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At least 19 recordsLinked to original sources
PubMed2025

Cell fate specification modes shape transcriptome evolution in the highly conserved spiral cleavage.

Early animal development can be remarkably variable, influenced by lineage-specific reproductive strategies and adaptations. Yet, early embryogenesis is also strikingly conserved in certain groups, such as Spiralia. In this clade, a shared cleavage program (i.e., spiral cleavage) and similar cell lineages are ancestral to at least seven phyla. Why early development is so conserved in specific groups and plastic in others is not fully understood. Here, we investigated two annelid species (Owenia fusiformis and Capitella teleta) with spiral cleavage but different modes of specifying their primary progenitor cells. By generating high-resolution transcriptomic time courses from the oocyte to gastrulation, we demonstrate that transcriptional dynamics differ markedly between these species during spiral cleavage and instead reflect their distinct timings of embryonic organiser specification. However, the end of cleavage and gastrulation exhibit high transcriptomic similarity, when orthologous transcription factors share gene expression domains, suggesting this period is a previously overlooked mid-developmental transition in annelid embryogenesis. Together, our data reveal hidden transcriptomic plasticity during spiral cleavage, indicating an evolutionary decoupling of morphological and transcriptomic conservation during early embryogenesis.

Animals↗
PubMed2026

Viral mimicry escape as a necessary feature of malignant transformation.

Malignant transformation is driven by disruption of pathways regulating proliferation and cell fate, but these same disruptions can create a collateral vulnerability: loss of transcriptional and epigenetic control over transposable elements and other normally silenced genomic regions. Consequently, emerging cancer cells can accumulate transposable element-derived and other endogenous immunogenic nucleic acids capable of triggering antiviral responses, a process termed viral mimicry. Increasing evidence indicates that viral mimicry can eliminate precancerous cells and shape tumour evolution, positioning it as an intrinsic tumour-suppressive mechanism. Here we highlight how cancer-associated changes in DNA methylation, histone modifications, splicing and RNA processing can lead to the presence of immunogenic nucleic acids that can activate viral mimicry pathways. We outline how cancer cells suppress viral mimicry, including compensatory epigenetic repression, RNA editing, nucleic acid decay and dampening of interferon signalling to enable cancer cell growth. Finally, we highlight the evidence suggesting that escaping viral mimicry is a fundamental process for cancer initiation and progression, and suggest that viral mimicry escape is necessary for cancer transformation and a therapeutic target in combination with immunotherapies. By framing viral mimicry escape as a necessary part of cancer transformation, this Review provides a unifying conceptual model for its translational exploitation.

Journal Article↗
PubMed1978

The nature of macrophages (foam cells) in neurinomas. Tissue culture study.

Fourteen cases of neurinomas of variable location are studied by tissue culture technic in an attempt to typify the foam cells as primary or superimposed elements in the tumor population. Our results demonstrate that the "in vitro" behavior of the neurinomas is constant and characteristic and that three cell types are found in them: fusiform, star-shaped cells and macrophages. There appears that the macrophage is an evolutive aspect of the star-shaped cells and probably of the fusiform one. On this basis, macrophage and foam cells of neurinomas must be considered as primary.

Adult↗
PubMed2026

Tumor evolution shapes metastatic competence in colorectal cancer.

In this issue of Cancer Cell, Manca et al. investigate the genomic evolution and metastatic tropism of over 7,000 colorectal cancers. Integrating primary tumor location, genomic alterations, and clinical variables, they reveal how distinct patterns of tumor evolution shape metastatic competence and impact organ tropism, offering a framework to refine surveillance.

Humans↗
PubMed2025

Molecular signature of primate astrocytes reveals pathways and regulatory changes contributing to human brain evolution.

Astrocytes contribute to the development and regulation of the higher-level functions of the brain, the critical targets of evolution. However, how astrocytes evolve in primates is unsettled. Here, we obtain human, chimpanzee, and macaque induced pluripotent stem-cell-derived astrocytes (iAstrocytes). Human iAstrocytes are bigger and more complex than the non-human primate iAstrocytes. We identify new loci contributing to the increased human astrocyte. We show that genes and pathways implicated in long-range intercellular signaling are activated in the human iAstrocytes and partake in controlling iAstrocyte complexity. Genes downregulated in human iAstrocytes frequently relate to neurological disorders and were decreased in adult brain samples. Through regulome analysis and machine learning, we uncover that functional activation of enhancers coincides with a previously unappreciated, pervasive gain of "stripe" transcription factor binding sites. Altogether, we reveal the transcriptomic signature of primate astrocyte evolution and a mechanism driving the acquisition of the regulatory potential of enhancers.

Astrocytes↗
PubMed2026

From wild to domestic: Single-cell transcriptomic perspectives on hippocampal regulation and evolution.

How domestication shapes brain evolution remains an open question. In this study, we integrated single-nucleus RNA sequencing (snRNA-seq), population genomics, and machine learning to investigate the hippocampal evolution under domestication. Across-species comparisons revealed that hippocampal cell type profiles are largely conserved across vertebrate species, while supporting the presence of adult hippocampal neurogenesis in birds. We further found that domestication and selective breeding likely influence the cellular composition and molecular regulation of the hippocampus. Our findings provide cellular evidence supporting the hypothesis that domestication affects adult hippocampal neurogenesis. Additionally, we showed that genes associated with neural progenitor cells (NPC) states and cell-marker programs are enriched for signatures of selection. Many of these genes function as regulators of neurogenesis and pathways mediating stress and fear reduction. Specifically, we identified selection at the FKBP5 promoter that may influence its expression in the NPC lineage, potentially contributing to stress-response regulation during domestication. Collectively, these results suggest that domestication is associated with hippocampal remodeling as part of an adaptive response to human-managed environments. This study provides a cellular and genetic perspective on how domestication reshapes the brain and offers a basis for further investigation into the mechanisms of neural evolution within the context of microevolution.

Animals↗
PubMed1995

Cell expansion and growth arrest phases during the transition from precursor (CD4-8-) to immature (CD4+8+) thymocytes in normal and genetically modified mice.

T cell early precursors belong to the CD3-CD4-CD8- triple negative (TN) thymocyte population that can be subdivided on the basis of CD44, CD25, and heat-stable Ag (HSA) expression. The kinetics and precursor product relationships of these subsets, as well as of the CD4/8low intermediates, were studied by using pulse labeling with bromodeoxyuridine (BrdUrd). The highest frequencies of DNA-synthesizing cells were found in CD44+CD25+ and CD44-CD25low or CD25- subsets. The major TN cell type (CD44-CD25high), as well as CD44+ CD25-HSAlow early precursors, contained a majority of resting cells. RAG-2-/- mice contained less cells in DNA synthesis than normal mice, and CD44-CD25-/low cells were absent. In female mice transgenic for the anti-HYTCR, CD44-CD25high cells were almost all cycling, but a high percentage of resting cells was found in CD44-CD25- cells. In days following the BrdUrd pulse, there was a reduction in the number of BrdUrd+ cells in most subsets, with the exception of the labeled CD44-CD25high cells that showed a bell-shaped curve. The kinetics and cell size evolution suggest that the majority of these cells do not give rise to CD4+CD8+ cells. In RAG-2-/- cells, the block at the CD44-CD25high stage involved all cells. In TCR transgenic (Tg) mice, no block was seen at the CD44-CD25high stage, suggesting that early expression of a complete TCR receptor precludes the normal selection step. However, another block in the differentiation process was observed at the CD44-CD25- step in TCR Tg mice, suggesting an additional selection point.

Animals↗
PubMed2026

A single-cell lens into the co-evolution of genotypes and phenotypes in cancer.

Genetic heterogeneity and clonal outgrowths are observed even in otherwise healthy human tissues, shaping the genetic composition of cell populations in non-malignant disease and during physiological ageing. This clonal mosaicism likely provides the pre-cancerous seeds for malignant transformation. Once a tumour arises, clonal evolution poses a major challenge to achieving cure, as clonal diversification provides an expanded number of substrates upon which therapy can act as a selective pressure, leading to the selection of resistant clones that ultimately fuel disease recurrence. Understanding somatic clonal evolution requires not only mapping genetic diversity but also defining the resulting phenotypes that provide a fitness advantage to mutated clones. This Review discusses multimodal single-cell technologies that enable the measurement of genotypes and additional molecular features from the same cell. These technologies unveil mutant-specific phenotypic traits, often show cell-state specificity in genotype-phenotype effects and can define therapeutic vulnerabilities for precision elimination of disease-propagating mutant cells. Furthermore, the combination of phylogenetic reconstruction with phenotypic measurements allows for the temporal mapping of clonal evolution and phenotypic plasticity. These breakthroughs have created a unique opportunity to define, directly in primary human samples, the mechanisms underlying clonal expansion in both healthy and malignant tissues.

Journal Article↗
PubMed2026

Stress-driven strategic games in cancer.

Tumor cells face chronic genotoxic, metabolic, hypoxic, and immune stress that shapes their evolution. While stress-response molecular pathways are well characterized, cancer biology lacks a predictive framework for how cells select among alternative adaptive strategies and how these selections interact to produce tumor-level behavior. We propose that evolutionary game theory, previously applied to cooperation in cancer, should be extended to position stress adaptation itself as the organizing principle of tumor evolution. In this framework, stress-adaptive strategies constitute frequency-dependent games whose payoffs depend on population composition. We introduce a three-level distinction between cell states (transcriptional snapshots), game states (local configurations of stress and neighbor composition that define the active payoff structure), and cell strategies (conditional behavioral policies mapping game states to fitness-relevant outputs). This perspective explains the maintenance of intratumor heterogeneity through frequency-dependent selection, the reversibility of resistance through bet-hedging dynamics, and therapy resistance as an equilibrium outcome rather than genetic inevitability. Integrating insights from single-cell genomics, spatial profiling, and lineage tracing, we outline testable predictions and experimental approaches for measuring payoff structures. Therapeutically, the framework suggests exploiting adaptive trade-offs, restricting phenotypic plasticity, and reshaping competitive landscapes. Re-framing cancer as an evolving game of stress adaptation provides a unifying structure for predictive oncology.

Animals↗
PubMed1987

Kaposi's sarcoma in AIDS. Multicentric angioneoplasia in early skin lesions.

Light-microscopic, immunohistochemical, and ultrastructural studies were performed on biopsy material from 15 young homosexual men with AIDS-associated mucocutaneous Kaposi's sarcoma; 19 Kaposi's sarcoma lesions in different developmental stages were investigated. These lesions showed multicentrically arising and proliferating vascular endothelia forming thick-walled and thin-walled capillaries and larger vessels, as well as spindle-shaped cells forming fascicles and bundles around them. Different amounts and organization of these two major cellular components were found in all stages of evolution of Kaposi's sarcoma lesions. Immunohistochemical and electron-microscopic techniques suggested that the spindle-shaped cells were of pericyte origin in different stages of maturation or, more rarely, lymphatic endotheliocytes. The skin lesions of AIDS-associated Kaposi's sarcoma occurred as a result of multicentric angioneoplasia of rather slow progression, together with the proliferation of pericyte-like mesenchymal cells, possibly representing a stromal reaction to the vascular proliferation. Both blood and lymphatic vessels seemed involved in this process. In early stages, scattered lymphocytic infiltration was an additional feature. Mitotic figures and cytologic atypia were not seen more frequently in early AIDS-associated Kaposi's sarcoma than in proliferating granulation tissue.

Acquired Immunodeficiency Syndrome↗
PubMed2026

A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.

INTRODUCTION: Cancer cell proliferation occurs within the context of persistent genomic instability. In this review, we propose the RS-CCD-CIN axis as a systems-level framework in which replication stress (RS), cell cycle deregulation (CCD) and chromosomal instability (CIN) form an interdependent triad that shapes tumour evolution. This axis represents a constrained metastable state in which genomic instability is tolerated and buffered. The objective of this review is to synthesize the current understanding of how the RS-CCD-CIN axis contributes to tumour heterogeneity, adaptability and therapy response. DISCUSSION: Evidence indicates that RS, CCD and CIN operate as a dynamic, interconnected network rather than as independent processes. Replication stress induces DNA damage and mutagenesis, while partial checkpoint disruption permits cells with unresolved lesions to proliferate. Chromosomal instability generates both structural and numerical alterations, contributing to intratumoural heterogeneity. Together, these processes facilitate adaptation to environmental and therapeutic pressures. Extrachromosomal DNA, micronuclei formation and cytosolic DNA signalling, including the cGAS-STING pathway, connect genomic instability to adaptive responses and immune modulation. Single-cell and spatial profiling reveal temporal and spatial variability in RS, CCD and CIN states, highlighting the limitations of static biomarkers. Therapeutically, targeting individual components often yields limited durability, whereas approaches that simultaneously perturb multiple aspects of the RS-CCD-CIN axis may improve clinical outcomes. CONCLUSIONS: This review highlights the RS-CCD-CIN axis as a fragile and metastable architecture that supports cancer evolution, while also being susceptible to collapse. A deeper understanding of this interconnected framework may inform the development of therapeutic strategies and enhance the management of resistance.

Humans↗
PubMed1979

[Study of uveal malignant melanoma with the electron microscope (author's transl)].

Twelve cases of uveal malignant melanoma, including the principal histologic types of this neoplasm according to Callender, were studied with the electron microscope. Nuclear inclusions were observed in each case, more frequently in epithelioid cells: they were probably correlated with nuclear hyperactivity. Melanogenesis in neoplastic cells was sometimes abnormal because of the granular structure of the premelanosomes, of the difference in size and in shape melanosomes, of the difference in size and in shape of the pigment granules and of the different stage of evolution of the premelanosomes in the cell. The size and the degree of reticulation of nucleoli and the number of free ribosomes and mitochondria increased from spindle A, to spindle B and epithelioid cells. This behaviour probably depends on an increasing metabolic activity which is related to the increasing degree of malignancy.

Adult↗
PubMed2026

Telomere Crisis Shapes Cancer Evolution.

Somatic mutations arise in normal tissues and precursor lesions, often targeting cancer-driver genes involved in cell cycle regulation. Most checkpoint-mutant clones, however, remain dormant throughout an individual's lifetime and seldom progress to malignancy, implying the presence of protective mechanisms that limit their expansion and malignant transformation. One such safeguard is telomere crisis-a potent tumor-suppressive barrier that eliminates cells lacking functional checkpoints and evading p53- and pRb-mediated surveillance. While the genomic instability unleashed during telomere crisis can drive clonal evolution, cell death is typically the dominant outcome, with only a rare subset of cells escaping elimination to initiate malignancy. Recognizing the dual role of telomere crisis-suppressing tumor initiation while enabling clonal evolution-is essential for understanding early cancer development and designing strategies to eliminate tumor-initiating cells.

Neoplasms↗
PubMed1983

Calcium, microfilaments and morphogenesis.

Morphogenesis, the generation of tissue form, is important not only in the embryogenesis of a new individual, but also because a change in morphogenesis may be involved in the establishment of differences between individuals during evolution. Morphogenetic movements are effected in part by coordinated changes in the shapes of individual cells and over the past decade the cellular organelles responsible for cell shape have been identified as microfilaments and microtubules. In non-embryonic systems the contraction of microfilaments is controlled by the level of intracellular free calcium, and so calcium is implicated as an intermediate control mechanism in morphogenisis. Through techniques which perturb the calcium balance of cells, or which measure calcium ion concentration directly, evidence is accumulating that calcium is involved in morphogenetic movements such as gastrulation and neurulation, and related phenomena such as wound healing. Thus fundamental questions about the control of morphogenesis in embryogenesis and evolution may now be couched in more precise terms of the control of intracellular calcium ion balance.

Animals↗
PubMed1990

[The development of the tongue in the chick embryo: observation under a scanning electron microscope].

The morphological features of the chick embryo tongue from the 8th day of incubation till hatching and during the early post incubation period have been investigated by means of Scanning Electron Microscope. At the SEM, it is possible to observe that already at the 8th day of incubation, the body and the root are separated by a low smooth-surfaced ridge. In the following days this ridge develops, giving rise to the so-called lingual spines, whose significance is still uncertain. As concerns the evolutive pattern of the superficial layer of the epithelium, in the first days of the considered incubation period the cells appear dome-shaped and have microvilli on their apical surface; afterwards they tend to become more flattened, and the microvilli are replaced by a thick net of microplicae. In the last days of incubation and after hatching desquamative phenomena become evident. The above described evolutive process can be regarded as a common feature of the whole dorsal lingual surface; only few regional differences are to be noted, such as the earlier development of the microplicae on the apex and borders of the tongue. In particular, the microplicae observed at the apex of the tongue show a typical aspect and arrangement; they run regularly parallel to each other. On the lingual dorsal surface taste bud-like structures have never been observed.

Animals↗
PubMed1980

Evaluation of the role of diacyglycerol in calcium-induced erythrocyte shape change and rigidity.

The intrusion of micromolar amounts of calcium into the calcium-poor interior of the human erythrocyte initiates a series of cataclysmic changes in cellular metabolism and morphology. These include (1) cellular shrinkage (elevated mean cell hemoglobin concentration), (2) loss of water and potassium, (3) rapid and near-total hydrolysis of intracellular ATP, (4) conversion of cell shape from biconcave disc to echinocyte and spheroechinocyte, (5) greatly diminished cellular deformability and elasticity, and (6) the accumulation of DAG. It has been suggested that this latter of phenomenon may account for the changes in cell shape and, perhaps, membrane viscoelastic properties. In the present study we have tested the hypothesis that DAG accumulation is important in the evolution of calcium-induced erythrocyte damage. Our results indicate that (1) calcium-loaded lamb erythrocytes become misshapen and inelastic but do not produce detectable DAG; (2) human red cells suspended in potassium-rich buffer do accumulate DAG after exposure to calcium and A23187 but do not become echinocytic or inflexible; (3) human erythrocytes artificially loaded with DAG are morphologically and elastically normal; and (4) human erythrocytes which have "naturally" accumulated DAG after prolonged incubation in the presence of calcium will retain this DAG after energy repletion. Despite marked elevations of DAG, these cells resume normal morphology and deformability. In aggregate, our data fail to support any direct role for DAG accumulation in the occurrence of calcium-induced damage to human erythrocytes.

Adenosine Triphosphate↗