Results 201 to 210 of about 10,361,402 (288)

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

Molecular 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, Hyung Seok Kim, Geum Ok Baek, Moon Gyeong Yoon, Su In Lee, Jee‐Yeong Jeong, Ji Eun Han, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun   +9 more
wiley   +1 more source

Cancer of unknown primary: the evolution of tissue of origin identification in the artificial intelligence era. [PDF]

Biomark Res
Zeng X, Lao IW, Sun Y, Wang Q, Zhang X, Luo Z, Zhou X, Xu M.   +7 more
europepmc   +1 more source

CEACAM1 participation in breast cancer progression

Molecular Oncology, EarlyView.
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin, Irina Kube‐Golovin, Anatolii Romaniuk, Gunther Wennemuth   +3 more
wiley   +1 more source

WeedNet: a foundation model-based global-to-local AI approach for weed species identification and classification. [PDF]

Nat Commun
Shen Y, Ayanlade TT, Boddepalli VN, Saadati M, Rairdin A, Deng ZK, Arshad MA, Chiranjeevi S, Balu A, Mueller D, Singh AK, Everman W, Merchant N, Ganapathysubramanian B, Anderson M, Sarkar S, Singh A.   +16 more
europepmc   +1 more source

Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer

Molecular Oncology, EarlyView.
Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas, Barbara Karakyriakou, Patricia C. Muskus, Alyssa M. Roberts, Justin Rendleman, Alexa Warren, Hanxu Lu, Kimberly A. Birmingham, Malone K. Friedman, Abigail E. Goen, Huijuan Yang, Owen M. Wilkins, Fred W. Kolling, Eugene Demidenko, Julie M. Jorns, Brock C. Christensen, Todd W. Miller   +16 more
wiley   +1 more source

Intrapatient tumour heterogeneity and clonal evolution in an autopsy study of metastatic salivary gland cancer

Molecular Oncology, EarlyView.
Tumour heterogeneity and clonal evolution of metastatic salivary gland cancer were evaluated in two patients with adenoid carcinoma and one patient with myoepithelial carcinoma. Radiology‐guided autopsy enabled multi‐region sampling (total samples n = 149), followed by whole‐genome sequencing and phylogenetic reconstruction (17 tumour samples, 4–7 per ...
Gerben Lassche, Niels J. van Ruitenbeek, Charlotte Adang, Luke O'Gorman, Pui Yuen Lee, Willemijn M. Klein, Adriana C. H. van Engen‐van Grunsven, Jack A. Schalken, Sander Bervoets, Gerald W. Verhaegh, Carla M. L. van Herpen   +10 more
wiley   +1 more source

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

Molecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee, Alessia Marin, Shivani Yalala, Harri M. Itkonen   +3 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular 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, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source