Journal September 26, 2026 4 min read

How does genomic instability work?

Genomic instability is the increased tendency of a cell to acquire genetic alterations. This page outlines its formal definition, the pathways involved, and findings from laboratory and clinical research, including evide

peptides-pro Editorial

Genomic instability is the increased tendency of a cell to acquire genetic alterations, including mutations, chromosomal rearrangements, and aneuploidy. It is a hallmark of cancer and aging and is defined operationally as a failure to maintain genomic integrity. The term encompasses both numerical instability (changes in chromosome number) and structural instability (breaks, deletions, translocations). No single molecular formula or identifier applies; it is a cellular phenotype.

The work centres on the DNA damage response (DDR) pathway, a signalling network that detects DNA lesions and coordinates repair, cell-cycle arrest, and apoptosis. Key nodes include ATM, ATR, p53, and the PARP family.

Research Studies

NMNAT-1 and NAD+ homeostasis in neuroprotection and aging

Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) catalyses the final step in NAD+ biosynthesis and is the major nuclear isoform of the mammalian NMNAT family. NAD+ is a cofactor for redox reactions, DNA repair, chromatin regulation, and stress adaptation. Age-associated NAD+ decline has been implicated in brain aging and neurodegenerative disorders, but the causal node and limiting compartment differ across tissues and disease states. Direct human genetic evidence establishes NMNAT-1 as a causal gene in inherited re [1].

Pathogenesis of nonfamilial somatotroph adenomas

Somatotroph cells express cognate G protein-coupled receptors for hypothalamic stimulatory GH-releasing hormone (GHRH) and inhibitory somatostatin. Excess growth hormone production leading to acromegaly most commonly emanates from an adenomatous pituitary somatotroph. Understanding the pathogenesis of these adenomas will elucidate how biologic behavior affects acromegaly treatment outcomes [2].

Alpha Ketoglutarate Enhances Geroprotection In Surgery (AEGIS)

Coronary artery bypass grafting (CABG) is performed in approximately 400,000 patients in the United States each year. CABG invokes a massive surgical stress response, with systemic epinephrine increasing 33-fold and norepinephrine increasing 3-fold. Initially, local tissue injury results in a sterile inflammation, releasing damage-associated molecular patterns (DAMPs). DAMPs activate neutrophils, bringing a cascade of cytokines, complement, and coagulation changes. Activation of nociceptors results in a neurometabolic response involving the sympathetic nervous system and hypothalamus-pituitary axis [3].

Survival Analysis of Early Triple Negative Breast Cancer (TNBC) Women Treated With Dose Dense Sequential Adjuvant Chemotherapy

Breast cancer remains the most commonly occurring cancer and leading cause of cancer death in women worldwide. According to specific clinical, molecular and genetic characteristics of patients, breast cancer is distinguished into subtypes with differences in disease progression, response to treatment and rate of metastasis. Breast cancer treatment decisions are based mainly on the presence or absence of established prognostic and predictive biomarkers, mainly the estrogen (ER) and progesterone (PR) hormone receptors, the human epidermal growth factor receptor 2 (HER2) oncoprotein in correlation with ki67 proliferation index. Tumor size, histological grade, lymph node status are also used as [4].

Nicotinamide Adenine Dinucleotide and Its Anti-aging Effects in the Context of Longevity and Menopause

Menopause is a complex biological condition associated with progressive estrogen depletion and increased susceptibility to several age-associated disorders. During this process, several biological mechanisms, such as mitochondrial dysfunction, oxidative stress, chronic inflammation, genomic instability, and immunosenescence, are implicated [5].

Ovarian aging and systemic health: Mechanisms and emerging intervention strategies

Ovarian aging may contribute to systemic aging via the ovarian-systemic axis. This review outlines intrinsic ovarian cellular defects such as genomic instability, epigenetic shifts, and mitochondrial and proteostasis damage, which may trigger senescence-associated secretory phenotype (SASP)-related inflammaging, fibrosis, and other age-related pathologies [6].

Complosome as a key modulator of cellular senescence, aging and age-related diseases

Aging is characterized by progressive physiological decline and accumulation of senescent cells that drive chronic "inflammaging" through the senescence-associated secretory phenotype (SASP). The complement system, traditionally viewed as a systemic extracellular defense mechanism, is now recognized as an essential intracellular [7].

Senotherapeutic strategies for ovarian aging: Mechanistic insights and translational perspectives

Ovarian aging manifests as progressive depletion of the primordial follicle reserve and declining oocyte quality, culminating in menopause and associated systemic comorbidities. Cellular senescence emerges as a central driver of this process, exerting effects through cell-cycle arrest pathways and a proinflammatory sen [8].

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