Results 181 to 190 of about 1,081,535 (384)

CRISPR targeting of FOXL2 c.402C>G mutation reduces malignant phenotype in granulosa tumor cells and identifies anti‐tumoral compounds

Molecular Oncology, Volume 19, Issue 4, Page 1092-1116, April 2025.
FOXL2 c.402C>G mutation drives granulosa cell tumors. Using CRISPR technology, we selectively corrected this mutation, reducing malignancy and increasing sensitivity to dasatinib and ketoconazole. Transcriptomic changes revealed potential therapeutic targets, demonstrating CRISPR's promise for treating this rare ovarian cancer.
Sandra Amarilla‐Quintana, Paloma Navarro, Iván Hernández, Alejandra Ramos, Ana Montero‐Calle, Pablo Cabezas‐Sainz, Maria J Barrero, Diego Megías, Borja Vilaplana‐Martí, Carolina Epifano, Déborah Gómez‐Dominguez, Sara Monzón, Isabel Cuesta, Laura Sánchez, Rodrigo Barderas, Jesús García‐Donas, Alberto Martín, Ignacio Pérez de Castro   +17 more
wiley   +1 more source

Porous polyethylene in reconstructive head and neck surgery [PDF]

, 1985
Berghaus, Alexander
core   +1 more source

Epidemiological review of multiple primary malignant neoplasms of the prostate, kidney, and bladder

, 2023
Artyom M. Mylnikov, Galina N. Maslyakova
openalex   +2 more sources

Integration of single‐cell and bulk RNA‐sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer

Molecular Oncology, EarlyView.
Prostate cancer is a leading malignancy with significant clinical heterogeneity in men. An 11‐gene signature derived from dysregulated epithelial cell markers effectively predicted biochemical recurrence‐free survival in patients who underwent radical surgery or radiotherapy.
Zhuofan Mou, Lorna W. Harries
wiley   +1 more source

0230 Multiple primary neoplasms on breast cancer survivors

, 2009
Nazar Lukavetskyy
openalex   +1 more source

Clinical significance of stratifying prostate cancer patients through specific circulating genes

Molecular Oncology, Volume 19, Issue 5, Page 1310-1331, May 2025.
We tested a specific panel of genes representative of luminal, neuroendocrine and stem‐like cells in the blood of prostate cancer patients, showing predictive value from diagnosis to late stages of disease. This approach allows monitoring of treatment responses and outcomes at specific time points in trajectories.
Seta Derderian, Edouard Jarry, Arynne Santos, Quentin Vesval, Lucie Hamel, Rafael Sanchez‐Salas, Alexis Rompré‐Brodeur, Wassim Kassouf, Raghu Rajan, Fadi Brimo, Marie Duclos, Armen Aprikian, Simone Chevalier   +12 more
wiley   +1 more source

Orthotopic Liver Transplantation for Benign Hepatic Neoplasms [PDF]

, 1995
Iwatsuki, S, Madariaga, JR, Selby, R, Starzl, TE, Tepetes, K, Webb, M   +5 more
core   +1 more source

A recommendation for the management of lesions of unknown malignancy in multiple primary malignant neoplasm patients: A case report

, 2014
Xiangyu Xia, Kaijun Cui
openalex   +2 more sources

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

Molecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita, Varda Shoshan‐Barmatz   +1 more
wiley   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

Molecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi, Kazunori Mori, Hidetsugu Nakagawa, Momoko Uchida, Fumihiro Ishikawa, Motoko Shibanuma   +5 more
wiley   +1 more source