Cellectis

Cellectis Publishes a Molecular Therapy Article on a SMART DUAL CAR T-cell Approach for Treating Recalcitrant Solid Tumors. To read the press release: https://lnkd.in/e-U_JD6D #celltherapy #cancer

Graft-versus-Host Disease (GvHD): a key consideration in allogeneic cell therapies?   In the world of allogeneic CAR T-cell therapies, Graft-versus-Host Disease (GvHD) is our double-edged sword.   Imagine these powerful T-cells as elite mercenaries, hired to eliminate a dangerous threat - cancer.   They're incredibly effective, but there's a catch: they're foreigners in your body's landscape.   Like a mercenary force that can't distinguish between civilians and enemies, these T-cells may mistakenly attack healthy tissues, leading to GvHD.   GvHD occurs when donor immune cells recognize the recipient's tissues as foreign and attack them. This can be a serious complication in treatments using donor-derived cells.   Allogeneic CAR T cell therapies are engineered to minimize GvHD risk.   Recent advancements have dramatically reduced this risk: For example, disruption of the T-cell receptor alpha constant (TRAC) gene minimizes risk of GvHD. Current data suggests that the GvHD risk in allogeneic CAR T-cell therapy is much lower than initially feared: A study (link at the end) involved the use of an allogeneic CAR T-cell product demonstrated a manageable safety profile with no clinically significant GvHD observed. Specifically, only 2 out of the 25 patients involved in the study developed grade 1 acute cutaneous GvHD, indicating a low incidence of GvHD in the trial. While allogeneic CAR T-cell therapy still carries a risk of GvHD, ongoing research and technological advancements are making it an increasingly safe option, potentially offering the benefits of "off-the-shelf" availability without significantly compromising patient safety. What are your thoughts on the future of allogeneic CAR T-cell therapies in minimizing GvHD? Drop them in the comments ⤵ https://lnkd.in/ebzkVm4i #celltherapy #genetherapy #cancer

Cellectis appoints Dr. Adrian Kilcoyne MD MPH MBA as Chief Medical Officer. To read the press release: https://lnkd.in/gnxQAZNS #celltherapy #genetherapy

Cellectis Provides Financial Results for the Second Quarter 2024. Full press release available here: https://lnkd.in/eF4gB3qV #celltherapy, #geneediting, #allogeneic

FDA Grants Orphan Drug Designation to Cellectis’ CLLS52 (alemtuzumab) For ALL Treatment. Full press release here: https://lnkd.in/esEkSr7P #allogeneic, #celltherapy, #genetherapy

FDA Grants Orphan Drug and Rare Pediatric Disease Designation Status to Cellectis’ UCART22 product candidate for Acute Lymphoblastic Leukemia (ALL) Treatment. Full press release available here: https://lnkd.in/g6Y5pNnE #allogeneic, #celltherapy, #genetherapy

When T-Cells Fail: The Struggle Against Cancer 🔍   T-cells are a key component of the body's natural defense against cancer.   But in this gripping video, we observe T-cells trying and failing to attack cancer cells. Despite their best efforts, the T-cells are outmatched. Tumors have evolved cunning ways to escape T-cell mediated killing. They've developed mechanisms to evade detection, such as downregulating tumor antigens or releasing immunosuppressive factors. This allows cancers to grow unchecked by the immune system.   Exhausted, the T-cells are forced to retreat, losing their ability to effectively kill cancer cells.   Harnessing and enhancing the anti-tumor activity of T-cells is a major focus of cancer immunotherapy research and treatment.   Immunotherapy works by blocking the inhibitory signals that cancer cells use to suppress T-cell activity, thereby reinvigorating the T-cell response against the tumor.   What do you think is the most promising approach to cancer immunotherapy? Share your thoughts below ⤵ Thanks to the team at Nanolive SA for sharing this video, which was captured label-free using a Nanolive holotomographic microscope. #cancer #celltherapy

The promise of universal CAR T-cells is to make personalized cancer treatments available off-the-shelf.   But there's been one hurdle: graft-versus-host disease. Graft-versus-Host Disease (GvHD) occurs when the donor T cells (the graft) recognize the recipient's body (the host) as foreign and attack it. This can lead to severe complications, such as skin damage, liver failure or immune system suppression.   Researchers are developing innovative strategies to prevent GvHD, such as:   ✅ TCR Elimination: The most widely used approach is to genetically remove or inactivate the T cell receptor (TCR) from allogeneic T cells. This prevents the donor T cells from recognizing host tissues as foreign and initiating a GvH response. Gene editing tool like TALEN® is used to disrupt the TCR gene. ✅ Specialized T Cell Subsets: Induced pluripotent stem cell (iPSC)-derived T cells: CAR T cells generated from iPSCs lack endogenous TCRs, eliminating the risk of GvHD.   ✅ iPSC-Derived T Cells: CAR T cells generated from iPSCs lack endogenous TCRs, eliminating the risk of GvHD.   ✅ Safety Switches: Incorporating mechanisms to eliminate the CAR T cells if GvHD occurs provides an additional safety measure.   These advances hold great promise for making allogeneic CAR T cells more accessible treatment option for cancer patients.   What other innovative approach do you have in mind? Drop them in the comments ⤵   #CancerImmunotherapy #CART #BiotechInnovation #CellTherapy

Cellectis Reports Results from Shareholders Meeting Held on June 28, 2024. To read the press release: https://lnkd.in/eN7AhjhE

We found 3 key factors determinant for efficient TALE base editing ✂ First, what are TALE base editors? TALE base editors are a recent and important addition to the gene editing landscape. By design, TALE base editors do not create break within DNA strands as does CRISPR/Cas9, or other engineered nucleases. They represent a promising therapeutic strategy for genetic diseases. Interesting, right? But, to broaden the scope of possible applications, we need to understand the design rules. TALE base editors rely on the deamination of cytidines within double strand DNA, leading to the formation of an uracil (U) intermediate. These molecular tools are fusions of transcription activator-like effector domains (TALE) for specific DNA sequence binding, split-DddA deaminase halves that will, upon catalytic domain reconstitution, initiate the conversion of a cytosine (C) to a thymine (T), and an uracil glycosylase inhibitor (UGI). Previous works have pointed towards the positioning of targeted cytosine to be a key determinant for efficient editing. That’s why we investigated whether the nature (length and composition) of the linker that connects the TALE array with the split deaminase catalytic heads could impact C-to-T conversion within the editing window. We found 3 key factors: 💡 Spacer length 💡TALEB architecture 💡Composition of surrounding bases All of them can impact editing outcomes and further improve our understanding of TALE base editors' activity and specificity, leading to the possibility to tune and control editing using educated designs. Any thoughts on this? Drop them in the comments ⤵ For those interested in gene editing advancements, the full paper is available in Scientific Reports : https://lnkd.in/eSRZxyfN #GeneEditing #MolecularBiology #Genetics #BiotechResearch