Neta Erez

The onset of p53-dependent DNA repair or apoptosis is determined by the level of accumulated damaged DNA.

Falkor, a novel cell growth regulator isolated by a functional genetic screen.

The murine telomerase catalytic subunit shares the PAb-240 mutant specific epitope of the p53 protein.

Prolonged culture of telomerase-immortalized human fibroblasts leads to a premalignant phenotype.

Expression of prolyl-hydroxylase-1 (PHD1/EGLN2) suppresses hypoxia inducible factor-1alpha activation and inhibits tumor growth.

Hypoxia-dependent regulation of PHD1: cloning and characterization of the human PHD1/EGLN2 gene promoter.

Activated p53 suppresses the histone methyltransferase EZH2 gene.

p53-dependent down-regulation of telomerase is mediated by p21waf1.

Monoclonal antibody to a DNA-binding domain of p53 mimics charge structure of DNA: anti-idiotypes to the anti-p53 antibody are anti-DNA.

Transcriptional programs following genetic alterations in p53, INK4A, and H-Ras genes along defined stages of malignant transformation.

Enhanced angiotensin II production by renal mesangium is responsible for apoptosis/proliferation of endothelial and epithelial cells in a model of malignant hypertension.

Plasticity in tumor-promoting inflammation: impairment of macrophage recruitment evokes a compensatory neutrophil response.

Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner.

Leukocytes as paracrine regulators of metastasis and determinants of organ-specific colonization.

The metastatic microenvironment: Brain-derived soluble factors alter the malignant phenotype of cutaneous and brain-metastasizing melanoma cells.

From sentinel cells to inflammatory culprits: cancer-associated fibroblasts in tumour-related inflammation.