Results 71 to 80 of about 6,549,693 (278)

Translating whole‐genome doubling into precision medicine in cancer

Molecular Oncology, EarlyView.
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
wiley   +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

A cell cycle checkpoint for the endoplasmic reticulum

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2020
The generation of new cells is one of the most fundamental aspects of cell biology. Proper regulation of the cell cycle is critical for human health, as underscored by many diseases associated with errors in cell cycle regulation, including both cancer and hereditary diseases.
openaire   +4 more sources

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

Molecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

The atypical cyclin-like protein Spy1 overrides p53-mediated tumour suppression and promotes susceptibility to breast tumourigenesis

Breast Cancer Research, 2019
Background Breast cancer is the most common cancer to affect women and one of the leading causes of cancer-related deaths. Proper regulation of cell cycle checkpoints plays a critical role in preventing the accumulation of deleterious mutations ...
Bre-Anne Fifield, Ingrid Qemo, Evie Kirou, Robert D. Cardiff, Lisa Ann Porter   +4 more
doaj   +1 more source

Cisplatinum and Taxol Induce Different Patterns of p53 Phosphorylation

Neoplasia: An International Journal for Oncology Research, 2001
Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines.
Giovanna Damia, Laura Filiberti, Faina Vikhanskaya, Laura Carrassa, Yoichi Taya, Maurizio Dincalci, Massimo Broggini   +6 more
doaj   +1 more source

Pds5A and Pds5B Display Non-redundant Functions in Mitosis and Their Loss Triggers Chk1 Activation

Frontiers in Cell and Developmental Biology, 2020
BackgroundPds5 is an abundant HEAT-repeat-containing protein that binds to cohesin and mediates sister chromatid cohesion. In vertebrates, Pds5A and Pds5B are known to protect DNA replication fork, as their loss leads to DNA damage.
Naif Al-Jomah, Naif Al-Jomah, Lubinda Mukololo, Lubinda Mukololo, Awais Anjum, Awais Anjum, Mohammed Al Madadha, Mohammed Al Madadha, Raj Patel   +8 more
doaj   +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

Chelidonine and Homochelidonine Induce Cell Death through Cell Cycle Checkpoints and MAP Kinase Pathways

Natural Product Communications, 2017
This study focuses on the comparative in vitro cytotoxicity of chelidonine and homochelidonine on human cancer and non-cancer cells. Both alkaloids produced a decrease in cellular growth in a dose-dependent manner exhibiting greater potency in cancer ...
Radim Havelek, Martina Seifrtova, Karel Kralovec, Klara Habartova, Lucie Cahlikova, Martina Rezacova   +5 more
doaj   +1 more source

Oncogenic mutations produce similar phenotypes in Drosophila tissues of diverse origins

Biology Open, 2014
An emerging interest in oncology is to tailor treatment to particular cancer genotypes, i.e. oncogenic mutations present in the tumor, and not the tissue of cancer incidence.
Stefanie Stickel, Tin Tin Su
doaj   +1 more source