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PubMed2026

Reframing early gastric carcinogenesis through lineage, niche, and evolution.

Early gastric cancer is still commonly conceptualized as the endpoint of a linear sequence from chronic gastritis to intestinal metaplasia, dysplasia, and invasion. Yet recent single-cell, spatial, genomic, and functional studies indicate that this model incompletely captures the biology of early gastric carcinogenesis. Malignant potential is established progressively within a precancerous gastric field already shaped by somatic evolution, chronic inflammatory injury, and epithelial lineage distortion. Within this field, progression is concentrated in a restricted set of precursor states, particularly incomplete, hybrid, and stem-like metaplastic populations that display plasticity, persistence, and increasing compatibility with a supportive microenvironment. Fibroblast niche remodeling, immune protection loss, endothelial rewiring, genomic instability, epigenetic drift, and selective retention of advantageous molecular alterations further promote malignant commitment. In parallel, diffuse gastric cancer appears to follow a distinct route that may arise independently of conventional intestinal metaplasia through E-cadherin-deficient epithelial transformation and downstream chromatin reprogramming. Here, we synthesize recent evidence to propose an updated framework for early gastric carcinogenesis based on field evolution, lineage instability, ecosystem support, and pathway divergence. Rather than replacing the classical Correa cascade, this framework seeks to refine it by shifting the unit of risk assessment from histologic stage alone to biologically defined precursor states shaped by lineage instability, clonal persistence, niche permissiveness, and pathway-specific molecular constraints. This perspective shifts the emphasis of prevention from detecting smaller cancers to identifying and intercepting biologically committed precursor states before invasion occurs.

Humans↗
PubMed1977

Immune status of mice tolerant of living cells. III. Presence and evolution of cells cytotoxic to the tolerated strain.

Spleen cells from CBA mice neonatally rendered highly tolerant to A/Jax (keeping a skin graft in perfect shape for more than 1 year and without detectable hemagglutinating or cytotoxic antibodies) contain cells cytotoxic for YAC 222 (A/Jax) in Cr release assay. The degree of the cytotoxicity depends on the age of the mouse, following a curve lower than, but parallel to, the one followed by the cytotoxicity of cells from CBA rendered immune by injecting them with A/Jax cells 1 week previously. The maximum of the cytotoxicity curve is reached during the 9th and 10th weeks. Normal CBA cells themselves are moderately cytotoxic to YAC 222. This "natural" cytotoxicity, significantly less intense and presumably directed against Moloney virus-related determinants, does not follow the same time pattern. The cytotoxic indices from both immune and tolerant cell populations are significantly reduced by CBA and anti-A/Jax immune serum. The tested sera of the tolerant mice did not contain hemagglutinating or in vitro-blocking antibodies in the Cr release assay (only the sera from unsuccessfully treated mice, having rejected their skin grafts, had some degree of blocking activity). However (and in agreement with previous experiments), these sera often contained synergistic hemagglutinins and in vivo enhancing properties of A/Jax tumors (Sal) grafted on CBA recipients.

Age Factors↗
PubMed2026

GATA2 deficiency: enhancer deregulation, immune surveillance failure, and clonal evolution.

Germline mutations in GATA2 cause a syndromic inborn error of immunity characterized by cytopenia, infections, immune dysregulation, and a marked predisposition to myelodysplastic syndrome and acute myeloid leukemia. Initially defined by the DCML phenotype-dendritic cell, monocyte, B- and NK-cell deficiency-GATA2 deficiency is now recognized as a disorder of global immune-hematopoietic homeostasis. Recent multi-omics and experimental models reveal enhancer-driven inflammatory rewiring, IRF8-dependent lineage imbalance, and premature hematopoietic aging. In parallel, adaptive immune defects, including impaired B- and T-cell development and function, contribute to defective immune surveillance. These alterations not only explain susceptibility to infection but also shape clonal evolution and malignant transformation. Clinically, improved risk stratification and transplant outcomes underscore the importance of early recognition and monitoring of immune dysfunction. GATA2 deficiency thus represents a paradigm linking immune dysregulation, inflammatory stress, and cancer predisposition.

Humans↗
PubMed1981

Study of two cases of ring 13 chromosome using high-resolution banding.

The chromosomes of two patients with ring 13 (r13) were studied using high-resolution RBG banding of prometaphase cells. The rings of the two patients differ slightly in breakpoints. Cell with multiple single, double-sized rings, quadruple-sized rings, rod- and ring-shaped fragments, and fragments showing varied states of condensation were seen, as were cells monosomic for chromosome 13. The evolution of these cell lines as a result of sister chromatid exchange, nondisjunction, ring breakage, and premature chromosome condensation is discussed. Clinical features of these patients reflect the heterogeneity of phenotype for r13 patients. Each case includes a feature of trisomy 13. The significance of mosaicism of cell lines in patients bearing ring chromosomes is considered with respect to variation in clinical findings.

Abnormalities, Multiple↗
PubMed1994

The evolution of echinoderm development is driven by several distinct factors.

We analyzed a comparative data base of gene expression, cell fate specification, and morphogenetic movements from several echinoderms to determine why developmental processes do and do not evolve. Mapping this comparative data onto explicit phylogenetic frameworks revealed three distinct evolutionary patterns. First, some evolutionary differences in development correlate well with larval ecology but not with adult morphology. These associations are probably not coincidental because similar developmental changes accompany similar ecological transformations on separate occasions. This suggests that larval ecology has been a potent influence on the evolution of early development in echinoderms. Second, a few changes in early development correlate with transformations in adult morphology. Because most such changes have occurred only once, however, it is difficult to distinguish chance associations from causal relationships. And third, some changes in development have no apparent phenotypic consequences and do not correlate with obvious features of either life history or morphology. This suggests that some evolutionary changes in development may evolve in a neutral or nearly neutral mode. Importantly, these hypotheses make specific predictions that can be tested with further comparative data and by experimental manipulations. Together, our phylogenetic analyses of comparative data suggest that at least three distinct evolutionary mechanisms have shaped early development in echinoderms.

Animals↗
PubMedDate not supplied

The effects of tumor sera on cell shape and photosynthesis of Euglena gracilis.

Cells of Euglena gracilis treated with human sera show a marked change in cell shape: Fully elongated cells have nearly totally been transformed to disk-shaped cells. This serum-mediated contraction is followed by irreversible cytolysis. Disintegration of chloroplast membranes leads to decreased photosynthetic O2 evolution. Sera from humans suffering from tumors reveal higher lytic activities than sera from individuals not suffering from tumors. Heating sera at 56 degrees C for 10 min or addition of EDTA destroyed or inhibited, respectively, the lytic activities completely. Polysaccharides transformed in polyanions by sulphatisation like dextransulphates or heparin seem to protect Euglena against serum activities. The effects described for human sera are believed to display the role of the complement pathway in the cytolysis of Euglena gracilis.

Animals↗
PubMed1992

Proteasomes: protein and gene structures.

Proteasomes are ring- or cylinder-shaped particles that have a sedimentation coefficient of 20S and are composed of a characteristic set of small polypeptides. These particles have a latent multicatalytic proteinase activity. Recently, proteasomes were found to combine reversibly with multiple protein components to form 26S proteolytic complexes that catalyze ATP-dependent, selective breakdown of proteins ligated with ubiquitin. This suggests that the 26S complexes are a new type of ATP-requiring protease in eukaryotic cells. We have studied the structures of various eukaryotic proteasomes at the molecular level by physicochemical and recombinant DNA techniques and have proposed that the gross structures of proteasomes, such as their size and shape, have been highly conserved during evolution. Proteasome subunits appear to be encoded by a family of homologous genes named the "proteasome gene family," which may have evolved from a common ancestral gene. Evidence obtained by genetic analyses in yeast and studies on the levels of proteasome expression in various eukaryotic cells indicates that proteasomes have essential roles in the cell. In this review, we summarize available information on the protein and gene structures of proteasomes and discuss the biological functions of proteasomes.

Amino Acid Sequence↗
PubMed2025

Pleiotropic mutational effects on function and stability constrain the antigenic evolution of influenza hemagglutinin.

The evolution of human influenza virus hemagglutinin (HA) involves simultaneous selection to acquire antigenic mutations that escape population immunity while preserving protein function and stability. Epistasis shapes this evolution, as an antigenic mutation that is deleterious in one genetic background may become tolerated in another. However, the extent to which epistasis can alleviate pleiotropic conflicts between immune escape and protein function/stability is unclear. Here, we measure how all amino acid mutations in the HA of a recent human H3N2 influenza strain affect its cell entry function, acid stability, and neutralization by human serum antibodies. We find that epistasis has entrenched certain mutations so that reverting to the ancestral amino acid identity in earlier strains is no longer tolerated. Epistasis has also enabled the emergence of antigenic mutations that were detrimental to HA's cell entry function in earlier strains. However, epistasis appears insufficient to overcome the pleiotropic costs of antigenic mutations that impair HA's stability, explaining why some mutations that strongly escape human antibodies never fix in nature. Our results refine our understanding of the mutational constraints that shape recent H3N2 influenza evolution: epistasis can enable antigenic change, but pleiotropic effects can restrict its trajectory.

Journal Article↗
PubMed1994

Modulation of cardiac myocyte phenotype in vitro by the composition and orientation of the extracellular matrix.

Cellular phenotype is the result of a dynamic interaction between a cell's intrinsic genetic program and the morphogenetic signals that serve to modulate the extent to which that program is expressed. In the present study we have examined how morphogenetic information might be stored in the extracellular matrix (ECM) and communicated to the neonatal heart cell (NHC) by the cardiac alpha 1 beta 1 integrin molecule. A thin film of type I collagen (T1C) was prepared with a defined orientation. This was achieved by applying T1C to the peripheral edge of a 100 mm culture dish. The T1C was then drawn across the surface of the dish in a continuous stroke with a sterile cell scraper and allowed to polymerize. When NHCs were cultured on this substrate, they spread, as a population, along a common axis in parallel with the gel lattice and expressed an in vivo-like phenotype. Individual NHCs displayed an elongated, rod-like shape and disclosed parallel arrays of myofibrils. These phenotypic characteristics were maintained for at least 4 weeks in primary culture. The evolution of this tissue-like organizational pattern was dependent upon specific interactions between the NHCs and the collagen-based matrix that were mediated by the cardiac alpha 1 beta 1 integrin complex. This conclusion was supported by a variety of experimental results. Altering the tertiary structure of the matrix or blocking the extracellular domains of either the cardiac alpha 1 or beta 1 integrin chain inhibited the expression of the tissue-like pattern of organization. Neither cell-to-cell contact or contractile function were necessary to induce the formation of the rod-like cell shape. However, beating activity was necessary for the assembly of a well-differentiated myofibrillar apparatus. These data suggest that the cardiac alpha 1 beta 1 integrin complex serves to detect and transduce phenotypic information stored within the tertiary structure of the surrounding matrix.

Animals↗
PubMed1989

The multicatalytic proteinase (prosome) is ubiquitous from eukaryotes to archaebacteria.

From the thermoacidophilic archaebacterium, Thermoplasma acidophilum, a proteolytically active particle has been isolated which is almost identical in size and shape with the multicatalytic proteinase (prosome) from rat. This result indicates that prosomes have been developed early in evolution and that they possibly serve functions common to all living cells.

Animals↗
PubMed1977

[Current findings on the asymmetric growth of the mullerian tract in female chick embryos].

Shape and orientation of the mesothelial cells were examined in the mullerian ducts of 8, 13 and 15 day female chick embryos with the scanning electron microscope. The observed evolution in the pattern of these cells likely reflects the mechanical conditions to which these organs are subjected during embryonic development: stretching for the left duct, slackening for the right duct. These observations, together with data concerning growth of these organs, suggest that topographical relationships between cells, which in this system result from mechanical factors, play an important role in controlling cell proliferation.

Animals↗
PubMedDate not supplied

Flagellar apparatus absolute orientations and the phylogeny of the green algae.

The absolute orientation of the flagellar apparatus in green algal motile cells is a feature of considerable value in studies of green algal systematics and phylogeny. The absolute orientation patterns found in those algae for which this feature is known or can be deduced are reviewed. Counterclockwise absolute orientation occurs in all classes except the Chlorophyceae and is considered primitive, while the clockwise absolute orientation present in most members of the Chlorophyceae is the result of progressive clockwise rotation of components during evolution. Extant intermediates documenting this rotation include Hafniomonas vegetative cells, which show counterclockwise absolute orientation, and Chaetopeltis quadriflagellate zoospores, in which the flagellar apparatus is strictly cruciate except for a slight clockwise offset of the microtubular rootlets. The V-shaped arrangement of the basal bodies in the flagellar apparatus, as well as the presence of proximal sheaths and of two layers of scales on the cell body, further identifies the Chaetopeltis zoospore as a primitive cell type within the Chlorophyceae . Trends towards the exsertion of basal bodies from a flagellar pit, either apically or laterally, the elimination of quadriflagellate cells, and, in the Chlorophyceae , an increasing amount of basal body offset, indicate advancement within the classes. Absolute orientation is conserved during flagellar apparatus replication and development. Events after flagellar apparatus division in the algae studied may be subdivided into component assembly, which is universal and preserves phylogenetically-useful features, and component reorientation, which occurs in relatively few green algae and adapts the flagellar apparatus to specialized functions. From these flagellar apparatus orientation studies, a major reevaluation of evolution within the Chlorophyceae is proposed, with weakly- thalloid algae possessing desmoschisis (e.g. Chaetopeltis ) considered primitive, and most other types, including the Volvocales , considered more advanced. The evolution of wall formation does not preclude the formation of scales in primitive chlorophycean genera. In addition, one or more previously undescribed major lineages may exist within the green algae, including one, the Pleurastrum lineage, whose members possess dorsiventrally -flattened motile cells, counterclockwise absolute orientation of the flagellar apparatus, and a phycoplast at cytokinesis. The Chlorophyceae , the Ulvophyceae , and the Pleurastrum lineage are considered to have a common ancestor that resembled the modern genus Pyramimonas , while the Charophyceae is thought to be of more ancient derivation. Th

Chlorophyta↗
PubMed1988

Stereological study of the early ultrastructural differentiation of chick embryo neuroepithelial cells during neurulation.

The neuroectodermal cells of chick embryos have been analyzed during neurulation by stereological and morphometrical ultrastructural methods in an attempt to describe their cytometric evolution. A profound change of cellular form coefficient was observed which is related to the typical process of columnarization of these cells. At stages 7 and 8, the nucleus appeared round in shape, probably due to a loss of pressure of the vitelline inclusions. In this sense, the volume density of these inclusions falls during this period. There was also a significant increase of the nuclear surface density, the significance of which is discussed on the basis of the nucleo-cytoplasmic interchanges and the differentiation process. At the same time, an increase in the number of mitochondria was observed, which is related to the neural folding process. Simultaneously, the amount of rough endoplasmic reticulum increases, presumably related to the remarkable changes of the embryonic extracellular matrix.

Animals↗
PubMed1992

Cone visual pigments are present in gecko rod cells.

The Tokay gecko (Gekko gekko), a nocturnal lizard, has two kinds of visual pigments, P467 and P521. In spite of the pure-rod morphology of the photoreceptor cells, the biochemical properties of P521 and P467 resemble those of iodopsin (the chicken red-sensitive cone visual pigment) and rhodopsin, respectively. We have found that the amino acid sequence of P521 deduced from the cDNA was very similar to that of iodopsin. In addition, P467 has the highest homology with the chicken green-sensitive cone visual pigment, although it also has a relatively high homology with rhodopsins. These results give additional strength to the transmutation theory of Walls [Walls, G. L. (1934) Am. J. Ophthalmol. 17, 892-915], who proposed that the rod-shaped photoreceptor cells of lizards have been derived from ancestral cone-like photoreceptors. Apparently amino acid sequences of visual pigments are less changeable than the morphology of the photoreceptor cells in the course of evolution.

Amino Acid Sequence↗
PubMed2026

Competing subclones and fitness diversity shape tumor evolution across cancer types.

MOTIVATION: Intratumor heterogeneity arises from ongoing somatic evolution and complicates cancer diagnosis, prognosis, and treatment. Reconstructing evolutionary dynamics typically requires spatiotemporal samples, which are often unavailable in clinical settings. Computational approaches that can infer tumor evolutionary history from single-timepoint bulk sequencing data remain limited. RESULTS: We present estimating evolutionary events through single-timepoint sequencing (TEATIME), a novel computational framework that models tumors as mixtures of two competing cell populations: an ancestral clone with baseline fitness and a derived subclone with elevated fitness. Using cross-sectional bulk sequencing data, TEATIME estimates mutation rates, timing of subclone emergence, relative fitness, and number of generations of growth. To quantify intratumor fitness asymmetries, we introduce a novel metric-fitness diversity-which captures the imbalance between competing cell populations and serves as a measure of functional intratumor heterogeneity. Applying TEATIME to 33 tumor types from The Cancer Genome Atlas, we revealed divergent as well as convergent evolutionary patterns. Notably, we found that immune-hot microenvironments constraint subclonal expansion and limit fitness diversity. Moreover, we detected temporal dependencies in mutation acquisition, where early driver mutations in ancestral clones epistatically shape the fitness landscape, predisposing specific subclones to selective advantages. These findings underscore the importance of intratumor competition and tumor-microenvironment interactions in shaping evolutionary trajectories, driving intratumor heterogeneity. Lastly, we demonstrate that TEATIME-derived evolutionary parameters and fitness diversity offer novel prognostic insights across multiple cancer types. AVAILABILITY AND IMPLEMENTATION: R implementation of TEATIME is available on GitHub (https://github.com/liliulab/TEATIME) and Zenodo (https://zenodo.org/records/17422174).

Neoplasms↗
PubMed1987

Effect of changes in neurofilament content on caliber of small axons: the beta,beta'-iminodipropionitrile model.

The structural role of neurofilaments in the normal axon and the consequences of altered axonal transport of neurofilaments have been extensively studied in large axons. These studies suggest that neurofilament numbers and interneurofilament spacing are major determinants of axonal cross-sectional area. In contrast, in small axons and dendrites, microtubules and membranous organelles appear to be the most closely correlated with size and shape of the cell process. In this study we have examined the effect of impairment in neurofilament transport on small axons, typical of most CNS pathways. Neurofilament transport was impaired by administration of beta,beta'-iminodipropionitrile (IDPN), resulting in proximal accumulation and distal depletion of neurofilaments. The evolution of these changes was studied in the optic nerves of guinea pigs treated with IDPN, 1-35 weeks following intoxication. The effect of this redistribution of neurofilaments on cross-sectional area of small axons was evaluated using quantitative ultrastructural methods. Our results show that with the alteration in neurofilament transport seen with IDPN intoxication, there is a wide spectrum of neurofilament densities, ranging from a 5-fold increase above normal in the proximal axon, to a 5-fold decrease below normal in the distal axon. Although the optic nerve fibers enlarge with the increase in neurofilament content, they do not atrophy significantly with the continued loss of neurofilaments. We conclude that factors other than neurofilament content are capable of maintaining size and shape of these small axons. Candidate organelles include microtubules and membranous organelles and possibly other axonal elements.

Animals↗
PubMed1995

Evolution and ultrastructure of the bovine spermatogonia precursor cell line.

The spermatogonial stem cell line in prepubertal and adult bovine testis was studied by electron microscopy and protein gene product 9.5 immunohistochemistry. Three successive spermatogonia precursor cell configurations were observed. Small basal stem cells were found to possess a spherical shape and nuclei with two to three nucleoli. They were observed in prepubertal testes (25 and 30 weeks) and in low numbers during all the stages of the seminiferous epithelial cycle in the adult. Aggregated spermatogonia precursor cells are the dominating germ cell type in the 25-week-old and 30-week-old calf. In the adult seminiferous epithelium, they cause expansion of the basal tubular compartment as they form dense groups containing up to 15 cells. These groups are observed concomitantly with cycling A-spermatogonia and preleptotenes at the beginning of spermatocytogenesis. At the end of A-spermatogonia propagation, the aggregated spermatogonia precursor cells separate and intermingle with cycling A-spermatogonia. The spermatogonia precursor cells can later be found together with I-spermatogonia as members of an interconnected cellular network of medium-sized cells. When the I-spermatogonia divide to form the smaller B-spermatogonia, the precursor cells, which stay connected with the cycling spermatogonial population, pass through a growth phase. They can now be considered as committed spermatogonia precursor cells and are continuously being transformed into A1-spermatogonia to start a new round of spermatocytogenesis. Ultrastructurally, all members of the precursor cell line are similar. However, a number of features have been found to show a quantitative increase (endoplasmic reticulum, mitochondria) or to exhibit a rising degree of complexity (nucleolus) during the progression from basal stem cells to committed spermatogonia precursor cells.

Animals↗