[8,11,12,13,14]. In both instances, natural or environmental, MN are the terminal result of the cellular repair of genomic errors which allow for cell survivability by the excision of fatal genomic errors that otherwise would be lethal to cells. DNA damage that occurs in MN induces chromosomal rearrangements, a process called chromothripsis which then allows these MN formations to serve a purpose in the pathogenesis of cancer [10].
After the baseline blood draw, the treatment cohort received either FOLFOX (n = 17), FOLFIRI (n = 4), or single agent inhibitors (i.e., leronlimab or cetuximab) (n = 4).
Figure 4.
(b) Patient B. A patient with progressive disease on FOLFOX was started on a single agent CCR5 inhibitor (Leronlimab, blue), which was followed by a decrease in MN correlating with a reduction (−39%) in tumor size. MNs then increased slightly, which correlated with a slight increase in tumor size (+11% and a possible new lung lesion) at which point FOLFIRI (purple) was started. After FOLFIRI induction, a drop in MN was seen which correlated with stable disease.
Funding
This manuscript was supported by the U.S. Army Research Office (ARO) and the Defense Advanced Research Projects Agency (DARPA) (W911NF-14-C-0098).
Publication Fees for this manuscript were paid for by Creatv MicroTech, Inc.
( Dr. Adams once again)
https://www.mdpi.com/2227-9059/10/11/2898
This was clinical trial NCT04504942
** the DOD also partially funded our 2024 FcRn abstract work