Ovarian cancer

Article
26 October 2022 | Open Access

Single-cell genomic variation induced by mutational processes in cancer

Single-cell whole-genome sequencing shows that 'foreground' cell-to-cell structural variation and alterations in copy number are associated with genomic diversity and evolution in triple-negative breast and high-grade serous ovarian cancers.

Tyler Funnell
, Ciara H. O’Flanagan
& Samuel Aparicio

Article
03 February 2021 | Open Access

IgA transcytosis and antigen recognition govern ovarian cancer immunity

In patients with high-grade serous ovarian cancer, robust and protective humoral responses are dominated by B-cell-derived polyclonal IgA that binds to polymeric IgA receptors that are universally expressed on ovarian cancer cells.

Subir Biswas
, Gunjan Mandal
& Jose R. Conejo-Garcia

Letter | 01 May 2019

Proteomics reveals NNMT as a master metabolic regulator of cancer-associated fibroblasts

The authors find that stromal methyltransferase nicotinamide N-methyltransferase (NNMT) regulates the transition of normal fibroblasts to cancer-associated fibroblasts through histone methylation and promotes ovarian cancer growth and metastasis.

Mark A. Eckert
, Fabian Coscia
& Ernst Lengyel

Article | 27 May 2015

Whole–genome characterization of chemoresistant ovarian cancer

Whole-genome sequencing of tumour and germline DNA samples from 92 patients with high-grade serous ovarian cancer identifies frequent gene breakages that inactivate the tumour suppressors RB1, NF1, RAD51B and PTEN, and contribute to chemotherapy resistance; acquired resistance was associated with diverse mechanisms such as reversions of germline BRCA1/2 mutations and overexpression of the drug efflux pump MDR1.

Ann-Marie Patch
, Elizabeth L. Christie
& David D. L. Bowtell

Letter | 04 September 2013

HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis

Interstrand crosslink (ICL) repair involves proteins whose mutation results in the disorder Fanconi anaemia: here gene knockdown studies in mice show that the absence of HELQ, a protein previously implicated in ICL repair, compromises germ cell development and results in tumour predisposition due to defective recombination at damaged replication forks.

Carrie A. Adelman
, Rafal L. Lolo
& Simon J. Boulton

Letter | 06 March 2013

Ovarian surface epithelium at the junction area contains a cancer-prone stem cell niche

The hilum (a transitional region) of the mouse ovary is identified as a stem cell niche of the ovarian surface epithelium, and its cells are prone to malignant transformation after inactivation of common tumour suppressor genes, suggesting that they may be the origin of ovarian carcinoma.

Andrea Flesken-Nikitin
, Chang-Il Hwang
& Alexander Yu. Nikitin

Letter | 16 December 2012

Mosaic PPM1D mutations are associated with predisposition to breast and ovarian cancer

Rare truncating mutations in the p53-inducible protein phosphatase PPM1D are shown to be associated with predisposition to breast cancer and ovarian cancer; notably, all of the mutations are mosaic in white blood cells but are not present in tumours, and probably have a gain-of-function effect.