Results 141 to 150 of about 6,437,662 (327)
The distribution of some extremum on the risk process whose income depend on the current reserve. [PDF]
Springerplus, 2016 He J, Liu Z, Zhang W.
europepmc +1 more source
Molecular Oncology, EarlyView.There is an unmet need in metastatic breast cancer patients to monitor therapy response in real time. In this study, we show how a noninvasive and affordable strategy based on sequencing of plasma samples with longitudinal tracking of tumour fraction paired with a statistical model provides valuable information on treatment response in advance of the ...
Emma J. Beddowes +20 more
wiley +1 more source
Low-income minority women at risk for cervical cancer: a process to improve adherence to follow-up recommendations [PDF]
, 2001 Virginia A Cardin +5 more
openalex +1 more source
Molecular Oncology, EarlyView.Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu +11 more
wiley +1 more source
The Psychophysiology of Real-Time Financial Risk Processing [PDF]
, 2001 Andrew W. Lo, Dmitry V. Repin
openalex +1 more source
Molecular Oncology, EarlyView.This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani +14 more
wiley +1 more source
Shortcuts in Cassava Processing and Risk of Dietary Cyanide Exposure in Zaire
, 1992 M. Banea, Nigel H. Poulter, Hans Rosling
openalex +1 more source
Molecular Oncology, EarlyView.Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen +12 more
wiley +1 more source