Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A Transient Pseudosenescent Secretome Promotes Tumor Growth after Antiangiogenic Therapy Withdrawal.

Cell reports - 26 Dec 2018

Mastri Michalis, Tracz Amanda, Lee Christina R, Dolan Melissa, Attwood Kristopher, Christensen James G, Liu Song, Ebos John M L

Abstract excerpt

VEGF receptor tyrosine kinase inhibitors (VEGFR TKIs) approved to treat multiple cancer types can promote metastatic disease in certain limited preclinical settings. Here, we show that stopping VEGFR TKI treatment after resistance can lead to rebound tumor growth that is driven by cellular changes resembling senescence-associated secretory phenotypes (SASPs) known to promote cancer progression. A SASP-mimicking...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Angiogenesis Inhibitors
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interleukin-6

Share to Mice, Inbred BALB C

Share to Neoplasm Metastasis

Share to Proteome

Share to Receptors, Vascular Endothelial Growth Factor

Share to TOR Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 30590043
DOI: 10.1016/j.celrep.2018.12.017
PMCID: PMC13277708

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Transient Pseudosenescent Secretome Promotes Tumor Growth after Antiangiogenic Therapy Withdrawal.PMID 30590043Read ↗

Effect of Cellular Senescence on the Growth of HER2-Positive Breast CancersSemantic proximity Read ↗

Non-Cell Autonomous Effects of the Senescence-Associated Secretory Phenotype in Cancer TherapySemantic proximity Read ↗

Oncogene inactivation-induced senescence facilitates tumor relapseSemantic proximity Read ↗

Senescent stromal cells promote cancer resistance through SIRT1 loss-potentiated overproduction of small extracellular vesiclesSemantic proximity Read ↗

Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistanceSemantic proximity Read ↗

Therapy-induced senescent tumor cells in cancer relapseSemantic proximity Read ↗

Controlling secretion to limit chemoresistance.Semantic proximity Read ↗

Could senescence phenotypes strike the balance to promote tumor dormancy?Semantic proximity Read ↗

Tumour-derived extracellular vesicles within the therapy-induced senescent secretome distinctly suppress breast cancer via DKK1-mediated inflammatory responseSemantic proximity Read ↗

Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppressionSemantic proximity Read ↗

Stromal Senescence By Prolonged CDK4/6 Inhibition Potentiates Tumor GrowthSemantic proximity Read ↗

Detection of the senescence-associated secretory phenotype (SASP).Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.