Results 101 to 110 of about 311,587 (357)

Epithelial–Mesenchymal Transition in Hepatocellular Carcinoma [PDF]

open access: yesFuture Oncology, 2009
The transition of epithelial cells to a mesenchymal phenotype is of paramount relevance for embryonic development and adult wound healing. During the past decade, the epithelial-mesenchymal transition (EMT) has been increasingly recognized to occur during the progression of various carcinomas such as hepatocellular carcinoma (HCC).
Christoph Kornauth   +9 more
openaire   +3 more sources

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

open access: yesMolecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu   +11 more
wiley   +1 more source

HDAC1 inhibition by MS-275 in mesothelial cells limits cellular invasion and promotes MMT reversal [PDF]

open access: yes, 2018
Peritoneal fibrosis is a pathological alteration of the peritoneal membrane occurring in a variety of conditions including peritoneal dialysis (PD), post-surgery adhesions and peritoneal metastases.
Battistelli, Cecilia   +14 more
core   +1 more source

ShcD adaptor protein drives invasion of triple negative breast cancer cells by aberrant activation of EGFR signaling

open access: yesMolecular Oncology, EarlyView.
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau   +11 more
wiley   +1 more source

Role of microRNA in epithelial to mesenchymal transition and metastasis and clinical perspectives

open access: yesCancer Management and Research, 2014
Antonio Díaz-López,1 Gema Moreno-Bueno,1,2 Amparo Cano11Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de Madrid, Instituto de Investigaciones Biomédicas “Alberto Sols” (CSIC-UAM ...
Díaz-López A   +2 more
doaj  

MUC1 marks collecting tubules, renal vesicles, comma- and S-shaped bodies in human developing kidney tubules, renal vesicles, comma- and s-shaped bodies in human kidney

open access: yesEuropean Journal of Histochemistry, 2012
MUC1 is a transmembrane glycoprotein, apically expressed in most epithelial cells, used in the differential diagnosis of carcinomas and for discrimination of tumors of non-epithelial origin showing epithelioid features.
V. Fanos   +9 more
doaj   +2 more sources

Breast Cancer Stem Cells Transition between Epithelial and Mesenchymal States Reflective of their Normal Counterparts

open access: yesStem Cell Reports, 2014
Previous studies have suggested that breast cancer stem cells (BCSCs) mediate metastasis, are resistant to radiation and chemotherapy, and contribute to relapse.
Suling Liu   +20 more
doaj   +1 more source

Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity [PDF]

open access: yes, 2011
Lung epithelial cells exhibit a high degree of plasticity. Alterations to lung epithelial cell function are critically involved in several chronic lung diseases such as pulmonary fibrosis.
Adamson IY   +66 more
core   +1 more source

Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry

open access: yesMolecular Oncology, EarlyView.
Elevated expression of transcriptional regulator inhibitor of DNA binding 1 (ID1) promoted cancer cell‐mediated vasculogenic mimicry (VM) through regulation of pro‐angiogenic and pro‐cancerous genes (e.g. VE‐cadherin (CDH5), TIE2, MMP9, DKK1). Higher ID1 expression also increased metastases to the lung and the liver.
Emma J. Thompson   +11 more
wiley   +1 more source

MET and NF2 alterations confer primary and early resistance to first‐line alectinib treatment in ALK‐positive non‐small‐cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu   +11 more
wiley   +1 more source

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