Results 111 to 120 of about 335,095 (291)

On null hypotheses in survival analysis

open access: yes, 2019
The conventional nonparametric tests in survival analysis, such as the log-rank test, assess the null hypothesis that the hazards are equal at all times. However, hazards are hard to interpret causally, and other null hypotheses are more relevant in many
Ryalen, Pål Christie   +2 more
core   +1 more source

Comprehensive omics‐based classification system in adult patients with B‐cell acute lymphoblastic leukemia

open access: yesMolecular Oncology, EarlyView.
The COMBAT classification system, developed through multi‐omics integration, stratifies adult patients with B‐cell acute lymphoblastic leukemia(B‐ALL) into three molecular subtypes with distinct surface antigen patterns, immune landscape, methylation patterns, biological pathways and prognosis.
Yang Song   +11 more
wiley   +1 more source

Incorporation of Frailties Into a Non-Proportional Hazard Regression Model and Its Diagnostics for Reliability Modeling of Downhole Safety Valves [PDF]

open access: gold, 2020
Francisco Louzada   +15 more
openalex   +1 more source

Likelihood-Based Estimation of a Proportional-Hazard, Competing- Risk Model with Grouped Duration Data [PDF]

open access: yes
This short paper demonstrates two important results related to the estimation of competing-risk models under the proportional-hazards assumption with grouped duration data.
Mark Yuying An
core  

Circulating tumor DNA monitoring and blood tumor mutational burden in patients with metastatic solid tumors treated with atezolizumab

open access: yesMolecular Oncology, EarlyView.
In patients treated with atezolizumab as a part of the MyPathway (NCT02091141) trial, pre‐treatment ctDNA tumor fraction at high levels was associated with poor outcomes (radiographic response, progression‐free survival, and overall survival) but better sensitivity for blood tumor mutational burden (bTMB).
Charles Swanton   +17 more
wiley   +1 more source

A multistate model for early decision making in oncology

open access: yes, 2018
The development of oncology drugs progresses through multiple phases, where after each phase a decision is made about whether to move a molecule forward.
Beyer, Ulrich   +4 more
core   +1 more source

The subcellular distribution of phosphorylated Y‐box‐binding protein‐1 at S102 in colorectal cancer patients, stratified by KRAS mutational status and clinicopathological features

open access: yesMolecular Oncology, EarlyView.
This study identifies nuclear YB‐1 S102 phosphorylation as a marker associated with KRAS and FBXW7 mutations in colorectal cancer. Mutated KRAS correlates specifically with nuclear, not cytoplasmic, S102 YB‐1. These findings provide the first ex vivo evidence of this link in CRC and suggest future studies should assess the prognostic and therapeutic ...
Konstanze Lettau   +9 more
wiley   +1 more source

The Use of Net Benefit in Modeling Non-Proportional Hazards

open access: yes, 2020
Background: The hazard ratio (HR), representing the quantified estimate of treatment effect in survival analysis, measures the instantaneous relative difference of failure risk between two groups. The HR is typically assumed to be independent of time; however, this assumption is usually violated in practice.
openaire   +2 more sources

Modeling of Distance Learners’ Retention Using Mixed-Model on Non-Proportional Hazard

open access: yesJournal of Open, Flexible and Distance Learning, 2023
Universitas Terbuka is a public university in Indonesia that implements an open-distance education system. The quality and success of higher education in Indonesia are indicated by the gross enrolment rate (GER). Modelling student retention is one indicator of the value of the GER.
openaire   +3 more sources

EGFR‐STAT3 activation provides a therapeutic rationale for targeting aggressive ETV1‐positive prostate cancer

open access: yesMolecular Oncology, EarlyView.
Cotargeting EGFR and STAT3 with Erlotinib and TTI‐101 impairs both 2D and 3D growth of ETV1‐overexpressing prostate cancer cells by disrupting a self‐sustaining ETV1–EGFR positive feedback loop that promotes EGFR and STAT3 expression and phosphorylation (activation).
Elsa Gomes Paiva   +5 more
wiley   +1 more source

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