Results 41 to 50 of about 359,688 (261)
THE ARTIFICIAL PRODUCTION IN MAMMALIAN PLASMA OF SUBSTANCES INHIBITORY TO THE GROWTH OF CELLS [PDF]
, 1915 Albert Walton
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Molecular 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
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Molecular 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
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Growth accessory substances in the nutrition of bacteria [PDF]
, 1921 Th. Thjötta, Oswald T. Avery
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Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry
Molecular 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
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On the Action of some Essential Oils and Other Volatile Substances on the Growth of the Bacillus Tuberculosis and in the Treatment of Phthisis [PDF]
, 1899 William Murrell
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Molecular 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
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Leaf Growth Factors II—The Activity of Pure Substances in Leaf Growth [PDF]
, 1939 David M. Bonner, A. J. Haagen‐Smit
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Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Molecular Oncology, EarlyView.Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
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Molecular Oncology, EarlyView.Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen +12 more
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