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Jazzeri et al (2002) compared gene expression profiles in BRCA1/2-associated EOC with sporadic EOC and showed that sporadic tumours may have mutations that resemble the molecular pathways seen in germline mutations as well as dysfunction in the downstream effects of these genes.
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Finally, because we expected Psn, Notch, and CBP to be involved in a related molecular pathway (see below), we examined the phenotypes produced when CBP was silenced with RNAi.
Several studies have identified cellular and molecular signals that participate in establishing these pathways (see review by [1]), including Ephrins [2] [4], Semaphorins [5] [9], Netrins and Slits [10], [11], Engrailed-1 [13], [13], and Sonic hedgehog [14].
Crucially, dual inhibition of EGFR and mTOR pathways by erlotinib and RAD001 combination therapy showed a synergistic and highly significant antitumour effect that could be explained on the molecular level by synergistic regulation of both pathways (see Figure 3C).
Recently, in vitro studies have demonstrated adiponectin involvement in various cancer cell types including breast, endometrial, colon, stomach, prostate, and leukemia [ 64, 65]; Adiponectin, in fact, inhibits cell growth and induces apoptosis in dose-dependent manner both in vitro and in vivo through different molecular pathways (for review, see [ 66, 67]).
A molecular subtype of melanoma is loosely defined as those tumors containing the same set of molecular (primarily genetic) defect(s) and their associated pathways (see Figure 1).
GEP of DLBCLs has identified molecular subgroups, which correlate with prognosis, and may have relevance for treatment based on signaling pathways (see below) [ 6– 9, 19].
On the other hand, we reported an important common CC molecular signature revealing the preservation of numerous growth factor signaling between the two types of treatments including the IGF, PDGF, FGF, and EGF pathways (See Figure SIII).
Lung cancer that develops in the absence of significant tobacco-smoke exposure appears to be a unique disease entity with novel genomic and epigenomic alterations and activation of molecular pathways that are not generally seen in tobacco-smoke-induced lung cancer.
Clustering was performed using a variational Bayesian mixture model [ 52] over the 8 largest molecular pathway modules to see if samples segregated significantly according to intrinsic subtype [ 46].
By binding to adrenoceptors in various organs, NE and EPI may modulate various intracellular molecular pathways already implicated in cancer (see below).
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