Oncology and Carcinogenesis

Oncology encompasses the study, diagnosis and treatment of neoplastic diseases, while carcinogenesis describes the multistep process by which normal cells acquire genetic and epigenetic alterations that endow them with malignant properties. Central hallmarks include sustained proliferative signalling, evasion of growth suppressors, resistance to cell death, replicative immortality, genomic instability, metabolic reprogramming and the capacity for invasion and metastasis. Carcinogens—chemical, physical or biological—can act as initiators by inducing DNA damage or as promoters by altering the tissue microenvironment or immune surveillance. Endogenous processes such as chronic inflammation, reactive oxygen species and replication errors further contribute to oncogenic transformation. Advances in molecular profiling have revealed key driver pathways—from mutant metabolic enzymes and epigenetic regulators to DNA‐repair defects and immune‐checkpoint circuits—informing targeted therapies and immunotherapies. Nevertheless, the interplay between tumour cell–intrinsic alterations and host factors continues to pose challenges for early detection, prevention and durable control of advanced disease.

Research from Nature Portfolio

Small‐molecule inhibitors of mutant isocitrate dehydrogenase (mIDH1) have achieved profound reductions in the oncometabolite 2‐hydroxyglutarate in low‐grade glioma, reversing DNA hypermethylation, attenuating stemness and proliferation programmes and triggering immune activation in the tumour microenvironment. One compound with superior brain penetrance has advanced to phase III trials. A first‐in‐class pan‐lysyl oxidase inhibitor remodels the desmoplastic stroma in pancreatic cancer, reducing collagen cross‐linking, matrix stiffness and metastatic spread, while enhancing gemcitabine delivery and efficacy. Loss of the tumour suppressor FAT1 has been shown to impair homologous recombination and promote both structural and numerical chromosomal instability via YAP1 dysregulation, linking Hippo signalling to genome doubling and intratumour heterogeneity.

Topic trend for the past 5 years

The graph below shows the article count in Nature Index journals for oncology and carcinogenesis.

Technical terms

Oncometabolite: A metabolite—such as 2‐hydroxyglutarate—whose accumulation perturbs epigenetic and metabolic programmes, driving oncogenesis.

Tumour microenvironment: The cellular (stromal, immune) and extracellular matrix components surrounding malignant cells that influence growth, invasion and therapy response.

Chromosomal instability (CIN): A rate of ongoing gains and losses of whole chromosomes or large segments, generating intratumour heterogeneity.

Replication stress: Impediments to normal DNA synthesis that slow or stall replication forks, leading to DNA damage and genomic instability.

Immune checkpoint: Regulatory pathways—such as PD-1/PD-L1—that modulate T-cell activity and can be co-opted by tumours to evade immune attack.

Desmoplasia: Fibrotic stromal remodelling characterised by collagen cross‐linking and increased matrix stiffness that can impede drug penetration.

Notable articles in oncology and carcinogenesis

1. Personalized RNA neoantigen vaccines stimulate T cells in pancreatic cancer. Nature (2023).
2. Genomic and Transcriptomic Features of Response to Anti-PD-1 Therapy in Metastatic Melanoma. Cell (2016).
3. Classification and mutation prediction from non–small cell lung cancer histopathology images using deep learning. Nature Medicine (2018).

Position of Oncology and Carcinogenesis in Nature Index by Count

Top 5 leading collaborators in Oncology and Carcinogenesis

Collaborating institutions