The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The UniProt accession Q07817 corresponds to human BCL2L1 (also called BCL-X, protein Bcl-2-like protein 1 / Bcl-xL), a canonical BCL-2 family apoptosis regulator with BH domains and a C-terminal transmembrane anchor. In a recent interactome reference table, BCL-XL is explicitly mapped to UniProt Q07817, annotated with localization to mitochondrial outer membrane (MOM) and endoplasmic reticulum (ER)/nuclear membrane, and described functionally as an inhibitor of cell death with BH1–BH4 plus a transmembrane domain. (ilyas2025exploringtherole pages 8-12)
BCL2L1 is best understood as an apoptosis-regulatory gene whose primary functional outputs are two antagonistic splice isoforms:
- Bcl-xL (long): ~233 aa, anti-apoptotic/pro-survival. (perezserna2025bcl2andbclxl pages 2-4, silva2026bcl2andbclxl pages 8-10)
- Bcl-xS (short): ~170 aa, pro-apoptotic. (perezserna2025bcl2andbclxl pages 2-4, silva2026bcl2andbclxl pages 8-10)
This isoform switch is central to the gene’s biology and is directly exploited therapeutically (see §2.2). (dou2024modificationofbclx pages 1-2, dou2024modificationofbclx pages 3-5)
Bcl-xL is a pro-survival BCL-2 family member containing conserved BH (Bcl-2 homology) domains and a hydrophobic C-terminal transmembrane region enabling organellar membrane association. (ilyas2025exploringtherole pages 8-12, silva2026bcl2andbclxl pages 8-10, silva2026bcl2andbclxl pages 10-11)
Structurally, BH1–BH3 regions create a hydrophobic BH3-binding groove (surface pocket) that binds BH3 helices from pro-apoptotic partners. This binding underlies the defining biochemical function of Bcl-xL: sequestering BH3-only activators/sensitizers and restraining pro-apoptotic effector activation (BAX/BAK). (perezserna2025bcl2andbclxl pages 2-4, perezserna2025bcl2andbclxl pages 4-6, silva2026bcl2andbclxl pages 2-3)
The primary function of Bcl-xL is to prevent mitochondrial outer membrane permeabilization (MOMP) by inhibiting BAX activity and/or sequestering BH3-only proteins, thereby blocking cytochrome c release and downstream caspase activation. (silva2026bcl2andbclxl pages 10-11, silva2026bcl2andbclxl pages 8-10, silva2026bcl2andbclxl pages 11-12, silva2026bcl2andbclxl pages 2-3)
A mechanistic example from a recent review highlights that BCL-xL can bind and restrain apoptosis activators, and that BH3-only proteins (e.g., PUMA) can competitively displace partners to free p53/BH3 proteins and allow BAX activation—illustrating how Bcl-xL’s anti-apoptotic function is executed through regulated protein–protein interactions. (silva2026bcl2andbclxl pages 10-11)
Bcl-xL localizes predominantly to the outer mitochondrial membrane, but is also found at ER, cytosol, and nuclear outer membrane/nuclear membrane, consistent with a role in apoptosis control at organelle membranes and contact sites. (ilyas2025exploringtherole pages 8-12, perezserna2025bcl2andbclxl pages 2-4, perezserna2025bcl2andbclxl pages 4-6)
Beyond canonical apoptosis suppression at mitochondria, Bcl-xL participates in ER–mitochondria functional coupling (including mitochondrial-associated ER membranes), integrating survival with Ca2+ homeostasis via interactions with ER Ca2+ channels (e.g., IP3R). (perezserna2025bcl2andbclxl pages 4-6, perezserna2025bcl2andbclxl pages 6-7)
A 2024 Cell Death & Disease study tested the hypothesis that high basal pro-survival BCL-XL and MCL-1 in BRAFV600E CRC raises the apoptotic threshold and limits response to BRAF-targeted therapy. (jenkins2024bclxlinhibitorsenhance pages 3-6, jenkins2024bclxlinhibitorsenhance pages 1-2)
Key quantitative findings:
- Clinically, BRAFV600E metastatic CRC represents ~10% of metastatic CRC; BRAF inhibitor monotherapy has ~5% objective responses, while encorafenib + cetuximab improves OS by 3.6 months with ~20% objective responses—underscoring incomplete apoptosis induction in this disease setting. (jenkins2024bclxlinhibitorsenhance pages 1-2)
- In vitro, encorafenib or encorafenib+cetuximab induced <25% apoptosis across lines; combining encorafenib with the BCL-XL inhibitor A-1331852 induced >50% apoptosis in 3/5 BRAFV600E CRC cell lines, while an MCL-1 inhibitor combination exceeded 20% apoptosis in only 1/5 lines; BCL-2 inhibition did not improve apoptosis beyond 25%. (jenkins2024bclxlinhibitorsenhance pages 3-6)
- Mechanistically, apoptosis induction by BRAF + BCL-XL inhibition was BIM-dependent (BIM deletion attenuated apoptosis). (jenkins2024bclxlinhibitorsenhance pages 3-6)
This work also evaluates platelet-toxicity mitigation strategies (see §3.2) using a BCL-XL degrader (DT2216) and a dendrimer-conjugated BCL-2/BCL-XL inhibitor (AZD0466). (jenkins2024bclxlinhibitorsenhance pages 6-8, jenkins2024bclxlinhibitorsenhance pages 1-2)
A 2024 Cell Death & Disease study in GBM demonstrated that BCLX/BCL2L1 is aberrantly spliced toward anti-apoptotic Bcl-xL in GBM cells and tested splice-switching oligonucleotides (SSOs) to shift isoform balance toward Bcl-xS. (dou2024modificationofbclx pages 1-2)
Key findings (mechanistic):
- SSOs/vivo-morpholinos targeting the exon junction shifted splicing to elevate Bcl-xS at the expense of Bcl-xL, activating apoptosis (CASP9/CASP3 activation) and inducing autophagy-related changes and mitochondrial damage, with antitumor effects in 2D/3D models and radiosensitization. (dou2024modificationofbclx pages 3-5, dou2024modificationofbclx pages 1-2)
- Radiation modality matters: low-energy X-rays increased the Bcl-xL/Bcl-xS ratio (potentially favoring resistance) whereas heavy (carbon) ions did not in the reported context. (dou2024modificationofbclx pages 1-2)
Quantitative details available from retrieved text include SSO/vMO concentrations (2–8 μM; often 4–8 μM for functional work) and timing (48 h harvest for splicing/protein readouts). (dou2024modificationofbclx pages 2-3)
A 2024 Blood Advances paper identifies CBFA2T3::GLIS2 pediatric AMKL as dependent on BCL-XL (BCL2L1) and sensitive to BCL-XL targeting by navitoclax and the BCL-XL degrader DT2216, including synergy with low-dose cytarabine in vivo. (gress2024cbfa2t3glis2pediatricacute pages 1-2)
Quantitative data in retrieved excerpts include:
- Cytarabine IC50 across CG2 models: 1–7 nM (in vitro). (gress2024cbfa2t3glis2pediatricacute pages 11-12)
- DT2216 xenograft dosing: every 4 days for 4–6 weeks, reducing leukemic burden and significantly prolonging survival in transplanted mouse models (without a numeric survival delta in the excerpt). (gress2024cbfa2t3glis2pediatricacute pages 11-12)
Current real-world implementations focus on BCL2L1/BCL-XL as a drug target in oncology, leveraging several strategies:
- BH3 mimetics / small-molecule inhibitors targeting the BH3-binding groove (e.g., A-1331852; broader inhibitors like navitoclax that bind BCL-XL among other BCL-2 family proteins). (gress2024cbfa2t3glis2pediatricacute pages 1-2, jenkins2024bclxlinhibitorsenhance pages 3-6)
- PROTAC degraders (e.g., DT2216) designed to degrade BCL-XL, motivated in part by improving the safety profile (platelet toxicity). (jenkins2024bclxlinhibitorsenhance pages 6-8, NCT04886622 chunk 1)
- Controlled-delivery formulations (e.g., AZD0466, a dendrimer-conjugate approach designed to reduce toxicity by altering exposure kinetics). (jenkins2024bclxlinhibitorsenhance pages 6-8)
- RNA therapeutics shifting BCL2L1 splicing toward Bcl-xS (SSOs/vivo-morpholinos). (dou2024modificationofbclx pages 3-5, dou2024modificationofbclx pages 1-2)
A central practical limitation for BCL-XL inhibition is thrombocytopenia, because platelets depend on BCL-XL for survival. (jenkins2024bclxlinhibitorsenhance pages 6-8, jenkins2024bclxlinhibitorsenhance pages 1-2)
The 2024 BRAFV600E CRC study provides a mechanistic rationale for potential platelet sparing by DT2216: it recruits the E3 ligase VHL, which has minimal expression in platelets, potentially biasing BCL-XL degradation toward tumor cells and away from platelets. (jenkins2024bclxlinhibitorsenhance pages 6-8)
ClinicalTrials.gov NCT04886622 (Dialectic Therapeutics) is a Phase 1, open-label dose-escalation/cohort-expansion study in relapsed/refractory malignancies, listed as COMPLETED, enrolling 20 subjects. (NCT04886622 chunk 1)
Implementation details extracted from the record:
- DT2216 administered IV over 30 minutes twice weekly, continuous dosing, 28-day cycles, starting dose 0.04 mg/kg with escalation. (NCT04886622 chunk 1)
- Thrombocytopenia is prespecified as a DLT concern: DLT criteria include Grade 4 thrombocytopenia and Grade 3 thrombocytopenia with clinically significant hemorrhage, and platelet counts are explicitly monitored as a secondary/PD endpoint. (NCT04886622 chunk 1)
No efficacy outcomes or thrombocytopenia incidence rates are reported in the retrieved registry chunks; those require the linked clinical publication(s), which were not retrieved as full text here. (NCT04886622 chunk 3, NCT04886622 chunk 1)
Functional annotation summary: The most precise primary molecular function of BCL2L1 (Q07817) is that Bcl-xL is a membrane-associated anti-apoptotic adaptor that binds BH3 motifs to inhibit activation/oligomerization of BAX/BAK and prevent MOMP, operating primarily on the mitochondrial outer membrane, and secondarily at ER and organelle contact sites where it also influences Ca2+ signaling and bioenergetic homeostasis. (perezserna2025bcl2andbclxl pages 2-4, perezserna2025bcl2andbclxl pages 4-6, silva2026bcl2andbclxl pages 8-10, silva2026bcl2andbclxl pages 11-12, perezserna2025bcl2andbclxl pages 6-7)
Why isoforms matter for annotation: Because the same gene also produces the pro-apoptotic Bcl-xS isoform, functional annotation should explicitly distinguish splice isoforms and note that cancer cells often favor Bcl-xL production; therapeutic strategies increasingly aim to either antagonize Bcl-xL (BH3 mimetics/PROTACs) or force isoform switching toward Bcl-xS (SSOs). (dou2024modificationofbclx pages 1-2, dou2024modificationofbclx pages 3-5)
Figure evidence from Jenkins et al. (2024) shows that combining encorafenib with AZD0466 in COLO201 xenografts yields stronger tumor suppression/regression than either agent alone, with associated endpoint tumor weights and excised tumor images. (jenkins2024bclxlinhibitorsenhance media f80a8fd4, jenkins2024bclxlinhibitorsenhance media 5fd567da)
| Topic | System/Indication | Intervention/Mechanism | Key quantitative findings | Key limitations/safety | Source (citation id) |
|---|---|---|---|---|---|
| Core function and localization of human BCL2L1/BCL-xL | Human BCL2L1 / BCL-xL protein | Anti-apoptotic BCL-2 family protein; BH1-BH4 domains plus C-terminal transmembrane anchor; BH3-binding groove sequesters BH3-only proteins and inhibits BAX/BAK, preventing MOMP/cytochrome c release; localizes mainly to mitochondrial outer membrane, also ER, cytosol, and nuclear membrane/outer nuclear membrane | Major isoforms: Bcl-xL ~233 aa (anti-apoptotic) and Bcl-xS ~170 aa (pro-apoptotic); Q07817 explicitly mapped to BCL-xL in recent interactome reference | Functionally important in normal cell survival; on-target inhibition can damage platelets because platelets depend on BCL-xL | (ilyas2025exploringtherole pages 8-12, perezserna2025bcl2andbclxl pages 2-4, silva2026bcl2andbclxl pages 10-11, silva2026bcl2andbclxl pages 8-10, silva2026bcl2andbclxl pages 2-3) |
| 2024 development: BRAF + BCL-XL targeting | BRAFV600E colorectal cancer | Encorafenib combined with BCL-XL inhibition/degradation (A-1331852, DT2216, AZD0466) to lower apoptotic threshold created by high basal BCL-XL/MCL-1 | Standard targeted therapy context: encorafenib + cetuximab gives ~20% objective responses and ~3.6-month OS benefit; encorafenib or encorafenib+cetuximab alone induced <25% apoptosis in cell lines; encorafenib + A-1331852 induced >50% apoptosis in 3/5 BRAFV600E CRC lines; MCL1 inhibitor combination exceeded 20% apoptosis in only 1/5 lines; encorafenib + AZD0466 caused significant xenograft suppression/regression and was well tolerated in mice | Some lines (HT29, RKO) were refractory; thrombocytopenia remains established on-target toxicity of BCL-XL inhibition; TUNEL signal not clearly different at sampled timepoint in vivo | (jenkins2024bclxlinhibitorsenhance pages 6-8, jenkins2024bclxlinhibitorsenhance pages 3-6, jenkins2024bclxlinhibitorsenhance pages 1-2, jenkins2024bclxlinhibitorsenhance media f80a8fd4) |
| 2024 development: splice-switching of BCL2L1 | Glioblastoma (GBM) | Splice-switching oligonucleotides / vivo-morpholino targeting BCLX pre-mRNA to shift splicing from anti-apoptotic Bcl-xL toward pro-apoptotic Bcl-xS | vMO/SSO tested at 2-8 uM (cells harvested 48 h; functional studies often 4-8 uM); shift lowered Bcl-xL/Bcl-xS ratio at mRNA and protein levels, triggered CASP9/CASP3-associated apoptosis, mitochondrial damage, autophagic flux, reduced 3D microsphere size, and enhanced radiosensitivity in 2D/3D GBM models | Quantitative percent splice-shift values were not given in the retrieved text; low-energy X-rays increased the Bcl-xL/Bcl-xS ratio, indicating some radiation regimens may favor the resistant isoform; normal astrocytes showed limited cytotoxicity in reported assays | (dou2024modificationofbclx pages 3-5, dou2024modificationofbclx pages 1-2, dou2024modificationofbclx pages 2-3) |
| 2024 development: BCL-XL dependency in pediatric leukemia | CBFA2T3::GLIS2 pediatric AMKL (also NUP98r AMKL models) | Genetic/functional vulnerability to BCL-XL targeted with navitoclax or selective BCL-XL PROTAC DT2216; combinations with low-dose cytarabine | Navitoclax or DT2216 induced apoptosis in vitro and in vivo; DT2216 dosed every 4 days for 4-6 weeks in xenograft models reduced circulating leukemic blasts and significantly prolonged survival; CG2 models were cytarabine-sensitive with IC50s of 1-7 nM; combinations further reduced leukemic burden | Retrieved text did not provide human response rates; navitoclax has known thrombocytopenia liability; DT2216 was developed to reduce this issue; minimal cross-toxicity reported on normal cord-blood CD34+ HSPCs in these models | (gress2024cbfa2t3glis2pediatricacute pages 1-2, gress2024cbfa2t3glis2pediatricacute pages 18-18, gress2024cbfa2t3glis2pediatricacute pages 11-12) |
| Clinical translation: first-in-human DT2216 monotherapy trial | Relapsed/refractory malignancies (solid + hematologic), NCT04886622 | Phase 1 open-label dose-escalation/cohort-expansion of IV DT2216, a BCL-XL PROTAC degrader | Enrollment 20; started 2021-08-25; completed June 2024; DT2216 IV over 30 min twice weekly on a continuous 28-day cycle; starting dose 0.04 mg/kg with escalation; PK/PD included Cmax, half-life, clearance, PBMC BCL-XL levels, serial platelet counts | DLT criteria explicitly included Grade 4 thrombocytopenia and Grade 3 thrombocytopenia with clinically significant hemorrhage; no efficacy outcomes were provided in the retrieved trial text | (NCT04886622 chunk 3, NCT04886622 chunk 1, NCT04886622 chunk 2) |
| Clinical translation: pediatric/AYA combination trial | Relapsed/refractory solid tumors and fibrolamellar carcinoma, NCT06620302 | Phase I/II DT2216 + irinotecan; BCL-xL degradation plus chemotherapy | Recruiting; estimated enrollment 81; DT2216 IV on days 1, 4, 8, 11, 15, 18 plus irinotecan on days 2-6 in cycle 1 then days 1-5 thereafter; 21-day cycles; PD includes PBMC Bcl-xL levels and paired tumor IHC when available | Primary goals are toxicity, MTD/RP2D, PK, preliminary activity; retrieved text did not include results or specific thrombocytopenia rates | (NCT06620302 chunk 1) |
| Clinical translation: ovarian cancer combination trial | Platinum-resistant ovarian cancer, NCT06964009 | Phase 1b dose-escalation of DT2216 + weekly paclitaxel | Recruiting; estimated enrollment ~30; primary aims are MTD/RP2D and DLTs during cycle 1/up to start of cycle 2 | DLTs include Grade >=3 non-hematologic and selected hematologic toxicities, treatment delays >14 days, death, or inability to receive >=75% of assigned doses; no outcome data yet in retrieved record | (NCT06964009 chunk 1) |
| Platelet-sparing rationale for PROTAC BCL-XL targeting | Cross-indication translational strategy | DT2216 links a BCL-XL-binding warhead to a VHL ligand so degradation is favored in VHL-expressing tumor cells, while platelets with minimal/low VHL expression are relatively spared | Preclinical rationale only in retrieved sources: DT2216 showed dose-dependent BCL-XL degradation in CRC models and was specifically designed/developed to limit thrombocytopenia | Human platelet-sparing efficacy still requires clinical confirmation; thrombocytopenia remains a prespecified safety concern and is closely monitored in trials | (jenkins2024bclxlinhibitorsenhance pages 6-8, gress2024cbfa2t3glis2pediatricacute pages 1-2) |
Table: This table condenses the main functional annotation points for human BCL2L1/BCL-xL and highlights the most relevant 2024 mechanistic, therapeutic, and clinical-translation findings. It is useful as a quick reference linking core biology to current drug-development efforts and available quantitative evidence.
References
(ilyas2025exploringtherole pages 8-12): Sidra Ilyas and Donghun Lee. Exploring the role of bcl2 interactome in cancer: a protein/residue interaction network analysis. Biology, 14:261, Mar 2025. URL: https://doi.org/10.3390/biology14030261, doi:10.3390/biology14030261. This article has 1 citations.
(perezserna2025bcl2andbclxl pages 2-4): Atenea A. Perez-Serna, Daniel Guzman-Llorens, Reinaldo S. Dos Santos, and Laura Marroqui. Bcl-2 and bcl-xl in diabetes: contributions to endocrine pancreas viability and function. Biomedicines, 13:223, Jan 2025. URL: https://doi.org/10.3390/biomedicines13010223, doi:10.3390/biomedicines13010223. This article has 13 citations.
(silva2026bcl2andbclxl pages 8-10): João P. N. Silva, Bárbara Pinto, Patrícia M. A. Silva, and Hassan Bousbaa. Bcl-2 and bcl-xl in cancer: regulation, function, and therapeutic targeting. International Journal of Molecular Sciences, 27:1123, Jan 2026. URL: https://doi.org/10.3390/ijms27021123, doi:10.3390/ijms27021123. This article has 5 citations.
(dou2024modificationofbclx pages 1-2): Zhihui Dou, Huiwen Lei, Wei Su, Taotao Zhang, Xiaohua Chen, Boyi Yu, Xiaogang Zhen, Jing Si, Chao Sun, Hong Zhang, and Cuixia Di. Modification of bclx pre-mrna splicing has antitumor efficacy alone or in combination with radiotherapy in human glioblastoma cells. Cell Death & Disease, Feb 2024. URL: https://doi.org/10.1038/s41419-024-06507-x, doi:10.1038/s41419-024-06507-x. This article has 12 citations and is from a peer-reviewed journal.
(dou2024modificationofbclx pages 3-5): Zhihui Dou, Huiwen Lei, Wei Su, Taotao Zhang, Xiaohua Chen, Boyi Yu, Xiaogang Zhen, Jing Si, Chao Sun, Hong Zhang, and Cuixia Di. Modification of bclx pre-mrna splicing has antitumor efficacy alone or in combination with radiotherapy in human glioblastoma cells. Cell Death & Disease, Feb 2024. URL: https://doi.org/10.1038/s41419-024-06507-x, doi:10.1038/s41419-024-06507-x. This article has 12 citations and is from a peer-reviewed journal.
(silva2026bcl2andbclxl pages 10-11): João P. N. Silva, Bárbara Pinto, Patrícia M. A. Silva, and Hassan Bousbaa. Bcl-2 and bcl-xl in cancer: regulation, function, and therapeutic targeting. International Journal of Molecular Sciences, 27:1123, Jan 2026. URL: https://doi.org/10.3390/ijms27021123, doi:10.3390/ijms27021123. This article has 5 citations.
(perezserna2025bcl2andbclxl pages 4-6): Atenea A. Perez-Serna, Daniel Guzman-Llorens, Reinaldo S. Dos Santos, and Laura Marroqui. Bcl-2 and bcl-xl in diabetes: contributions to endocrine pancreas viability and function. Biomedicines, 13:223, Jan 2025. URL: https://doi.org/10.3390/biomedicines13010223, doi:10.3390/biomedicines13010223. This article has 13 citations.
(silva2026bcl2andbclxl pages 2-3): João P. N. Silva, Bárbara Pinto, Patrícia M. A. Silva, and Hassan Bousbaa. Bcl-2 and bcl-xl in cancer: regulation, function, and therapeutic targeting. International Journal of Molecular Sciences, 27:1123, Jan 2026. URL: https://doi.org/10.3390/ijms27021123, doi:10.3390/ijms27021123. This article has 5 citations.
(silva2026bcl2andbclxl pages 11-12): João P. N. Silva, Bárbara Pinto, Patrícia M. A. Silva, and Hassan Bousbaa. Bcl-2 and bcl-xl in cancer: regulation, function, and therapeutic targeting. International Journal of Molecular Sciences, 27:1123, Jan 2026. URL: https://doi.org/10.3390/ijms27021123, doi:10.3390/ijms27021123. This article has 5 citations.
(perezserna2025bcl2andbclxl pages 6-7): Atenea A. Perez-Serna, Daniel Guzman-Llorens, Reinaldo S. Dos Santos, and Laura Marroqui. Bcl-2 and bcl-xl in diabetes: contributions to endocrine pancreas viability and function. Biomedicines, 13:223, Jan 2025. URL: https://doi.org/10.3390/biomedicines13010223, doi:10.3390/biomedicines13010223. This article has 13 citations.
(jenkins2024bclxlinhibitorsenhance pages 3-6): Laura J. Jenkins, Ian Y. Luk, Fiona Chionh, Tao Tan, Kristen Needham, Jamieson Ayton, Camilla M. Reehorst, Natalia Vukelic, Oliver M. Sieber, Dmitri Mouradov, Peter Gibbs, David S. Williams, Niall C. Tebbutt, Jayesh Desai, Frédéric Hollande, Amardeep S. Dhillon, Erinna F. Lee, Delphine Merino, W. Douglas Fairlie, and John M. Mariadason. Bcl-xl inhibitors enhance the apoptotic efficacy of braf inhibitors in brafv600e colorectal cancer. Cell Death & Disease, Mar 2024. URL: https://doi.org/10.1038/s41419-024-06478-z, doi:10.1038/s41419-024-06478-z. This article has 10 citations and is from a peer-reviewed journal.
(jenkins2024bclxlinhibitorsenhance pages 1-2): Laura J. Jenkins, Ian Y. Luk, Fiona Chionh, Tao Tan, Kristen Needham, Jamieson Ayton, Camilla M. Reehorst, Natalia Vukelic, Oliver M. Sieber, Dmitri Mouradov, Peter Gibbs, David S. Williams, Niall C. Tebbutt, Jayesh Desai, Frédéric Hollande, Amardeep S. Dhillon, Erinna F. Lee, Delphine Merino, W. Douglas Fairlie, and John M. Mariadason. Bcl-xl inhibitors enhance the apoptotic efficacy of braf inhibitors in brafv600e colorectal cancer. Cell Death & Disease, Mar 2024. URL: https://doi.org/10.1038/s41419-024-06478-z, doi:10.1038/s41419-024-06478-z. This article has 10 citations and is from a peer-reviewed journal.
(jenkins2024bclxlinhibitorsenhance pages 6-8): Laura J. Jenkins, Ian Y. Luk, Fiona Chionh, Tao Tan, Kristen Needham, Jamieson Ayton, Camilla M. Reehorst, Natalia Vukelic, Oliver M. Sieber, Dmitri Mouradov, Peter Gibbs, David S. Williams, Niall C. Tebbutt, Jayesh Desai, Frédéric Hollande, Amardeep S. Dhillon, Erinna F. Lee, Delphine Merino, W. Douglas Fairlie, and John M. Mariadason. Bcl-xl inhibitors enhance the apoptotic efficacy of braf inhibitors in brafv600e colorectal cancer. Cell Death & Disease, Mar 2024. URL: https://doi.org/10.1038/s41419-024-06478-z, doi:10.1038/s41419-024-06478-z. This article has 10 citations and is from a peer-reviewed journal.
(dou2024modificationofbclx pages 2-3): Zhihui Dou, Huiwen Lei, Wei Su, Taotao Zhang, Xiaohua Chen, Boyi Yu, Xiaogang Zhen, Jing Si, Chao Sun, Hong Zhang, and Cuixia Di. Modification of bclx pre-mrna splicing has antitumor efficacy alone or in combination with radiotherapy in human glioblastoma cells. Cell Death & Disease, Feb 2024. URL: https://doi.org/10.1038/s41419-024-06507-x, doi:10.1038/s41419-024-06507-x. This article has 12 citations and is from a peer-reviewed journal.
(gress2024cbfa2t3glis2pediatricacute pages 1-2): Verena Gress, Mathieu Roussy, Luc Boulianne, Mélanie Bilodeau, Sophie Cardin, Nehme El-Hachem, Véronique Lisi, Banafsheh Khakipoor, Alexandre Rouette, Azer Farah, Louis Théret, Léo Aubert, Furat Fatima, Éric Audemard, Pierre Thibault, Éric Bonneil, Jalila Chagraoui, Louise Laramée, Patrick Gendron, Loubna Jouan, Safa Jammali, Bastien Paré, Shawn M. Simpson, Thai Hoa Tran, Michel Duval, Pierre Teira, Henrique Bittencourt, Raoul Santiago, Frédéric Barabé, Guy Sauvageau, Martin A. Smith, Josée Hébert, Philippe P. Roux, Tanja A. Gruber, Vincent-Philippe Lavallée, Brian T. Wilhelm, and Sonia Cellot. Cbfa2t3::glis2 pediatric acute megakaryoblastic leukemia is sensitive to bcl-xl inhibition by navitoclax and dt2216. Dec 2024. URL: https://doi.org/10.1182/bloodadvances.2022008899, doi:10.1182/bloodadvances.2022008899. This article has 28 citations and is from a peer-reviewed journal.
(gress2024cbfa2t3glis2pediatricacute pages 11-12): Verena Gress, Mathieu Roussy, Luc Boulianne, Mélanie Bilodeau, Sophie Cardin, Nehme El-Hachem, Véronique Lisi, Banafsheh Khakipoor, Alexandre Rouette, Azer Farah, Louis Théret, Léo Aubert, Furat Fatima, Éric Audemard, Pierre Thibault, Éric Bonneil, Jalila Chagraoui, Louise Laramée, Patrick Gendron, Loubna Jouan, Safa Jammali, Bastien Paré, Shawn M. Simpson, Thai Hoa Tran, Michel Duval, Pierre Teira, Henrique Bittencourt, Raoul Santiago, Frédéric Barabé, Guy Sauvageau, Martin A. Smith, Josée Hébert, Philippe P. Roux, Tanja A. Gruber, Vincent-Philippe Lavallée, Brian T. Wilhelm, and Sonia Cellot. Cbfa2t3::glis2 pediatric acute megakaryoblastic leukemia is sensitive to bcl-xl inhibition by navitoclax and dt2216. Dec 2024. URL: https://doi.org/10.1182/bloodadvances.2022008899, doi:10.1182/bloodadvances.2022008899. This article has 28 citations and is from a peer-reviewed journal.
(NCT04886622 chunk 1): A Study of DT2216 in Relapsed/Refractory Malignancies. Dialectic Therapeutics, Inc. 2021. ClinicalTrials.gov Identifier: NCT04886622
(NCT04886622 chunk 3): A Study of DT2216 in Relapsed/Refractory Malignancies. Dialectic Therapeutics, Inc. 2021. ClinicalTrials.gov Identifier: NCT04886622
(NCT06620302 chunk 1): Testing the Addition of an Anti-cancer Drug, DT2216, to the Usual Chemotherapy Treatment for Relapsed or Refractory Solid Tumors and Fibrolamellar Carcinoma. Children's Oncology Group. 2025. ClinicalTrials.gov Identifier: NCT06620302
(NCT06964009 chunk 1): Elizabeth Stover, MD, PhD. DT2216 + Paclitaxel in Platinum-Resistant Ovarian Cancer. Elizabeth Stover, MD, PhD. 2025. ClinicalTrials.gov Identifier: NCT06964009
(jenkins2024bclxlinhibitorsenhance media f80a8fd4): Laura J. Jenkins, Ian Y. Luk, Fiona Chionh, Tao Tan, Kristen Needham, Jamieson Ayton, Camilla M. Reehorst, Natalia Vukelic, Oliver M. Sieber, Dmitri Mouradov, Peter Gibbs, David S. Williams, Niall C. Tebbutt, Jayesh Desai, Frédéric Hollande, Amardeep S. Dhillon, Erinna F. Lee, Delphine Merino, W. Douglas Fairlie, and John M. Mariadason. Bcl-xl inhibitors enhance the apoptotic efficacy of braf inhibitors in brafv600e colorectal cancer. Cell Death & Disease, Mar 2024. URL: https://doi.org/10.1038/s41419-024-06478-z, doi:10.1038/s41419-024-06478-z. This article has 10 citations and is from a peer-reviewed journal.
(jenkins2024bclxlinhibitorsenhance media 5fd567da): Laura J. Jenkins, Ian Y. Luk, Fiona Chionh, Tao Tan, Kristen Needham, Jamieson Ayton, Camilla M. Reehorst, Natalia Vukelic, Oliver M. Sieber, Dmitri Mouradov, Peter Gibbs, David S. Williams, Niall C. Tebbutt, Jayesh Desai, Frédéric Hollande, Amardeep S. Dhillon, Erinna F. Lee, Delphine Merino, W. Douglas Fairlie, and John M. Mariadason. Bcl-xl inhibitors enhance the apoptotic efficacy of braf inhibitors in brafv600e colorectal cancer. Cell Death & Disease, Mar 2024. URL: https://doi.org/10.1038/s41419-024-06478-z, doi:10.1038/s41419-024-06478-z. This article has 10 citations and is from a peer-reviewed journal.
(gress2024cbfa2t3glis2pediatricacute pages 18-18): Verena Gress, Mathieu Roussy, Luc Boulianne, Mélanie Bilodeau, Sophie Cardin, Nehme El-Hachem, Véronique Lisi, Banafsheh Khakipoor, Alexandre Rouette, Azer Farah, Louis Théret, Léo Aubert, Furat Fatima, Éric Audemard, Pierre Thibault, Éric Bonneil, Jalila Chagraoui, Louise Laramée, Patrick Gendron, Loubna Jouan, Safa Jammali, Bastien Paré, Shawn M. Simpson, Thai Hoa Tran, Michel Duval, Pierre Teira, Henrique Bittencourt, Raoul Santiago, Frédéric Barabé, Guy Sauvageau, Martin A. Smith, Josée Hébert, Philippe P. Roux, Tanja A. Gruber, Vincent-Philippe Lavallée, Brian T. Wilhelm, and Sonia Cellot. Cbfa2t3::glis2 pediatric acute megakaryoblastic leukemia is sensitive to bcl-xl inhibition by navitoclax and dt2216. Dec 2024. URL: https://doi.org/10.1182/bloodadvances.2022008899, doi:10.1182/bloodadvances.2022008899. This article has 28 citations and is from a peer-reviewed journal.
(NCT04886622 chunk 2): A Study of DT2216 in Relapsed/Refractory Malignancies. Dialectic Therapeutics, Inc. 2021. ClinicalTrials.gov Identifier: NCT04886622