Results 151 to 160 of about 4,807,572 (318)

PAK1 activation drives divergent resistance mechanisms to aromatase inhibition and tamoxifen in a luminal: A breast cancer model

open access: yesMolecular Oncology, EarlyView.
Breast cancer remains a major cause of cancer death in women, frequently developing endocrine therapy resistance. This study demonstrates that upregulated p21‐activated kinase 1 (PAK1) activity drives resistance to tamoxifen and long‐term estrogen deprivation in ER+ breast cancer models.
Luisa Schwarzmüller   +10 more
wiley   +1 more source

Regulation of cancer cell metabolism

open access: yes, 2011
Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways ...
Rob A. Cairns   +5 more
core   +1 more source

Spatial and single‐nuclei transcriptomics reveals idiosyncratic and generic patterns in papillary and anaplastic thyroid cancers

open access: yesMolecular Oncology, EarlyView.
Matched spatial transcriptomics and single‐nuclei RNA‐seq were generated for anaplastic and BRAFV600E papillary thyroid cancers revealing generic and tumor‐specific states occurring in cancer cells and in the tumor microenvironment. In this context, cancer dedifferentiation mirrored organoid maturation through ordered thyroid marker gain/loss ...
Adrien Tourneur   +11 more
wiley   +1 more source

Circulating microRNA signatures of cachexia and cancer in Canis familiaris as a comparative oncology model for human disease

open access: yesMolecular Oncology, EarlyView.
Circulating microRNAs as biomarkers of cachexia and sex‐specific cancer in senior dogs. In 25 client‐owned dogs, four circulating miRNAs (miR‐15a, miR‐15b, miR‐16, miR‐140) were downregulated in cachexia, with miR‐16 the strongest individual biomarker (AUC = 0.899).
Soon‐Seok Park   +6 more
wiley   +1 more source

Targeting MTHFD2 to exploit cancer-specific metabolism and the DNA damage response

open access: yes
The one-carbon metabolism enzyme methylenetetrahydrofolate dehydrogenase/cyclohydrolase 2 (MTHFD2) is a promising therapeutic target in cancer. MTHFD2 is upregulated across numerous cancer types, promotes growth and metastasis of cancer, and correlates ...
Green, A.C.   +7 more
core   +1 more source

Nutrition, Metabolism, and Cancer

open access: yesVeterinary Quarterly, 1998
(1998). Nutrition, Metabolism, and Cancer. Veterinary Quarterly: Vol. 20, Voorjaarsdagen Congress 1998, pp. S75-S75.
openaire   +2 more sources

Epigenetic silencing of the liver‐specific lncRNA LUNAR promotes liver cancer progression via NOTCH activation

open access: yesMolecular Oncology, EarlyView.
LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang   +9 more
wiley   +1 more source

The metabolic response to cancer [PDF]

open access: yesProceedings of the Nutrition Society, 1992
J, Gelin, K, Lundholm
openaire   +2 more sources

PANoptosis in the pathogenesis of myelodysplastic syndromes

open access: yesMolecular Oncology, EarlyView.
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla   +4 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

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