Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Get in touch with Xinying
Contact Xinying, search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck RackActions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Articles
New Binding Sites for JAK2 Inhibition in Myeloproliferative Neoplasms: Structural Insights, Therapeutic Potential, and Future Directions
1 Introduction Myeloproliferative neoplasms are myeloid malignancies defined byhypercellular bone marrow and elevated peripheral blood cell counts [1]. The classical subtypes (Figure 1) include polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF). MF can present asprimary myelofibrosis (PMF) or develop from a pre-existing MPN such as PV or ET, in which case it is referred to assecondary myelofibrosis (SMF) [2, 3].
Quercetagetin-rich flavonoids from marigold induce apoptosis inhibit metastasis of non-small cell lung cancer via the p53/p21 signaling pathway
Abstract Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, with limited therapeutic efficacy and severe side effects associated with conventional chemotherapy, creating an urgent need for safe and effective natural anti-tumor agents. Quercetagetin-rich marigold flavonoids (QG-MF), isolated from the lutein-extracted inflorescence residues of Tagetes erecta L.
Reversing adenosine-mediated immunosuppression in triple-negative breast cancer by synergistic chemo-immunotherapy via stimuli-responsive nanomedicines
Keywords Triple-negative breast cancer Adenosine-receptor signalling pathway Immunogenic cell death Tumor immune microenvironment Chemo-immunotherapy synergy Nanomedicines Evidence before this study EPI, a first-line chemotherapeutic agent for TNBC, has been extensively studied because it can directly kill tumor cells and induce ICD. Evidence indicates that EPI triggers ICD through high mobility group box 1 (HMGB1) release, calreticulin (CRT) exposure, and ATP secretion.
Actions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Get in touch with Xinying
Contact Xinying, search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck Rack