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Metformin and TP53

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https://www.readbyqxmd.com/read/27869650/inhibiting-mitochondrial-respiration-prevents-cancer-in-a-mouse-model-of-li-fraumeni-syndrome
#1
Ping-Yuan Wang, Jie Li, Farzana L Walcott, Ju-Gyeong Kang, Matthew F Starost, S Lalith Talagala, Jie Zhuang, Ji-Hoon Park, Rebecca D Huffstutler, Christina M Bryla, Phuong L Mai, Michael Pollak, Christina M Annunziata, Sharon A Savage, Antonio Tito Fojo, Paul M Hwang
Li-Fraumeni syndrome (LFS) is a cancer predisposition disorder caused by germline mutations in TP53 that can lead to increased mitochondrial metabolism in patients. However, the implications of altered mitochondrial function for tumorigenesis in LFS are unclear. Here, we have reported that genetic or pharmacologic disruption of mitochondrial respiration improves cancer-free survival in a mouse model of LFS that expresses mutant p53. Mechanistically, inhibition of mitochondrial function increased autophagy and decreased the aberrant proliferation signaling caused by mutant p53...
November 21, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27793936/impact-of-h3k27-demethylase-inhibitor-gskj4-on-nsclc-cells-alone-and-in-combination-with-metformin
#2
Hikaru Watarai, Masashi Okada, Kenta Kuramoto, Hiroyuki Takeda, Hirotsugu Sakaki, Shuhei Suzuki, Shizuka Seino, Hiroyuki Oizumi, Mitsuaki Sadahiro, Chifumi Kitanaka
BACKGROUND: GSKJ4, an H3K27 demethylase inhibitor, reportedly exhibits antitumor activity against specific cancers harboring genetic alterations in genes encoding chromatin modulators. However, its potential as an anticancer agent against human cancers not associated with such genetic alterations, including non-small cell lung cancer (NSCLC), remains unknown. MATERIALS AND METHODS: The effect of GSKJ4 on the growth of three NSCLC cell lines and normal lung fibroblasts was investigated using the WST-8, dye exclusion, and colony formation assays...
November 2016: Anticancer Research
https://www.readbyqxmd.com/read/26655904/the-genomic-landscape-of-renal-oncocytoma-identifies-a-metabolic-barrier-to-tumorigenesis
#3
Shilpy Joshi, Denis Tolkunov, Hana Aviv, Abraham A Hakimi, Ming Yao, James J Hsieh, Shridar Ganesan, Chang S Chan, Eileen White
Oncocytomas are predominantly benign neoplasms possessing pathogenic mitochondrial mutations and accumulation of respiration-defective mitochondria, characteristics of unknown significance. Using exome and transcriptome sequencing, we identified two main subtypes of renal oncocytoma. Type 1 is diploid with CCND1 rearrangements, whereas type 2 is aneuploid with recurrent loss of chromosome 1, X or Y, and/or 14 and 21, which may proceed to more aggressive eosinophilic chromophobe renal cell carcinoma (ChRCC)...
December 1, 2015: Cell Reports
https://www.readbyqxmd.com/read/26031332/sestrin2-protects-dopaminergic-cells-against-rotenone-toxicity-through-ampk-dependent-autophagy-activation
#4
Yi-Sheng Hou, Jun-Jie Guan, Hai-Dong Xu, Feng Wu, Rui Sheng, Zheng-Hong Qin
Dysfunction of the autophagy-lysosomal pathway (ALP) and the ubiquitin-proteasome system (UPS) was thought to be an important pathogenic mechanism in synuclein pathology and Parkinson's disease (PD). In the present study, we investigated the role of sestrin2 in autophagic degradation of α-synuclein and preservation of cell viability in a rotenone-induced cellular model of PD. We speculated that AMP-activated protein kinase (AMPK) was involved in regulation of autophagy and protection of dopaminergic cells against rotenone toxicity by sestrin2...
August 2015: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/25051360/deregulation-of-the-egfr-pi3k-pten-akt-mtorc1-pathway-in-breast-cancer-possibilities-for-therapeutic-intervention
#5
REVIEW
Nicole M Davis, Melissa Sokolosky, Kristin Stadelman, Steve L Abrams, Massimo Libra, Saverio Candido, Ferdinando Nicoletti, Jerry Polesel, Roberta Maestro, Antonino D'Assoro, Lyudmyla Drobot, Dariusz Rakus, Agnieszka Gizak, Piotr Laidler, Joanna Dulińska-Litewka, Joerg Basecke, Sanja Mijatovic, Danijela Maksimovic-Ivanic, Giuseppe Montalto, Melchiorre Cervello, Timothy L Fitzgerald, Zoya Demidenko, Alberto M Martelli, Lucio Cocco, Linda S Steelman, James A McCubrey
The EGFR/PI3K/PTEN/Akt/mTORC1/GSK-3 pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance and metastasis. The expression of this pathway is frequently altered in breast cancer due to mutations at or aberrant expression of: HER2, ERalpha, BRCA1, BRCA2, EGFR1, PIK3CA, PTEN, TP53, RB as well as other oncogenes and tumor suppressor genes. In some breast cancer cases, mutations at certain components of this pathway (e.g., PIK3CA) are associated with a better prognosis than breast cancers lacking these mutations...
July 15, 2014: Oncotarget
https://www.readbyqxmd.com/read/24190252/destabilization-of-myc-mycn-by-the-mitochondrial-inhibitors-metaiodobenzylguanidine-metformin-and-phenformin
#6
Stephanie S Wang, Ruth Hsiao, Mariko M Limpar, Sarah Lomahan, Tuan-Anh Tran, Nolan J Maloney, Naohiko Ikegaki, Xao X Tang
In the present study, we investigated the anticancer effects of the mitochondrial inhibitors, metaiodobenzylguanidine (MIBG), metformin and phenformin. 131I-MIBG has been used for scintigraphic detection and the targeted radiotherapy of neuroblastoma (NB), a pediatric malignancy. Non-radiolabeled MIBG has been reported to be cytotoxic to NB cells in vitro and in vivo. However, the mechanisms behind its growth suppressive effects have not yet been fully elucidated. Metformin and phenformin are diabetes medications that are being considered in anticancer therapeutics...
January 2014: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/22090360/tp53-disruptive-mutations-lead-to-head-and-neck-cancer-treatment-failure-through-inhibition-of-radiation-induced-senescence
#7
Heath D Skinner, Vlad C Sandulache, Thomas J Ow, Raymond E Meyn, John S Yordy, Beth M Beadle, Alison L Fitzgerald, Uma Giri, K Kian Ang, Jeffrey N Myers
PURPOSE: Mortality of patients with head and neck squamous cell carcinoma (HNSCC) is primarily driven by tumor cell radioresistance leading to locoregional recurrence (LRR). In this study, we use a classification of TP53 mutation (disruptive vs. nondisruptive) and examine impact on clinical outcomes and radiation sensitivity. EXPERIMENTAL DESIGN: Seventy-four patients with HNSCC treated with surgery and postoperative radiation and 38 HNSCC cell lines were assembled; for each, TP53 was sequenced and the in vitro radioresistance measured using clonogenic assays...
January 1, 2012: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/22041887/anti-estrogen-resistance-in-breast-cancer-is-induced-by-the-tumor-microenvironment-and-can-be-overcome-by-inhibiting-mitochondrial-function-in-epithelial-cancer-cells
#8
Ubaldo E Martinez-Outschoorn, Allison Goldberg, Zhao Lin, Ying-Hui Ko, Neal Flomenberg, Chenguang Wang, Stephanos Pavlides, Richard G Pestell, Anthony Howell, Federica Sotgia, Michael P Lisanti
Here, we show that tamoxifen resistance is induced by cancer-associated fibroblasts (CAFs). Coculture of estrogen receptor positive (ER+) MCF7 cells with fibroblasts induces tamoxifen and fulvestrant resistance with 4.4 and 2.5-fold reductions, respectively, in apoptosis compared with homotypic MCF7 cell cultures. Treatment of MCF7 cells cultured alone with high-energy mitochondrial "fuels" (L-lactate or ketone bodies) is sufficient to confer tamoxifen resistance, mimicking the effects of coculture with fibroblasts...
November 15, 2011: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/21720999/individualizing-antimetabolic-treatment-strategies-for-head-and-neck-squamous-cell-carcinoma-based-on-tp53-mutational-status
#9
Vlad C Sandulache, Heath D Skinner, Thomas J Ow, Aijun Zhang, Xuefeng Xia, James M Luchak, Lee-Jun C Wong, Curtis R Pickering, Ge Zhou, Jeffrey N Myers
BACKGROUND: Mutations in the tumor protein 53 (TP53) tumor suppressor gene are common in head and neck squamous cell carcinoma (HNSCC) and correlate with radioresistance. Currently, there are no clinically available therapeutic approaches targeting p53 in HNSCC. In this report, the authors propose a strategy that uses TP53 mutational status to individualize antimetabolic strategies for the potentiation of radiation toxicity in HNSCC cells. METHODS: Glycolytic flux and mitochondrial respiration were evaluated in wild-type (wt) and mutant (mut) TP53 HNSCC cell lines...
February 1, 2012: Cancer
https://www.readbyqxmd.com/read/21655990/evidence-for-biological-effects-of-metformin-in-operable-breast-cancer-a-pre-operative-window-of-opportunity-randomized-trial
#10
RANDOMIZED CONTROLLED TRIAL
Sirwan Hadad, Takayuki Iwamoto, Lee Jordan, Colin Purdie, Susan Bray, Lee Baker, Gera Jellema, Steve Deharo, D Grahame Hardie, Lajos Pusztai, Stacy Moulder-Thompson, John A Dewar, Alastair M Thompson
Metformin may reduce the incidence of breast cancer and enhance response to neoadjuvant chemotherapy in diabetic women. This trial examined the effects of metformin on Ki67 and gene expression in primary breast cancer. Non-diabetic women with operable invasive breast cancer received pre-operative metformin. A pilot cohort of eight patients had core biopsy of the cancer at presentation, a week later (without treatment; internal control), then following metformin 500-mg o.d. for 1 week increased to 1-g b.d. for a further week continued to surgery...
August 2011: Breast Cancer Research and Treatment
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