Results 111 to 120 of about 7,503,880 (242)

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Molecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

DNA damage response and hematological malignancy [PDF]

International Journal of Hematology, 2017
DNA damage is a serious threat to cellular homeostasis. Damaged DNA leads to genomic instability, mutation, senescence, and/or cell death. DNA damage triggers a cellular response called the DNA damage response (DDR), followed by activation of the DNA repair machinery. DDR both maintains cellular homeostasis and prevents cancer development.
openaire   +3 more sources

The multiple roles of A-type lamins in cellular aging, cell cycle progression and the DNA damage response. [PDF]

, 2011
A-type lamins are a group of type V intermediate filaments whose main members are lamin A and C. Lamins A/C are components of the nuclear lamina and are encoded by the LMNA gene.
GIBBS-SEYMOUR, IAN,DAVID
core  

"Adaptive response" - some underlying mechanisms and open questions [PDF]

, 2008
Organisms are affected by different DNA damaging agents naturally present in the environment or released as a result of human activity. Many defense mechanisms have evolved in organisms to minimize genotoxic damage. One of them is induced radioresistance
Stephka G. Chankova, Dimova, Evgeniya G, Chankova, Stephka G, Peter E. Bryant, Bryant, Peter Edward, Evgeniya G. Dimova   +5 more
core   +1 more source

Transcriptional profiling of circulating extracellular vesicles from prebiopsy prostate cancer patients

Molecular Oncology, EarlyView.
RNA profiling of circulating extracellular vesicles (EVs) from blood samples of men undergoing prostate biopsy identifies transcripts associated with clinically significant prostate cancer. Integrative analysis with public tumor datasets links EV‐derived gene signatures to tumor stage and progression‐free survival, highlighting CASP3, XRCC2, and RIT1 ...
Stefan Werner, Pierre Tennstedt, Randi C. Pose, Christian Müller, Katharina Besler, Svenja Schneegans, Malik Alawi, Marie C. Roesch, Sven Peine, Desiree Bonci, Joanna Budna‐Tukan, Evi Lianidou, Catherine Alix‐Panabières, Derya Tilki, Klaus Pantel   +14 more
wiley   +1 more source

Human checkpoint proteins hRad9, hHus1, and hRad1 form a DNA damage-responsive complex [PDF]

, 2004
Human cells have evolved protective mechanisms such as DNA repair and cell cycle checkpoints in order to promote stability of the genome. Studies on hereditary instability syndromes associated with a higher incidence of malignancies like Xeroderma ...
Volkmer, Elias
core   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

Molecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder, Klaas de Lint, Hồ Mỹ Phúc Võ, Mariana M. Góis, Rosalie A. Kampen, Marta San Martin Alonso, Ilse Nootenboom, Veronica Garzero, Tiemen J. Wendel, Rob M. F. Wolthuis, Sylvie M. Noordermeer   +10 more
wiley   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

The involvement of single-stranded DNA, replication protein A, and the DNA double-strand break dose in the damage checkpoint of Saccharomyces cerevisiae. [PDF]

, 2007
In response to DNA damage, eukaryotic cells activate a checkpoint signalling cascade, resulting in cell cycle arrest, stabilisation of replication forks and activation of repair.
Zierhut, C.
core