Results 81 to 90 of about 1,237,731 (267)

Certified 2011 Population Estimates for Oregon and Counties

open access: yes, 2011
Certified Population Estimates for Oregon and Its Counties.
Portland State University. Population Research Center
core  

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

Population Estimates, Oregon Counties and Incorporated Cities

open access: yes, 1975
This report contains the estimates for each of the thirty-six counties and the 240 incorporated cities of Oregon from 1975-1986. The estimates are based on data such as births, deaths, school enrollment, housing, number of privately owned passenger ...
Portland State University. Center for Population Research and Census
core  

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

2000 Oregon Population Estimates Report

open access: yes, 2001
This report presents the population estimates for Oregon and its counties and incorporated cities for July 1, 2000, based on the April 1, 2000 census information.
Portland State University. Population Research Center   +3 more
core  

Inference From Gene to Population: Propagating Uncertainty In Estimates of Population Characteristics Through Ecological Scales [PDF]

open access: yes, 2010
A current trend in population biology is the increasing realisation of the effect of individual variability on some of the big patterns of population dynamics.
Chipperfield, Joseph
core  

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Official Population Estimates: Oregon Counties and Cities July 1, 1978 - July 1, 1988

open access: yes, 1988
This report contains the following tables: Population Estimates of Oregon by Area Type and Specific Metropolitan Areas: 1978-1988 Population Estimates for Counties and Cities: 1978-1988 Population of Oregon Cities by Alphabetical Order : April 1, 1980 ...
Portland State University. Population Research Center   +1 more
core  

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak   +10 more
wiley   +1 more source

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