Long-term followup of bi-shRNAfurin and GMCSF augmented autologous tumor cell immunotherapy treated colorectal cancer patients in phase I and IIa studies.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e15100-e15100
Author(s):  
Minal A. Barve ◽  
Anton M. Melnyk ◽  
Luisa Manning ◽  
Gladice Wallraven ◽  
Martin Birkhofer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cell ◽  
Phase I ◽  
Checkpoint Inhibitors ◽  
Disease Free Survival ◽  
Stage Iii ◽  
Autologous Tumor Cell ◽  
Autologous Tumor ◽  
Disease Free

e15100 Background: Vigil is an immuno-stimulatory autologous tumor cell therapy, which uses patient tumor cells transfected with a plasmid encoding genes to upregulate GM-CSF and down regulate TGFβ 1&2. It is administered monthly by intra-dermal injection. In Phase I and IIa trials patients with over 19 different tumor types were safely treated. Rapid and durable systemic immune activation was demonstrated using an IFNγ ELISPOT assay. Methods: Data are summarized for a group of 9 patients with advanced colorectal cancer followed for up to 3.5 years. Results: Six women and 3 men with Stage III or IV colorectal cancer were treated between March, 2010 and September, 2013. Six patients received Vigil as a monotherapy and 3 in combination with FOLFOX chemotherapy. Results: Demographics and treatment details are displayed below. Two patients with Stage III disease received combination therapy after complete surgical resection, and remain disease free over 3 years from surgery. The patients received 9 and 12 Vigil injections with a brisk and durable ELISPOT reactions. Conclusions: Preliminary results suggest that Vigil can be combined safely with FOLOX chemotherapy and still elicit a systemic immune response. Long term disease free survival has been observed in several patients justifying further exploration of this combination. More detailed molecular characterization and neoantigen identification of patient tumor will be undertaken in future studies. A combination with immune checkpoint inhibitors may also be explored. [Table: see text]

scholarly journals Comparative analysis ofBRAF,NRASandc-KITmutation status between tumor tissues and autologous tumor cell-lines of stage III/IV melanoma

2014 ◽  
Vol 24 (1) ◽  
pp. 70-73 ◽  
Author(s):  
Anne-Chantal Knol ◽  
Marie-Christine Pandolfino ◽  
Audrey Vallée ◽  
Frédérique Nguyen ◽  
Virginie Lella ◽  
...  
Keyword(s):  
Comparative Analysis ◽  
Tumor Cell ◽  
Cell Lines ◽  
Stage Iii ◽  
Autologous Tumor Cell ◽  
Autologous Tumor ◽  
Tumor Cell Lines ◽  
Tumor Tissues

Clinical relevance of tumor cell ploidy and N-myc gene amplification in childhood neuroblastoma: a Pediatric Oncology Group study.

1991 ◽  
Vol 9 (4) ◽  
pp. 581-591 ◽  
Author(s):  
A T Look ◽  
F A Hayes ◽  
J J Shuster ◽  
E C Douglass ◽  
R P Castleberry ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Gene Amplification ◽  
Gene Copy Number ◽  
Disease Free Survival ◽  
Gene Copy ◽  
Early Treatment Failure ◽  
Free Survival ◽  
Myc Gene ◽  
Disease Free

We assessed tumor cell DNA content (ploidy) and N-myc gene copy number as predictors of long-term disease-free survival in 298 children with neuroblastoma. Diploid tumor stem lines were identified in 101 patients (34%), clonal hyperdiploid abnormalities in 194 (65%), and hypodiploid stem lines in three (1%). In children with widely disseminated tumors at diagnosis (stage D), ploidy had a highly age-dependent influence on prognosis. Among infants (less than 12 months) treated with cyclophosphamide-doxorubicin, hyperdiploidy was closely associated with long-term disease-free survival (greater than 90% of cases), while diploidy invariably predicted early treatment failure (P less than .001). Similarly, in children 12 to 24 months of age who were treated with cisplatin-teniposide and cyclophosphamide-doxorubicin, diploidy uniformly predicted early failure, whereas half of the children with hyperdiploidy achieved long-term disease-free survival (P less than .001). There was no relationship between ploidy and treatment outcome in children older than 24 months with stage D tumors who had a very low probability of long-term disease-free survival (less than 10%). N-myc gene amplification was detected in 37 (25%) of the 147 tumors tested, with the remainder showing single-copy levels of the gene. N-myc gene amplification was more frequent in diploid than in hyperdiploid tumors (23 of 57 v 14 of 87, P = .001) and predicted a high likelihood of early treatment failure. In children younger than 2 years with disseminated neuroblastoma, tumor cell ploidy and N-myc gene copy number provide complementary prognostic information that will distinguish patients who can be cured on current regimens from those who require new treatment strategies.

scholarly journals Retrospective analysis of the effect of CAPOX and mFOLFOX6 dose intensity on survival in colorectal patients in the adjuvant setting

2016 ◽  
Vol 23 (3) ◽  
pp. 171 ◽  
Author(s):  
A. Mamo ◽  
J. Easaw ◽  
F. Ibnshamsah ◽  
A. Baig ◽  
Y.S. Rho ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dose Reduction ◽  
Real Life ◽  
Disease Free Survival ◽  
Dose Intensity ◽  
Sensory Neuropathy ◽  
Stage Iii ◽  
Cancer Centre ◽  
Peripheral Sensory ◽  
Disease Free

Background Despite lack of a true comparative study, the FOLFOX (5-fluorouracil–leucovorin–oxaliplatin) and CAPOX (capecitabine–oxaliplatin) regimens are believed to be similar in their efficacy and tolerability in the treatment of stage III colorectal cancer. However, that belief has been disputed, because real-life data suggest that the CAPOX regimen is more toxic, leading to more frequent reductions in the delivered dose intensity—thus raising questions about the effect of dose intensity on clinical outcomes.Methods A retrospective data review for two Canadian institutions, the Segal Cancer Centre and the Tom Baker Cancer Centre, considered patients diagnosed with stage III colorectal cancer during 2006–2013. Primary endpoints were dose intensity and toxicity, with a secondary endpoint of disease-free survival.Results The study enrolled 180 eligible patients (80 at the Segal Cancer Centre, 100 at the Tom Baker Cancer Centre). Of those 180 patients, 75 received CAPOX, and 105 received mFOLFOX6. In the CAPOX group, a significant dose reduction was identified for capecitabine compared with 5-fluorouracil in mFOLFOX6 group (p = 0.0014). Similarly, a significant dose reduction was observed for oxaliplatin in mFOLFOX6 compared with oxaliplatin in CAPOX (p = 0.0001). Compared with the patients receiving CAPOX, those receiving mFOLFOX6 were twice as likely to experience a treatment delay of more than 1 cycle-length (p = 0.03855). Toxicity was more frequent in patients receiving mFOLFOX6 (nausea: 30% vs. 18%; diarrhea: 47% vs. 24%; peripheral sensory neuropathy: 32% vs. 3%). At a median follow-up of 40 months, preliminary data showed no difference in disease-free survival (p = 0.598). Pooled data from both institutions were also separately analyzed, and no significant differences were found.Conclusions Our results support the use of CAPOX despite a lack of head-to-head randomized trial data.

Phase I/II Trial of Autologous Tumor Cell Line–Derived Vaccines for Recurrent or Metastatic Sarcomas

2004 ◽  
Vol 19 (5) ◽  
pp. 581-588 ◽  
Author(s):  
Robert Dillman ◽  
Neil Barth ◽  
Senthamil Selvan ◽  
Linda Beutel ◽  
Cristina de Leon ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Phase I ◽  
Cell Line ◽  
Tumor Cell Line ◽  
Autologous Tumor Cell ◽  
Autologous Tumor

scholarly journals Phase I Trial of TGF-β2 Antisense GM-CSF Gene-Modified Autologous Tumor Cell (TAG) Vaccine

2011 ◽  
Vol 17 (1) ◽  
pp. 183-192 ◽  
Author(s):  
Jairo Olivares ◽  
Padmasini Kumar ◽  
Yang Yu ◽  
Phillip B. Maples ◽  
Neil Senzer ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Phase I ◽  
Phase I Trial ◽  
Autologous Tumor Cell ◽  
Autologous Tumor ◽  
Gm Csf

Phase I/II Trial of Autologous Tumor Cell Line–Derived Vaccines for Recurrent or Metastatic Sarcomas

2004 ◽  
Vol 19 (5) ◽  
pp. 581-588 ◽  
Author(s):  
Robert Dillman ◽  
Neil Barth ◽  
Senthamil Selvan ◽  
Linda Beutel ◽  
Cristina de Leon ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Phase I ◽  
Cell Line ◽  
Tumor Cell Line ◽  
Autologous Tumor Cell ◽  
Autologous Tumor
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