# Publications Search Within Results Search Within Results search ## 450 results Show filters filter\_alt Sort by Year of PublicationAlphabetical A-Z sort ## 450 results Download 450 citations download- [BibTeX](/node/1850976/export?format=bibtex) - [EndNote X3 XML](/node/1850976/export?format=endnote8) - [EndNote 7 XML](/node/1850976/export?format=endnote7) - [Endnote tagged](/node/1850976/export?format=tagged) - [Marc](/node/1850976/export?format=marc) - [PubMedId](/node/1850976/export?format=pubmed_id) - [RIS](/node/1850976/export?format=ris) ### 2026 Lee, Y. S. *et al.* [Synergistic targeting of eIF4A-mediated translation initiation and apoptosis in acute myeloid leukemia.](https://pubmed.ncbi.nlm.nih.gov/41815287/) *Blood neoplasia* **3**, 100202 (2026). Lee, Y. S. *et al.* [Synergistic targeting of eIF4A-mediated translation initiation and apoptosis in acute myeloid leukemia.](https://pubmed.ncbi.nlm.nih.gov/41815287/) *Blood neoplasia* **3**, 100202 (2026). - add\_circle do\_not\_disturb\_on Abstract Targeted therapies, such as the BCL-2 inhibitor venetoclax, have expanded the treatment options for patients with acute myeloid leukemia (AML), but survival remains poor because of drug resistance and disease relapse. We found that the translation... Wu, B. *et al.* [TROP2/claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer.](https://pubmed.ncbi.nlm.nih.gov/41932810/) *Journal for immunotherapy of cancer* **14**, (2026). Wu, B. *et al.* [TROP2/claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer.](https://pubmed.ncbi.nlm.nih.gov/41932810/) *Journal for immunotherapy of cancer* **14**, (2026). - add\_circle do\_not\_disturb\_on Abstract **BACKGROUND:** Immune exclusion inhibits antitumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. In triple-negative breast cancer (TNBC), an aggressive and generally immune-rich subtype, an immune-cold microenvironment... Goyette, M.-A. *et al.* [HER2 heterogeneous breast cancer models reveal novel therapeutic targets and subclonal dynamics during evolution to resistance to HER2-targeted therapies.](https://pubmed.ncbi.nlm.nih.gov/41925564/) *Cancer discovery* (2026) doi:10.1158/2159-8290.CD-25-1459. Goyette, M.-A. *et al.* [HER2 heterogeneous breast cancer models reveal novel therapeutic targets and subclonal dynamics during evolution to resistance to HER2-targeted therapies.](https://pubmed.ncbi.nlm.nih.gov/41925564/) *Cancer discovery* (2026) doi:10.1158/2159-8290.CD-25-1459. - add\_circle do\_not\_disturb\_on Abstract Intratumor heterogeneity for HER2 in HER2-positive breast cancer is a driver of resistance to HER2-targeted therapies. The advancement of treatments for HER2 heterogeneous tumors has been hindered by the lack of preclinical models that accurately mimic... Lee, S. M. *et al.* [Host microRNA-31-5p regulates KHDRBS3 expression and modulates viral gene expression during KSHV lytic reactivation.](https://pubmed.ncbi.nlm.nih.gov/41931390/) *Cell reports* **45**, 117160 (2026). Lee, S. M. *et al.* [Host microRNA-31-5p regulates KHDRBS3 expression and modulates viral gene expression during KSHV lytic reactivation.](https://pubmed.ncbi.nlm.nih.gov/41931390/) *Cell reports* **45**, 117160 (2026). - add\_circle do\_not\_disturb\_on Abstract Oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) employs a biphasic life cycle consisting of latency and lytic replication to achieve lifelong infection. Despite its essential role in KSHV persistence and tumorigenicity, much remains unknown about... Meylan, M. *et al.* [Persistent T cell activation and cytotoxicity against glioblastoma following single oncolytic virus treatment in a clinical trial.](/publication/persistent-t-cell-activation-and-cytotoxicity-against-glioblastoma-following-single) *Cell* **189**, 1287–1304.e18 (2026). Meylan, M. *et al.* [Persistent T cell activation and cytotoxicity against glioblastoma following single oncolytic virus treatment in a clinical trial.](/publication/persistent-t-cell-activation-and-cytotoxicity-against-glioblastoma-following-single) *Cell* **189**, 1287–1304.e18 (2026). - add\_circle do\_not\_disturb\_on Abstract A recent first-in-human clinical trial demonstrated that survival in glioblastoma (GBM) patients following rQNestin34.5v.2 oncolytic virus treatment was associated with immune activation signatures. This study was registered at ClinicalTrials.gov... Campisi, M. *et al.* [Vascular STING activation facilitates NK cell anti-tumor immunity in small cell lung cancer.](https://pubmed.ncbi.nlm.nih.gov/41791380/) *Cancer cell* (2026) doi:10.1016/j.ccell.2026.02.008. Campisi, M. *et al.* [Vascular STING activation facilitates NK cell anti-tumor immunity in small cell lung cancer.](https://pubmed.ncbi.nlm.nih.gov/41791380/) *Cancer cell* (2026) doi:10.1016/j.ccell.2026.02.008. - add\_circle do\_not\_disturb\_on Abstract Small cell lung cancer (SCLC) typically displays a "cold" tumor microenvironment with a paucity of immune infiltrate. Neuroendocrine SCLC cells also profoundly repress MHC-I expression, rendering them vulnerable to NK cell-mediated cytotoxicity. Here, we... Xu, R. *et al.* [Live-cell Pick-Seq (LiP-Seq): Interrogating ultra-rare mantle cell lymphoma persistent cells after CART19 therapy.](https://pubmed.ncbi.nlm.nih.gov/41855504/) *Blood advances* (2026) doi:10.1182/bloodadvances.2025016688. Xu, R. *et al.* [Live-cell Pick-Seq (LiP-Seq): Interrogating ultra-rare mantle cell lymphoma persistent cells after CART19 therapy.](https://pubmed.ncbi.nlm.nih.gov/41855504/) *Blood advances* (2026) doi:10.1182/bloodadvances.2025016688. - add\_circle do\_not\_disturb\_on Abstract Many cancer therapies induce high response rates, with some resulting in undetectable disease as assessed using standard clinical assays. This is particularly true in leukemia and lymphoma, where patients often achieve deep remission yet ultimately suffer... Doh, H. M., Kozlova, N., Cruz, K. A. & Muranen, T. [Interaction of NDRG1 and TGM2 modulates DNA replication and repair.](https://pubmed.ncbi.nlm.nih.gov/41914984/) *Molecular cancer research : MCR* (2026) doi:10.1158/1541-7786.MCR-25-0743. Doh, H. M., Kozlova, N., Cruz, K. A. & Muranen, T. [Interaction of NDRG1 and TGM2 modulates DNA replication and repair.](https://pubmed.ncbi.nlm.nih.gov/41914984/) *Molecular cancer research : MCR* (2026) doi:10.1158/1541-7786.MCR-25-0743. - add\_circle do\_not\_disturb\_on Abstract In tumor cells, DNA replication is constantly challenged by endogenous and exogenous sources, referred to as replication stress, and various pathways have evolved to mitigate this stress in cancer. We recently identified a novel extracellular matrix... Mills, C. E. *et al.* [Polypharmacology of an Optimal Kinase Library.](https://pubmed.ncbi.nlm.nih.gov/41889995/) *bioRxiv : the preprint server for biology* (2026) doi:10.64898/2026.03.17.711623. Mills, C. E. *et al.* [Polypharmacology of an Optimal Kinase Library.](https://pubmed.ncbi.nlm.nih.gov/41889995/) *bioRxiv : the preprint server for biology* (2026) doi:10.64898/2026.03.17.711623. - add\_circle do\_not\_disturb\_on Abstract Despite decades of research, current understanding of the spectrum of targets bound by kinase inhibitors remains incomplete. This complicates mechanism of action studies, drug repurposing, and understanding of adverse responses. Here, we describe kinome... Brunette, G. J. *et al.* [Haplotype-resolved reconstruction and functional interrogation of cancer karyotypes.](https://pubmed.ncbi.nlm.nih.gov/41856042/) *Cell systems* **17**, 101477 (2026). Brunette, G. J. *et al.* [Haplotype-resolved reconstruction and functional interrogation of cancer karyotypes.](https://pubmed.ncbi.nlm.nih.gov/41856042/) *Cell systems* **17**, 101477 (2026). - add\_circle do\_not\_disturb\_on Abstract Complex karyotype changes are widespread in cancer genomes. A major gap in cancer genome characterization is the resolution of rearranged chromosomes with chromosome-length continuity. Here, we describe a two-tiered approach to determine the segmental... Zhu, G. *et al.* [HPV16 E6 oncoprotein promotes microhomology-mediated viral integration by increasing PolΘ protein expression.](https://pubmed.ncbi.nlm.nih.gov/41785316/) *Proceedings of the National Academy of Sciences of the United States of America* **123**, e2532479123 (2026). Zhu, G. *et al.* [HPV16 E6 oncoprotein promotes microhomology-mediated viral integration by increasing PolΘ protein expression.](https://pubmed.ncbi.nlm.nih.gov/41785316/) *Proceedings of the National Academy of Sciences of the United States of America* **123**, e2532479123 (2026). - add\_circle do\_not\_disturb\_on Abstract Integration of the high-risk human papillomavirus 16 (HPV16) genome into the host chromosome, frequently driven by microhomology-mediated end joining (MMEJ), is a critical step in the carcinogenesis of HPV-associated tumors. However, the mechanisms by... Rojas-Jimenez, E. *et al.* [Evaluation of targeted and immune combination therapies in a rat model of hormone receptor-positive breast cancer.](https://pubmed.ncbi.nlm.nih.gov/41642991/) *Proceedings of the National Academy of Sciences of the United States of America* **123**, e2501052123 (2026). Rojas-Jimenez, E. *et al.* [Evaluation of targeted and immune combination therapies in a rat model of hormone receptor-positive breast cancer.](https://pubmed.ncbi.nlm.nih.gov/41642991/) *Proceedings of the National Academy of Sciences of the United States of America* **123**, e2501052123 (2026). - add\_circle do\_not\_disturb\_on Abstract Estrogen receptor (ER) positive breast cancer is the most prevalent subtype, commonly responsive to endocrine therapies. Immune checkpoint inhibitors (ICIs) have limited efficacy in ER-positive disease, highlighting the need for the development of... - Previous page chevron\_left - [1](?page=0 "Current page") - [2](?page=1 "Go to page 2") - [3](?page=2 "Go to page 3") - [ Last page 38 ](?page=37 "Go to last page") - [ Next page chevron\_right ](?page=1 "Go to next page")