Results 61 to 70 of about 892,099 (304)
Background Novel immune checkpoint inhibitors have been often utilized for different types of malignancies as salvage therapy with varying success. One obstacle to immune checkpoint inhibitor use is the higher incidence of immune-mediated side effects ...
Linh Ngo +3 more
doaj +1 more source
Targeting sphingosine kinase 1 in carcinoma cells decreases proliferation and survival by compromising PKC activity and cytokinesis [PDF]
Sphingosine kinases (SK) catalyze the phosphorylation of proapoptotic sphingosine to the prosurvival factor sphingosine 1-phosphate (S1P), thereby promoting oncogenic processes.
Zangemeister-Wittke, Uwe +15 more
core +2 more sources
Epigenetic reprogramming of lineage switching in cancer
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı +4 more
wiley +1 more source
Checkpoint inhibitors in hematological malignancies [PDF]
Inhibitory molecules such as PD-1, CTLA-4, LAG-3, or TIM-3 play a role to keep a balance in immune function. However, many cancers exploit such molecules to escape immune surveillance. Accumulating data support that their functions are dysregulated in lymphoid neoplasms, including plasma cell myeloma, myelodysplastic syndrome, and acute myeloid ...
Chi Young Ok, Ken H. Young
openaire +3 more sources
Ligand‐dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry
EGF and HRG induce distinct G1/S progression programs in ErbB2‐amplified BT474 breast cancer cells. Despite activating the potent ErbB2–ErbB3 heterodimer, HRG does not accelerate cell‐cycle entry. Instead, EGF promotes earlier restriction‐point passage via ERK–FOS signaling, whereas HRG activates the AKT–MYC axis, driving transcriptional heterogeneity ...
Ririn Rahmala Febri +5 more
wiley +1 more source
A context‐dependent modulatory role for eIF6 in acquired resistance to vemurafenib in melanoma
Acquired resistance to vemurafenib upregulates the translation factor eIF6 in melanoma cells. Silencing eIF6 in resistant cells reduces proliferation and partially restores drug sensitivity, whereas its overexpression increases sensitivity across melanoma lines regardless of BRAF status, via modulation of mTOR, S6K, and MAPK signaling.
George Kyriakopoulos +9 more
wiley +1 more source
Background Immune checkpoint inhibitors have traditionally been understood to exert their effects primarily within the tumor microenvironment, particularly targeting CD8 + T cells. However, recent studies have highlighted a pivotal role of tumor-draining
Jinzhu Zhang +13 more
doaj +1 more source
Efficacy and Safety of Amrubicin in Small Cell Carcinoma Previously Treated with Immune Checkpoint Inhibitors and Chemotherapy [PDF]
三重大学博士(医学)application/pdfAdding an immune checkpoint inhibitor to chemotherapy to treat extensive-stage small cell lung cancer is effective. However, there are no reports of an effective second-line treatment in patients previously treated with ...
西村, 正, ニシムラ, タダシ
core +1 more source
The ubiquitin system in normal and infected germinal center B cells
The ubiquitin system plays a central role in germinal center (GC) B cells, influencing differentiation to long‐lived memory B cells. Oncogenic gammaherpesviruses gain access to memory B cells by establishing latency in GC B cells. Mapping ubiquitin mechanisms in normal and infected GC B cells will define specific molecular circuits in B cells germane ...
Destiny Davis +2 more
wiley +1 more source
Negative Immune Checkpoint Inhibitors
Checkpoint inhibitors are a modern therapeutic approach for treating various types of cancer, metabolic diseases, and chronic infections. The main goal of this therapy is to specifically unlock the immune system, allowing it to recognize and eliminate cancer cells or pathogens, primarily through the activation of T lymphocytes.
Magda Drewniak-Świtalska +2 more
openaire +4 more sources

