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Results for “tumour escape”

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At least 19 recordsLinked to original sources

PubMed1977

Alterations of mononuclear phagocyte function induced by Lewis lung carcinoma in C57BL mice.

The function of the reticulo-endothelial system in mice bearing Lewis lung carcinomas has been measured by(1) the rate of clearance of carbon particles from the circulation in vivo and calculation of the phagocytic index K; (2) chemotactic locomotion of macrophages in vitro in the presence or absence of serum or tumour supernate. The ability of the bone marrow to develop macrophage colonies in vitro in the presence or absence of sera from tumour-bearing mice has also been tested. A clear depression of macrophage locomotion and macrophage colony formation in vitro was found in the presence of sera or tumour supernates from tumour-bearing mice as early as 24 to 72 h after tumour inoculation. Similarly, tumour-bearing mice showed marked depression of carbon clearance in tests repeated throughout the first 72 h after tumour inoculation. This early depression of macrophage function may be an important step in allowing escape of tumour cells from host resistance.

Animals↗

PubMed2025

Epigenetic orchestration of cancer-immune dynamics: mechanisms, technologies, and clinical advancements.

BACKGROUND: Epigenetic dysregulation plays a pivotal role in cancer immune evasion by orchestrating tumour antigen silencing, immune cell dysfunction, and the formation of an immunosuppressive microenvironment. By disrupting successive phases of the cancer-immunity cycle-from antigen presentation to T cell exhaustion-these aberrations facilitate immune escape and tumour progression, highlighting the need for targeted epigenetic intervention. AIM OF REVIEW: This review systematically dissects how epigenetic alterations impair anti-tumour immunity at each stage of the CI cycle. It not only integrates fragmented mechanistic evidence but also emphasizes underexplored crosstalk between specific epigenetic regulators and immune cell types. It further highlights emerging technologies-such as single-cell epigenomics, spatial multi-omics, and CRISPR-based screens-that are driving discovery of novel therapeutic targets and refining patient stratification. Key scientific concepts of review. We discuss how epigenetic interventions, alone or in combination with immunotherapies, can reinvigorate immune responses and overcome resistance to current treatments. A particular focus is given to how integrative high-resolution platforms are mapping immunoepigenetic landscapes, enabling mechanism-informed, precision immunotherapy strategies. By bridging epigenetic regulation with translational immuno-oncology, this review outlines a future where epigenetic reprogramming becomes central to overcoming immune evasion in cancer.

Humans↗

PubMed1975

Serum factors modifying cell mediated immunity to rat hepatoma d23 correlated with tumour growth.

Sera from rats bearing a progressively growing transplanted aminoazo-dye-induced hepatoma (hepatoma D23) have been examined for the presence of hepatoma D23-specfic antigen, antibody and immune complexes throughout the course of tumour growth. The levels of these factors have been correlated with the in vitro blocking and inhibition of cytotoxic lymph-node cells from immunized animals for cultured tumour cells. Sera from animals bearing small tumours (7-14 days after tumour implantation contain free tumour-specific antigen whilst immune complexes could not be detected. Although these sera were neither blocking nor inhibitory under the normal conditions of the test, when concentrated two and fourfold, inhibition but not blocking of lymph-node cell cytotoxicity could be detected. In comparison sera from animals bearing large tumours (24-28 days) blocked but did no inhibit in vitro lymph-node cell cytotoxicity and this correlates with the presence of tumour-specific immune complexes in antibody excess. Animals with intermediate-sized tumours had high levels of both blocking and inbibitory activity in the serum, these effects becoming apparent when neither free antibody nor free antigen could be detected. The relevance of these findings to the mechanism by which a growing tumour may escape specific cellular immune destruction is discussed.

Animals↗

PubMed1979

[Tumour immunology (author's transl)].

The anti-tumour immune mechanism as it operates in vivo and in vitro is reviewed. Tumour-specific antigens on the surface of the tumour cell induce cellular (lymphocytes, macrophages) and humoral (antibodies, mediators) reactions which are capable of destroying the tumour cell. The combined operation of these mechanisms is described in detail, e.g. opsonization of tumour cells, enhancement, escape mechanism, specific versus unspecific reactions, potentiation. Analyses of tumour-specific cell-mediated reactions gain more and more importance as attempts to influence the function and differentiation of individual cells become more and more successful.

Antibodies, Neoplasm↗

PubMed1978

[Topical immunochemical consideration of the structure of the tumour cell membrane (author's transl)].

Fundamental experiments and results in the elucidation of cell membrane structure are reviewed in detail. Special consideration is given to the topochemical organisation and immunochemistry of the glycolipids and glycoproteins that are integrated into the cell membrane, and which form a major component of the surface receptor mosaic. This, in turn, underlies a transmembrane, cytoskeletal control, a mechanism that can only be explained by the modern concept of a fluid membrane. The investigations discussed here provide an interpretation of the behaviour and properties of the membranes of the tumour cell, as observed in the effect of cell transformation on the topography of the plasma membrane, and during the cell cycle and cell growth. In this connection, the so-called tumour associated antigens are discussed fully and their biochemistry and immunology treated in detail. Concepts of tumour immunity and escape mechanisms are then elucidated and defined with the aid of model systems. Using examples, it is shown why the results of this fundamental research form a sound basis for the immunodiagnosis and therapy of tumours.

Animals↗

PubMed2026

Engineered Bacteriophages in Cancer Immunotherapy: Emerging Concepts and Potential Integration with CAR-T Cell Therapy.

Due to antigen heterogeneity, restricted immune cell trafficking and an immunosuppressive, nutrient-restricted tumour microenvironment, solid tumours remain resistant to modern immunotherapies. Engineered bacteriophages offer a modular framework to overcome these obstacles: programmable virus-like particles with scalable production. Through genome engineering, capsid decoration with mammalian cell-targeting ligands, or hybrid AAV/phage systems, engineered bacteriophages can display tumour-associated antigens, enhance receptor-mediated uptake and deliver therapeutic payloads such as cytokines, chemokines and suicide genes without naturally infecting mammalian cells. These features support their use as vaccine platforms, immunological adjuvants and targeted gene-delivery vehicles. These may enable more precise, tumour-localized therapeutic intervention. Phages can engage innate immune pathways, including TLR9, TLR3/7/8, cGAS-STING and AIM2, promoting dendritic cell maturation and inflammatory mediators that may convert immunologically "cold" tumours into inflamed microenvironments. Their multivalent antigen display enhances B- and T-cell priming, while cDC1-mediated cross-presentation supports cytotoxic CD8+ T-cell responses and immunological memory. In CAR-T therapy, engineered phages may improve tumour homing through chemokine modulation, support persistence through local cytokine delivery, reduce antigen escape by presenting multiple tumour epitopes, and limit T-cell exhaustion through dominant-negative receptor strategies or local checkpoint blockade. This review summarizes engineering approaches, delivery systems, manufacturing, biodistribution, dosing, and safety issues, including immunogenicity, pre-existing anti-phage antibodies and horizontal gene transfer. It also distinguishes therapeutic engineered phage particles from phage display technologies used for molecular discovery. Despite encouraging results integrating modified bacteriophages with CAR-T cell therapy, the evidence remains mostly preclinical, indicating both substantial translational prospects and crucial obstacles for future clinical development.

CAR-T cell therapy↗

PubMed2026

ChromCall: assigning chromatin status to defined genomic regions using epigenomic profiling data.

MOTIVATION: Chromatin regulation is crucial for modulating gene expression and cellular function by altering DNA accessibility. Defining and understanding chromatin regulation across diverse biological conditions, including health and disease, requires quantification of both the presence and enrichment level of diverse DNA-binding factors and chromatin modifications across defined genomic regions. Existing approaches mainly rely on peak-based or genome-wide models, which identify high-signal regions but do not annotate chromatin status at predefined functional genomic regions, such as promoters or enhancers. This lack of region-based annotation limits downstream comparative and integrative analyses across multiple factors and datasets, prompting us to create ChromCall. RESULTS: ChromCall is an R package for region-based chromatin enrichment analysis that provides a robust and extensible foundation for transparent and reproducible epigenomic profiling at predefined genomic regions. We applied ChromCall to ChIP-seq data from glioblastoma (GBM) brain tumours and found that the promoters of genes implicated in treatment resistance are significantly more likely to exhibit a combination of histone marks associated with phenotypic plasticity. This highlights a potential novel mechanism of therapeutic escape in these deadly tumours. AVAILABILITY AND IMPLEMENTATION: The R package is available on https://github.com/GliomaGenomics/ChromCall and the version used in this paper is archived at https://doi.org/10.5281/zenodo.19580967.

Chromatin↗

PubMedDate not supplied

The role of immunological factors in the treatment of cancer.

Evidence has accumulated in the last 15 years that many experimentally-induced tumours in animals carry a tumour-specific transplantation-type antigen (TSTA) in their plasma membrane and that the tumour-bearing host responds to the TSTAs with the production of antibodies and cytotoxic mononuclear cells. In man the situation is not yet clear but there are indications that a similar situation may apply in many human malignancies. These findings have led to a resurgence in interest in the role of immunotherapy in the treatment of malignant disease, but as yet there is no clear evidence from properly controlled clinical trials that immunotherapy is the treatment of choice for any tumour. At present clinical immunotherapy constitutes a field for careful investigation but it cannot be considered a proven modality of treatment. At present its use must be confined to controlled studies in which benefit or possible harm can be determined. When giving immunotherapy it is necessary to monitor carefully the specific immune reaction of the host against the tumour. Further progress in immunotherapy requires a better understanding of why tumour cells succeed in vivo to escape destruction by the immune responses of the host. This review summarizes the current state of knowledge concerning the nature of TSTAs, the effect of the immune response to TSTAs on metastatic spread and the mechanisms of escape with special reference to the role which circulating soluble TSTA plays in 'neutralizing' the action of cytotoxic cells and antibodies. It is stressed that there is no support for the hypothesis of a 'blocking antibody'. Finally the different types of immunotherapy which have been developed in animal systems are described and possible clinical applications are discussed.

Animals↗

PubMed2026

Cancer Immune Responsiveness and MHC Class I Antigen Presentation: Mechanisms of Immune Escape and Immunotherapy Resistance in Gastrointestinal Cancers.

The Antigen Processing and Presentation Machinery (APM) is essential for immune surveillance by enabling the presentation of antigenic peptides to T lymphocytes and facilitating the elimination of infected or transformed cells. In cancer, the integrity of this process influences cancer immune responsiveness (CIR), defined as a tumour's capacity to be recognised by the immune system and respond to immunotherapy. Tumours with intact antigen presentation pathways are more likely to generate effective antitumour responses, whereas APM defects promote immune escape and therapeutic resistance. Cancer cells frequently evade immune detection through altered antigen processing or reduced expression of major histocompatibility complex (MHC) class I molecules, limiting tumour antigen presentation to cytotoxic T lymphocytes. These alterations are increasingly recognised as determinants of response to immune checkpoint inhibitors and potential predictive biomarkers. APM defects may be reversible or irreversible. Interferon-mediated signalling can restore MHC class I expression and T-cell cytotoxicity in some tumours, whereas permanent genomic alterations affecting human leukocyte antigen (HLA) class I genes, β2-microglobulin (β2-m), or interferon-γ (IFN-γ) pathway components can severely impair antigen presentation. Emerging evidence highlights four mechanistic levels of APM perturbation: peptide generation, peptide loading, MHC class I integrity, and epigenetic regulation. Each contributes to distinct patterns of immune evasion. This review examines how MHC class I alterations influence CIR and contribute to immune evasion and immunotherapy resistance in gastrointestinal malignancies, while discussing therapeutic strategies to restore or bypass APM deficiencies.

Humans↗

PubMed1978

Influence of environmental factors excluding ultra violet radiation on the incidence of skin cancer.

Cancers of the skin are not properly registered and our lack of precise knowledge of the influence of environmental factors is due both to a failure to report and a failure to attribute because many tumours are not recognised as due to environmental factors and escape notification due to lack of knowledge and teaching. The long latent period also interferes. The commonest cancer is squamous cell carcinoma followed by basal cell carcinoma. Melanoma is exceedingly rarely environmental. The main causative agents are: Polycyclic aromatic hydrocarbons (PAH), inorganic arsenic and ionising radiation. PAH induce 4 times more cancer of the scrotum in workers using cutting oils or pitch than expected. These subjects have also increased incidence of second primaries of both the skin and internal organs. The latent period varies from 20 years (exposure to coal tar) to 50 years or more (exposure to mineral oils). Exposure to pitch may result in 11 fold increase incidence of squamous cell carcinoma. Skin cancer due to arsenic is rare. It has been seen in sheep dip workers, in patients treated with Fowler's solution and in vineyard workers using arsenical pesticides and drinking contaminated wine. The latent period may go up to 60 years. Ionising radiation over 1,000 rems may cause basal and squamous cell carcinoma. The latent period varies from 7 weeks to 56 years (average 25--30 yrs).

Arsenic↗

PubMed1978

[Comparative immunogenicity of irradiated and nonirradiated syngeneic and xenogeneic tumor cells containing a common specific transplantation antigen].

The authors compared the immunogenic activity for Syrian hamsters of native and irradiated syngeneic and xenogeneic tumour cells bearing on their surface common and SV40-specific transplantational antigen. The results obtained showed syngeneic tumour cells to be more immunogenic for the recipient than the xenogeneic tumour cells containing an antigen of the same specificity. Irradiation renders tumour cells, including the xenogeneic ones, more immunogenic, this possibly being associated with the capacity of nonirradiated cells to escape from immune recognition through their ability to divide.

Animals↗

PubMed1979

Trophoblast transferrin and transferrin receptors in the host--parasite relationship of human pregnancy.

Transferrin and specific transferrin receptors are demonstrated on the microvillous surface of syncytiotrophoblast in human immature and term placentae by immuno histological techniques with the use of light and electron microscopy. That the distribution of transferrin is limited to the materno-foetal interface supports the hypothesis that binding of maternal transferrin to trophoblast receptors is involved in the process of iron transport to the foetus. Parallel studies with baboon placentae demonstrate the presence of trophoblast receptors which bind both baboon and human transferrin, thereby putting forward an experimental model which might be used to test the biological significance of placental transferrin receptors in primates. In addition, investigation of a large number of human cell lines shows that many transformed cells, but no normal cells (such as blood lymphocytes) or cells from primary culture (such as neonatal foreskin fibroblasts), possess the ability to bind transferrin to their membranes. These findings suggest that transferrin receptors may play important biological roles in addition to that of iron transport from mother to foetus. One such role could be the limitation of iron in intervillous spaces, thus depriving iron-requiring microorganisms of iron, hence serving as a non-specific factor of resistance for placentae. Another role for foetal transferrin receptors on trophoblasts could be to bind maternal transferrin at the materno-foetal interface, thus frustrating maternal immunosurveillance. This is similar to a mechahism used by schistosomes in the host-parasite relation where host proteins are bound by the parasite to escape immunological recognition. The presence of transferrin receptors on transformed cells suggests that this mechanism might also be employed by tumour cells. Finally, in view of previous studies which show that transferrin is required by stimulated lymphocytes to pass from the G1 to the S phase of cellular replication, it is proposed that trophoblast transferrin receptors could limit the amount of transferrin in intervillous spaces and thus impede the proliferation and possible cytotoxicity of maternal activated lymphocytes at the materno-foetal interface.

Female↗

PubMed1979

The lipoxygenase of reticulocytes. Purification, characterization and biological dynamics of the lipoxygenase; its identity with the respiratory inhibitors of the reticulocyte.

A lipoxygenase has been purified from rabbit reticulocyte-rich anaemic blood cells. It possesses a molecular weight of 78 000 and an isoelectric point of 5.5 and contains 5% neutral sugars and two iron atoms per enzyme molecule. The lipoxygenase has proved to be identical with the inhibitors of respiratory proteins described formerly. The actions of the lipoxygenase on linoleic acid, phospholipids, mitochondrial and erythrocyte membranes and electron transfer particles were studied. A special feature of the reticulocyte lipoxygenase is the suicidal character of its action on lipids. With electron transfer particles the reticulocyte lipoxygenase causes a loss of acid-labile sulfur which accompanies respiratory inhibition; the strong respiratory inhibition is not exerted by soybean lipoxygenase. The reticulocyte lipoxygenase acts preferably on mitochondrial membranes as compared with cell membranes of the erythrocyte; erythrocyte cytosol moderates the action on mitochondrial membranes. Furthermore, the lipoxygenase reaction can concomitantly and irreversibly inactivate sulfhydryl enzymes as demonstrated with muscle glyceraldehyde-3-phosphate dehydrogenase. The occurrence of the lipoxygenase here described is restricted to reticulocytes; very low amounts were observed in bone marrow and no lipoxygenase was detectable in normal blood. During the course of an experimental anaemia the lipoxygenase is produced owing to superinduction in large amounts, which may persist for a long time since they escape inactivation. Preliminary evidence was obtained for the occurrence of other lipoxygenases in tissues of lung, spleen, kidney and also epithelial tumours.

Amino Acids↗

PubMed1977

Assay of immune cytolysis of lymphocytes and tumour cells by automatic determination of cell volume distribution.

Immune cytolysis (lysis) of cells due to the action of antibody in the presence of complement is usually substantiated by the uptake of vital dye by the cells, or by the escape of radiolabel from the cells. Immune cytolysis has now been assayed by determination of cell volume distribution with a Coulter multi-channel particle size analyser used in conjunction with a Coulter counter. For Ehrlich ascites and sarcoma-180 cells, volume degradation corresponding to vital staining was obtained only if trypsin (final concentration 625 microgram/ml) was added immediately after the usual 1 h incubation period for cells, antibody and complement. For L1210 leukaemia cells, trypsin was added at 0 degrees just 1 min before Coulter evaluation, to avoid potentiation of antibody-mediated cell lysis by trypsin. Immune cytolysis of mouse thymic, splenic and lymph node lymphocytes required addition of pronase (final concentration 625 microgram/ml) at 0 degrees for further disruption of antibody-damaged cells, prior to determination of cell volume distribution in the Coulter equipment. Scanning electron micrographs of L1210 cells undergoing immune cytolysis illustrated the changes in cell volume recorded by the Coulter apparatus. This new method for determination of immune cytolysis provides detailed information about the volume distribution of target cells, which permits detection of subtle changes and gives insight into the process of cytolysis. It is not intended to displace other procedures in routine use, except that complete automation of the present method is possible in future.

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↗

PubMed1975

Influence of geometry on control of cell growth.

The assembled evidence suggests that geometry plays an important role in regulation of cell growth, at least at two levels: (1) For non-transformed individual cells in culture, there may be a continuous range of shapes, from spherical all the way to extremely flat or extended, which correlates with increasing proliferative capacity or increasing ability to respond to serum growth factors. In other words, sensitivity to a variety of mitotic stimulators and growth factors may be modulated by cell conformation. Fully transformed cells appear to lose the modulating effect of shape, and thus are able to proliferate even when spherical. (2) For transformed cells which can grow in three-dimensional populations, the shape of the population itself eventually limits growth. The most likely mechanism is based upon the limiting effects of diffusion gradients of nutrients, oxygen and catabolites which build up across the surface of a three-dimensional population of cells. Tumor cells which are able to make tumour angiogenesis factor (TAF), induce new capillary blood vessels from the host. These vessels penetrate the tumor and permit further rapid growth. In this sense, tumor angiogenesis is a mechanism by which "successful" tumors escape the growth restriction imposed upon three-dimensional cell population by geometry [49].

Animals↗

PubMed1977

[Carcinoid heart disease secondary to a tumor of the small intestine. Apropos of a case with associated tricuspid and pulmonary insufficiency].

The authors report a case of carcinoid heart disease secondary to a tumour of the small bowel with liver metastases. There were severe lesions of the endocardium on the right side of the heart, with gross pulmonary and tricuspid incompetence. The left side of the heart did not escape but the fibrous plaques were limited to the papillary muscle of the mitral valve, and had no effect upon the haemodynamics. The pathogenesis of the strange cardiac lesion may be partly explained in terms of the toxicity to the endothelium of bradykinin. In spite of the serious nature of the valvular damage is it right to consider surgical correction, bearing in mind the fact that the prognosis of carcinoid syndrome is still very poor despite treatment?

Aged↗

PubMed1975

[The diagnosis of carcinoma of the breast in relation to growth rate (author's transl)].

The doubling time (DT) was estimated quantitatively for 16 carcinomas of the breast according to the method described by Collins and co-workers in 1956. This is based on the concept of constant and exponential growth. Observation interval for these mammographically confirmed tumors was between 83 and 1,034 days. The DT was calculated to vary from 45 to 260 days; in order to reach a diameter of 1 cm. after 30 divisions would require a period of 3.7 to 21.4 years. Mammography frequently demonstrates small, clinically occult, tumours. Axillary lymph node metastases are relatively rare from small tumours; growth rate of 70% of breast carcinomas in such that an annual clinical and radiological check-up will prove to be the best means of reducing mortality from carcinoma of the breast. The risk inherent in the radiation resulting from annual mammography is acceptable in women over 35 years. This leaves the problem of rapidly growing carcinomas which would escape early diagnosis by early examinations. Half-yearly examinations of women in high risk groups (1. Previous mastectomy for carcinoma, 2. Biopsy-proven mastopathy with atypical proliferation) comprising about 30% of carcinomas with a short doubling time would appear to be reasonable.

Adenocarcinoma↗