Inhibitor Therapy
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2021 ◽  
Vol 38 ◽  
pp. 100872
Author(s):  
Stephen M. Graves ◽  
Floor J. Backes

Blood ◽  
2021 ◽  
Author(s):  
Naseema Gangat ◽  
Natasha Szuber ◽  
Hassan B Alkhateeb ◽  
Aref Al-Kali ◽  
Animesh D Pardanani ◽  
...  

2021 ◽  
pp. molcanres.0442.2021
Author(s):  
Mark Lee ◽  
Brian R. Untch ◽  
Bin Xu ◽  
Ronald Ghoissein ◽  
Catherine Han ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
So Yeon Oh ◽  
Soyeon Kim ◽  
Bhumsuk Keam ◽  
Tae Min Kim ◽  
Dong-Wan Kim ◽  
...  

AbstractCirculating soluble programmed death-1 ligand (sPD-L1) is measurable in the serum of cancer patients. This study aimed to investigate the significance of sPD-L1 in cancer patients receiving immune checkpoint inhibitor therapy. Blood samples were obtained before and after immune checkpoint inhibitor therapy (January 2015 to January 2019). The study cohort consisted of 128 patients who were diagnosed with non-small cell lung cancer (n = 50), melanoma (n = 31), small cell lung cancer (n = 14), urothelial carcinoma (n = 13), and other cancers (n = 20). Patients with a high level (> 11.0 pg/μL) of sPD-L1 were more likely to exhibit progressive disease compared with those with a low level (41.8% versus 20.7%, p = 0.013). High sPD-L1 was also associated with worse prognosis; the median PFS was 2.9 (95% confidence interval [CI] 2.1–3.7) months versus 6.3 (95% CI 3.0–9.6) months (p = 0.023), and the median OS was 7.4 (95% CI 6.3–8.5) months versus 13.3 (95% CI 9.2–17.4) months (p = 0.005). In the multivariate analyses, high sPD-L1 was an independent prognostic factor for both decreased PFS (HR 1.928, p = 0.038) and OS (HR 1.788, p = 0.004). sPD-L1 levels did not correlate with tissue PD-L1 expression. However, sPD-L1 levels were positively correlated with neutrophil to lymphocyte ratios and negatively correlated with both the proportion and the total number of lymphocytes. We found that high pretreatment sPD-L1 levels were associated with progressive disease and were an independent prognostic factor predicting lower PFS and OS in these patients.


Author(s):  
N Pannell ◽  
D Joseph ◽  
MMTM Ally ◽  
M Bida ◽  
G R Tintinger

2021 ◽  
Vol 9 (10) ◽  
pp. e002886corr1

CHEST Journal ◽  
2021 ◽  
Vol 160 (4) ◽  
pp. A981-A982
Author(s):  
Parth Patel ◽  
Tarang Patel ◽  
SACHIN PATIL ◽  
Shaili Patel ◽  
Jonathan Ross Ang

2021 ◽  
pp. 100877
Author(s):  
Angela L. Liang ◽  
Payam Katebi Kashi ◽  
Mark Hopkins ◽  
Anna Beavis ◽  
Stephanie Gaillard ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jian Ma ◽  
Qing Shi ◽  
Gaofeng Cui ◽  
Haoyue Sheng ◽  
Maria Victoria Botuyan ◽  
...  

AbstractGeminin and its binding partner Cdt1 are essential for the regulation of DNA replication. Here we show that the CULLIN3 E3 ubiquitin ligase adaptor protein SPOP binds Geminin at endogenous level and regulates DNA replication. SPOP promotes K27-linked non-degradative poly-ubiquitination of Geminin at lysine residues 100 and 127. This poly-ubiquitination of Geminin prevents DNA replication over-firing by indirectly blocking the association of Cdt1 with the MCM protein complex, an interaction required for DNA unwinding and replication. SPOP is frequently mutated in certain human cancer types and implicated in tumorigenesis. We show that cancer-associated SPOP mutations impair Geminin K27-linked poly-ubiquitination and induce replication origin over-firing and re-replication. The replication stress caused by SPOP mutations triggers replication catastrophe and cell death upon ATR inhibition. Our results reveal a tumor suppressor role of SPOP in preventing DNA replication over-firing and genome instability and suggest that SPOP-mutated tumors may be susceptible to ATR inhibitor therapy.


2021 ◽  
Author(s):  
BD Nguyen-Sträuli ◽  
P Meyer-Wilmes ◽  
J Baum ◽  
A Kreklau ◽  
C Buschmann ◽  
...  

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