Cancer progression and therapeutic failure are increasingly understood as consequences of cancer cell plasticity—the capacity of malignant cells to reversibly transition between phenotypic and functional states in response to intrinsic cues and external stress. This Collection will focus on the cellular and molecular mechanisms that enable adaptive state switching, including therapy-induced tolerance, non-genetic resistance, and lineage reprogramming, as well as the tumor microenvironment and tumor ecology that shape these adaptive processes. Emphasis will be placed on dynamic and reversible processes that allow cancer cells to evade targeted, cytotoxic, or immune-based therapies through mechanisms that may occur independently of, precede, or cooperate with the acquisition of genetic resistance.

Contributions should prioritize mechanistic insight into how transcriptional, epigenetic, metabolic, and stress-response programs interact with microenvironmental cues—including hypoxia, inflammation, stromal signaling, nutrient availability, immune pressure, and therapy-induced niche remodeling—to generate adaptive cell states over time. Studies leveraging single-cell, lineage-tracing, spatially resolved, and longitudinal approaches are particularly welcome, as are integrative reviews that synthesize emerging frameworks for plasticity-driven disease progression and relapse. We also encourage submissions exploring therapeutic strategies to target plastic states, disrupt adaptive transitions, or exploit transient cellular vulnerabilities.

Potential topics of interest include (but are not limited to):

• Drug-tolerant persister cells and reversible resistance
• Lineage plasticity and cell fate reprogramming
• Epigenetic and transcriptional control of adaptive states
• Therapy-induced stress responses and survival programs
• Microenvironmental drivers of plasticity
• Immune evasion and immune-mediated selection of adaptive cell states
• Spatial and ecological determinants of cell-state transitions
• Single-cell, spatial, and lineage-tracing approaches to plasticity
• Therapeutic targeting of plastic states and adaptive vulnerabilities

This Collection supports and amplifies research related to SDG 3, Good Health and Well-Being.

All submissions in this collection undergo the journal’s standard peer review process. Similarly, all manuscripts authored by a Guest Editor(s) will be handled by the Editor(s)-in-Chief. As an open access publication, this journal levies an article processing fee (details here). We recognize that many key stakeholders may not have access to such resources and are committed to supporting participation in this issue wherever resources are a barrier. For more information about what support may be available, please visit OA funding and support, or email OAfundingpolicy@springernature.com or the Editor-in-Chief.

Survival of the fittest! Sadly this also applies to cancer cells. In the early phase of cancer, (epi)genetic mutations in initiated cells may be selected for their ability to exploit cell competition to eliminate neighboring less competent cells, thereby facilitating tumor expansion.

These tumor cells' competitive skills include but are not limited to the ability to live under hypoxia and acidic microenvironment, clonal expansion of cancer stem cells that contributes to tumor heterogeneity, as well as evading host immune cell surveillance. Interestingly, it has been recently shown that cell competition can also occur in later phases of cancer.

More importantly, cancer risk factors (such as unhealthy diet and chronic inflammation) could also produce variations of niche supplying the tumor and might dictate the outcome of cell competition in tumorigenesis.

It is anticipated that strategies pinpointing competitive cell interactions in various phases and microenvironments of cancers might help to suppress cancer initiation, expansion, and progression. In this collection, we welcome original articles focusing on tumor cell competition research.