patients had biopsy-proven radiation necrosis (RN), 20 had recurrent tumor (TM) and 3 had no biopsy. Mean age was 58 years, 60% of subjects were female and median KPS was 85 (range 60-100). Predominant primary tumor pathologies were lung (48%), breast (17%) and melanoma (10%). Mean tumor volume was 6.5cc (range 0.4-38.6). Median length of hospital stay was 2.2 days. Approximately 40% of subjects were able to stop or reduce steroid usage at both 12 and 26 weeks after surgery. Median KPS scores for the group did not change significantly over 26 weeks. PFS and QoL data is being analyzed (will be presented at meeting). OS for the whole group was 89.7% at 12 weeks and 74.9% at 26 weeks. Analysis based on pathology showed OS at 12 and 26 weeks to be 100% and 80%, respectively, for RN patients compared with 78.9% and 72.4% for TM patients. These preliminary results suggest that laser ablation can be effective in preserving KPS and can have a steroid sparing effect in patients with progressive brain metastases or radiation necrosis after radiosurgery.
Sethi G, Ahn KS, Pandey MK, Aggarwal BB. Celastrol, a novel triterpene, potentiates TNF-induced apoptosis and suppresses invasion of tumor cells by inhibiting NF-κB-regulated gene products and TAK1-mediated NF-κB activation. Blood. 2007;109(7):2727-2735.
Journal: Blood (2013)
Lymphoproliferative Disease Risk in Patients with Autoimmune Disease: Clustering of Primary CNS Lymphoma with Drug Regimen and Disease Process
Authors: Genevieve Marie Crane, Helen Powell, Rumen Kostadinov, Peter C. Burger, Richard F. Ambinder, Lode J. Swinnen, Michael J. Borowitz, Amy S. Duffield
Journal: Blood (2015)
Characteristics of homologous recombination deficiency (HRD) in paired primary and recurrent high-grade serous ovarian cancer (HGSOC)
Authors: J. Patel, J. Sehouli, K. Timms, C. Solimeno, J. Reid, J. Lanchbury, I. Braicu, S. Darb-Esfahani, M. Ganapathi, R. Ganapathi
Journal: Annals of Oncology (2016)
A phase 2 study of the aurora kinase A inhibitor alisertib for patients with neuroendocrine prostate cancer (NEPC)
Authors: H. Beltran, D. Danila, B. Montgomery, R. Szmulewitz, U. Vaishampayan, A. Armstrong, M. Stein, C. Hoimes, J. Pinski, H. Scher, L. Puca, R. Bareja, W. Wong, M. Rubin, J.M. Mosquera, A. Sboner, C. Oromendia, D. Nanus, K. Ballman, S.T. Tagawa
Journal: Annals of Oncology (2016)
Neutrophil to lymphocyte ratio (NLR) impact on the survival and response duration of patients with metastatic castration resistant prostate cancer (mCRPC) treated with abiraterone acetate (AA)
Authors: A.B. Mansinho, D. Macedo, I.C. Fernandes, A. Quintela, L.A.M. Costa
Journal: Annals of Oncology (2016)
DRES-02. YOUNG ADULT PATIENTS WITH ANAPLASTIC GLIOMA MAY NOT BENEFIT FROM RADIATION PLUS TMZ TREATMENT COMPARED TO RADIATION ONLY
Authors: Yang Pei
Journal: Neuro-Oncology (2016)

Age is the major therapy-independent prognostic factor in malignant gliomas, but few studies have investigated treatment and survival of young adults. We aim to assess the relevance of survival and treatment in age-specific subgroups, especially younger adult patients with high-grade gliomas in a large-scale population from the Chinese Glioma Genome Atlas (CGGA). 726 patients with confirmed anaplastic glioma or glioblastoma were enrolled in this study. Overall survival and progression-free survival were analyzed according to treatment in young adults (age<50) and older adults (age≥50). In total, 264 of 726 of the patients were older patients (OP), and 462 were young patients (YP). Among all GBM patients and OP with anaplastic gliomas, patients assigned to RT plus TMZ had significantly longer OS and PFS than patients assigned to RT alone (P<0.05). In contrast, among YP with anaplastic gliomas, a more favorable survival benefit was not observed in the RT plus TMZ treatment group compared to the RT only group. We observed no survival benefit in young adult patients (age<50) with anaplastic glioma when TMZ was added to RT. Our findings should provoke discussion in relation to younger patients with anaplastic glioma who are receiving radiotherapy plus TMZ chemotherapy.
Efficacy of R723, a Potent and Selective JAK2 Inhibitor, in JAK2V617F-Induced Murine MPD Model.
Authors: Kotaro Shide, Takuro Kameda, Vadim Markovtsov, Takuya Matsunaga, Haruko Shimoda, Tomonori Hidaka, Keiko Katayose, Yoko Kubuki, Somasekhar Bhamidipati, Gary Park, Allan Torneros, Matt Duan, Yasumichi Hitoshi, Kazuya Shimoda
Journal: Blood (2009)
Prediction of tumor response after neoadjuvant chemoradiotherapy in rectal cancer using 18fluorine-2-deoxy-d-glucose positron emission tomography-computed tomography: a prospective study
Authors: A. Del Freo, R. Della Seta, F. Federici, M.P. Muttini, P. Pacetti, M. Pedata, M.C. Pennucci, C. Valsuani, S. Venturini, A. Tagliagambe, A. Grandinetti, M. Rotellini, A. Ginori, A. Mambrini
Journal: Annals of Oncology (2016)
Final results of the FAST study, an international, multicenter, randomized, phase II trial of epirubicin, oxaliplatin, and capecitabine (EOX) with or without the anti-CLDN18.2 antibody IMAB362 as first-line therapy in patients with advanced CLDN18.2+ gastric and gastroesophageal junction (GEJ) adenocarcinoma
Authors: M. Schuler, S.-E. Al-Batran, Z. Zvirbule, G. Manikhas, F. Lordick, A. Rusyn, Y. Vinnyk, I. Vynnychenko, N. Fadeeva, M. Nechaeva, A. Dudov, E. Gotovkin, A. Pecheniy, I. Bazin, I. Bondarenko, B. Melichar, C. Huber, Ö Türeci, U. Sahin
Journal: Annals of Oncology (2016)
PDTB-19. EphA RECEPTOR TYROSINE KINASES AS TARGETS FOR THERAPY IN PAEDIATRIC MEDULLOBLASTOMA
Authors: Benjamin Carrington, Fares Al-Ejeh, Yi Chieh Lim, Kathleen Ensbey, Zara Bruce, Paul Jamieson, Adrian Fuchs, Kristofer Thurecht, Brett Stringer, Andrew Boyd, Bryan Day
Journal: Neuro-Oncology (2016)

Medulloblastoma is a malignant neuroepithelial tumor that arises in the cerebellum. The overall long term survival is approximately 75%, the prospects are much less optimistic for children under five where survival is less than 50%. To achieve optimal survival, treatment involves both surgery and chemoradiotherapy. The long term effects on quality of life from radiation therapy are very significant, particularly cognitive impairment in young children. This motivates a search for novel therapies to provide better outcomes for this disease. Eph receptors and ephrin ligands are widely expressed and function normally during early embryonic development. They have been shown to be re-expressed and functional in a number of human cancers. Recent published findings have shown that EphA receptors are over expressed in glioblastoma and functionally promote a more aggressive stem cell-like phenotype in a kinase independent manner. Very little is known about Eph family receptors in medulloblastoma. We therefore undertook a study to examine EphA receptor function and to determine if these receptors might be alternative therapeutic targets in this disease. Our findings show elevated subtype-specific expression and activation of both EphA2 and EphA3 in paediatric medulloblastoma. Interestingly, EphA2 and EphA3 were most highly activated in the WNT subtype, which has the best ­prognosis, suggesting that EphA receptor activation may have tumor-suppressive functions in this subtype. EphA2 and EphA3 kinase function were intact, showing robust activation following stimulation with ephrin ligand. Furthermore, EphA2 activation led to a significant decrease in medulloblastoma cell migration in-vitro. Either EphA2 or EphA3 shRNA mediated knockdown attenuated medulloblastoma cell growth in-vitro and reduced tumor formation in-vivo. As a therapeutic proof of principle, we tested EphA2 and EphA3 specific monoclonal antibody drug conjugate targeting. Robust cell killing was observed in-vitro, while an EphA3-maytansine conjugate significantly reduced the size of developed orthotopic tumors in-vivo with minimal toxicity.
IMST-18. LOW-DOSE RADIATION ALTERS ONCOGENE LEVELS AND ENHANCES T-CELL IMMUNE RECOGNITION IN HUMAN MEDULLOBLASTOMA CELLS
Authors: Stephen Lowe, Ramin Eskandari, Daniel G. McDonald, Amy-Lee Bredlau, Kenneth N Vanek, Naren L Banik, Joseph M Jenrette, Samuel Cheshier, Arabinda Das
Journal: Neuro-Oncology (2016)

Group 3 and 4 Medulloblastoma have very poor survival rates compared with groups 1 and 2, and are strongly associated with elevated levels of the oncogenes c-MYC, CDK6, MYCN, but also have several pro-tumor molecular alterations; 1) defects in β2-microglobulin (β2m) synthesis, 2)loss of the gene(s) encoding HLA antigen heavy chain(s), 3) mutations inhibiting HLA antigen heavy chain transcription or translation, 4) defects in the regulatory mechanisms controlling HLA antigen expression and 5) abnormalities in one or more of the antigen processing machinery (APM) components. Although many of c-MYC’s functions for Group 3 and CDK6 and MYCN functions for Group 4 have been elucidated, medulloblastoma cell presentation of antigen through the HLA class I/II pathway has not been reported. Thus, our aim was to study the effect of low-dose X-ray radiation (LDXR: 1 Gy) on the functional immunological responses of Group 3 and 4 MB cells (D283, and D341) with respect to c-MYC, CDK6 and MYCN functions. Western blot analysis showed LDXR reduced expression of c-Myc in group 3 and CDK6 and MYCN expression in group 4 medulloblastoma cells respectively by 20%. Interestingly, LDXR reduced the expression of histone methylases EZH2 and KDM6A, which are exclusively expressed in group 3 and 4 medulloblastoma. At the same time LDXR upregulated medulloblastoma cell expression of human leukocyte antigen (HLA) class I, and HLA II molecules (i.e. HLA-DP, HLA-DQ, HLA-DR complex, HLA-DM) by greater than 20% compared to non-irradiated cells in vitro. Invariant chain expression was also reduced by greater than 25%in the LDXR group, corresponding to increased activation of cytotoxic CD8+T and helper CD4+ T-cells and for enhanced effector T-cell responses. These results suggest that LDXR may alter several immune modulating molecules, enhancing T-cell/tumor-cell interaction and potentially enhance T-cell mediated medulloblastoma cell death.