Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

Genetic analysis of senataxin and RNase H2-deficient mice reveals that genome stability during class switch recombination and antibody generation can be uncoupled, suggesting a role for R loop metabolism dysfunction in lymphomagenesis in patients without immune deficiency.

Interaction with PUMILIO is essential for maintenance of genomic stability by the cytoplasmic long noncoding RNA NORAD, whereas binding to RBMX is dispensable for this function.

Genetic predisposition to uterine leiomyomas arises from variation at loci for genetic stability and genitourinary development, and in part explains the frequent occurrence of the condition in women with African origin.

Fifteen continuous high-grade serous ovarian carcinoma patient-derived organoids are characterized by transcriptomic, genomic, and drug sensitivity assays to reveal that they comprise communities of clonal populations and represent models of different causes of chromosomal instability and degrees of genome complexity.

When a protein involved in DNA repair malfunctions, it can anneal RNA molecules to DNA molecules, creating hybrids that increase the frequency of mutations in the DNA.

A new role for Endonuclease G with respect to the generation of mtDNA deletions is identified, which is dependent on the formation of G4 DNA within human mitochondria.

p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.

Genetic analysis combined with whole genome sequencing elucidates mechanisms and pathways that form and prevent a specific class of genome rearrangements, foldback inversions, seen in many human cancers.

Complex chromosomal rearrangements similar to those described in cancer and developmental syndromes occur in plants during postzygotic genome elimination, a centromeric-derived incompatibility.