Autologous Cell-Based Products

Author(s):  
Eduardo Bravo ◽  
Magdalena Blanco-Molina
Keyword(s):  
2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
M. Arar ◽  
A. Rotärmel ◽  
A.-K. Knoefel ◽  
H. Baraki ◽  
I. Kutschka ◽  
...  

2021 ◽  
pp. 1-6
Author(s):  
Joseph Stavas ◽  
Maria Diaz-Gonzalez de Ferris ◽  
Ashley Johns ◽  
Deepak Jain ◽  
Tim Bertram

Background: Advanced cell therapies with autologous, homologous cells show promise to affect reparative and restorative changes in the chronic kidney disease (CKD) nephron. We present our protocol and preliminary analysis of an IRB-approved, phase I single-group, open-label trial that tests the safety and efficacy of Renal Autologous Cell Therapy (REACT; NCT 04115345) in adults with congenital anomalies of the kidney and urinary tract (CAKUT). Methods: Adults with surgically corrected CAKUT and CKD stages 3 and 4 signed an informed consent and served as their “own” baseline control. REACT is an active biological ingredient acquired from a percutaneous tissue acquisition from the patient’s kidney cortex. The specimen undergoes a GMP-compliant manufacturing process that harvests the selected renal cells composed of progenitors for renal repair, followed by image-guided locoregional reinjection into the patient’s renal cortex. Participants receive 2 doses at 6-month intervals. Primary outcomes are stable renal function and stable/improved quality of life. Additional exploratory endpoints include the impact of REACT on blood pressure, vitamin D levels, hemoglobin, hematocrit and kidney volume by MRI analysis. Results: Four men and 1 woman were enrolled and underwent 5 cell injections. Their characteristics were as follows: mean 52.8 years (SD 17.7 years), 1 Hispanic, 4 non-Hispanic, and 5 white. There were no renal tissue acquisition, cell injection, or cell product-related complications at baseline. Conclusion: REACT is demonstrating feasibility and patient safety in preliminary analysis. Autologous cell therapy treatment has the potential to stabilize or improve renal function in CAKUT-associated CKD to delay or avert dialysis. Patient enrollment and follow-up are underway.


Author(s):  
Massis Krekorian ◽  
Gerwin G. W. Sandker ◽  
Kimberley R. G. Cortenbach ◽  
Oya Tagit ◽  
N. Koen van Riessen ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akira Yoshida ◽  
Tomoaki Takata ◽  
Tsutomu Kanda ◽  
Naoyuki Yamaguchi ◽  
Hitomi Minami ◽  
...  

AbstractThe tumour microenvironment (TME) plays an important role in cancer development, progression, and metastasis. Various cytokines are present in the TME in oesophageal cancer. Oesophageal stricture is a major complication of endoscopic submucosal dissection (ESD) for oesophageal cancer, and inflammatory cytokines are closely related to its pathogenesis. However, the cytokine crosstalk involved in the oesophageal cancer TME and post-ESD stricture has not been fully elucidated. This study investigated the comprehensive cytokine dynamics following ESD in patients with oesophageal cancer. In addition, the effect of a novel preventive technique for post-ESD stricture, autologous cell sheet engraftment, on cytokine levels was evaluated. Various pro-inflammatory and anti-tumorigenic cytokines were elevated in patients with oesophageal cancer, and ESD transiently influenced cytokine concentrations. IL-1β and TNF-α, two major pro-inflammatory cytokines that induce oesophageal stricture, were significantly suppressed by cell sheet engraftment. In conclusion, this study revealed the distinct cytokine dynamics after ESD in patients with oesophageal cancer, together with the effect of autologous cell sheet engraftment on cytokine fluctuation. These results can accelerate research on the TME and therapeutic strategies for oesophageal cancer.


Cytotherapy ◽  
2017 ◽  
Vol 19 (5) ◽  
pp. S41
Author(s):  
S. Luther ◽  
S. Punreddy ◽  
T. Lawson ◽  
A. Verma ◽  
S. Rigby ◽  
...  

Spine ◽  
2013 ◽  
Vol 38 (4) ◽  
pp. E217-E222 ◽  
Author(s):  
Roger Kirk Owens ◽  
Charles H. Crawford ◽  
Mladen Djurasovic ◽  
Chelsea E. Canan ◽  
Lauren O. Burke ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document