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Results for “Cancer immunosurveillance”

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13 recordsLinked to original sources
PubMed1977

Immunosurveillance and cancer: epidemiologic observations.

To evaluate the immunologic surveillance theory of cancer, we reviewed the epidemiologic observations that have been made on cancer risk among population groups with immune deficiency. Lymphoproliferative neoplasms predominate in various groups, most notably renal transplant recipients treated with immunosuppressive agents and patients with primary immunodeficiency syndromes. In some immune disorders, specific forms of nonlymphoid neoplasia seem to occur excessively, although the patterns are not clear-cut or consistent. The available epidemiologic evidence fails to support the concept that immunosurveillance mechanisms are generally involved in carcinogenesis but does provide clues to immunologic processes that may predispose to particular neoplasms.

Adult↗
PubMed2015

Patrolling monocytes control tumor metastasis to the lung.

The immune system plays an important role in regulating tumor growth and metastasis. Classical monocytes promote tumorigenesis and cancer metastasis, but how nonclassical "patrolling" monocytes (PMo) interact with tumors is unknown. Here we show that PMo are enriched in the microvasculature of the lung and reduce tumor metastasis to lung in multiple mouse metastatic tumor models. Nr4a1-deficient mice, which specifically lack PMo, showed increased lung metastasis in vivo. Transfer of Nr4a1-proficient PMo into Nr4a1-deficient mice prevented tumor invasion in the lung. PMo established early interactions with metastasizing tumor cells, scavenged tumor material from the lung vasculature, and promoted natural killer cell recruitment and activation. Thus, PMo contribute to cancer immunosurveillance and may be targets for cancer immunotherapy.

Animals↗
PubMed2025

N6-methyladenosine RNA base modification regulates NKG2D-dependent and cytotoxic genes expression in natural killer cells.

BACKGROUND: Breast cancer (BC) is the most commonly diagnosed cancer in women. N6-methyladenosine (m6A) is the most prevalent internal modification in mammalian mRNAs and plays a crucial role in various biological processes. However, its function in Natural killer (NK) cells in BC remains unclear. NK cells are essential for cancer immunosurveillance. This study aims to assess m6A levels in transcripts involved in the NKG2D cytotoxicity signaling pathway in NK cells of BC patients compared to controls and find out its impact on mRNA levels. Additionally, it evaluates how deliberately altering m6A levels in NK cells affects mRNA and protein expression of NKG2D pathway genes and NK cell functionality. METHODS: m6A methylation in transcripts of NKG2D-pathway-related genes in BC patients and controls was determined using methylated RNA immunoprecipitation-reverse transcription-PCR (MERIP-RT-PCR). To deliberately alter m6A levels in primary cultured human NK cells, the m6A demethylases, FTO and ALKBH5, were knocked out using the CRISPR-CAS9 system, and FTO was inhibited using Meclofenamic acid (MA). The impact of m6A alteration on corresponding mRNA and protein levels was assessed using RT-qPCR and Western blot analysis or flow cytometry, respectively. Additionally, NK cell functionality was evaluated through degranulation and 51Cr release cytotoxicity assays. RESULTS: Transcripts of NKG2D, an activating receptor that detects stressed non-self tumour cells, had significantly higher m6A levels in the 3' untranslated region (3'UTR) accompanied by a marked reduction in their corresponding mRNA levels in BC patients compared to controls. Conversely, transcripts of ERK2 and PRF1 exhibited significantly lower m6A levels escorted with higher mRNA expression in BC patients relative to controls. The mRNA levels of PI3K, PAK1 and GZMH were also significantly elevated in BC patients. Furthermore, artificially increasing transcripts' m6A levels via MA in cultured primary NK cells reduced mRNA levels of NKG2D pathway genes and death receptor ligands but did not affect protein expression or NK cell functionality. CONCLUSION: Transcripts with higher m6A levels in the 3'UTR region were less abundant, and vice versa. However, changes in mRNA levels of the target genes didn't impact their corresponding protein levels or NK cell functionality.

Humans↗
PubMed2026

Systemic immune activation in hereditary cancer predisposition syndromes: a cross-sectional study.

BACKGROUND: Immune surveillance mechanisms contribute to the elimination of precancerous lesions in hereditary cancer predisposition syndromes (HCPSs). METHODS: By combining single-cell transcriptomics, multiparametric mass cytometry and cytokine profiling of the systemic immune environment in 391 individuals among whom 227 are living with HCPSs we investigated phenotypic alterations in cancer-free individuals with HCPS. RESULTS: A decrease in peripheral B cell abundance and their more differentiated phenotype have been confirmed both in breast cancer patients with germline pathogenic variants in BRCA1 (gpath(BRCA1)) and in patients living with Lynch syndrome (LS). Pre-cancer women with gpath(BRCA1) exhibited an activated phenotype of multiple immune cell lineages, similar to those with manifest disease. In LS, B cell phenotypes exhibited the largest changes in response to cancer eradication, while increased peripheral IL-6 levels was detected even in presymptomatic individuals with LS. CONCLUSIONS: HCPS-specific differences in the phenotype of the systemic immune system might be leveraged in future risk-reducing strategies.

Humans↗
PubMed1979

Lymphocyte transformation to phytohaemagglutinin and delayed hypersensitivity related to age and previous cancer history.

Declining immunosurveillance in old age has been considered one possible explanation for the increased incidence of cancer in the elderly. This study was set up to search for evidence of persistent immunodeficiency in patients with a past history of cancer. Lymphocyte responses to phytohaemagglutinin and cutaneous delayed hypersensivity were assessed in fifty-seven elderly subjects who had successfully completed treatment for cancer more than 18 months previously and compared with those of forty-three healthy controls matched for age and sex. Although a significant difference between mean tritiated thymidine uptake was observed in the lymphocyte response to phytohaemagglutinin (cancer patients 1859 cpm, control 2502 cpm), this could be explained by an unexpectedly prolonged effect of radiotherapy. Mean counts for those twenty-six cancer patients receiving radiotherapy within the period 18 months to 4 years were low (1257 cpm), but were normal (2366 cpm) for the remainder. A significant negative correlation of lymphocyte transformation with age was confirmed in both groups. There was no significant difference in cutaneous delayed hypersensitivity response to commonly encountered antigens. Whilst recognising that these tests do not comprehensively assess immune function, the present results provide no support for the theory that an age-related decline in immune function contributes to the heightened incidence of cancer in the elderly.

Aged↗
PubMed1977

Some immunological considerations relevant to the study of human bladder cancer.

The likelihood that immunosurveillance, concomitant immunity, and immunodepression play a role in the development and spread of neoplasms of the urinary bladder is discussed. The circumstantial evidence for the existence of concomitant immunity to bladder cancer-associated antigens is briefly reviewed, and the implications of the hypothesis of Zinkernagel and Dougherty of a genetic restriction to the cytotoxicity of T-cells for virally determined target cell antigens and of the concept of immunoregulatory cells for our understanding of the immunology of bladder carcinoma are discussed.

Aged↗
PubMed1978

Tumor immunology and interferon.

Host defense mechanisms against cancer depend on an intact cellular immunity system. Immunosurveillance depends on thymus lymphocytes which, when sensitized, form lymphokines. One of the important lymphokines produced by T-lymphocytes is called interferon, well known for its antiviral effects. Recent experimental evidence points also to the potential effectiveness of interferon against malignancies. Interferon and interferon-inducers have been found to alter the course of solid tumors, leukemia, sarcomas and lymphomas in experimental animals, possibly by stimulating the reticuloendothelial system to produce tumor rejection or by altering the surface of cells to change tumor and host reactions.

Animals↗
PubMed2024

A comprehensive meta-analysis of tissue resident memory T cells and their roles in shaping immune microenvironment and patient prognosis in non-small cell lung cancer.

Tissue-resident memory T cells (TRM) are a specialized subset of long-lived memory T cells that reside in peripheral tissues. However, the impact of TRM-related immunosurveillance on the tumor-immune microenvironment (TIME) and tumor progression across various non-small-cell lung cancer (NSCLC) patient populations is yet to be elucidated. Our comprehensive analysis of multiple independent single-cell and bulk RNA-seq datasets of patient NSCLC samples generated reliable, unique TRM signatures, through which we inferred the abundance of TRM in NSCLC. We discovered that TRM abundance is consistently positively correlated with CD4+ T helper 1 cells, M1 macrophages, and resting dendritic cells in the TIME. In addition, TRM signatures are strongly associated with immune checkpoint and stimulatory genes and the prognosis of NSCLC patients. A TRM-based machine learning model to predict patient survival was validated and an 18-gene risk score was further developed to effectively stratify patients into low-risk and high-risk categories, wherein patients with high-risk scores had significantly lower overall survival than patients with low-risk. The prognostic value of the risk score was independently validated by the Cancer Genome Atlas Program (TCGA) dataset and multiple independent NSCLC patient datasets. Notably, low-risk NSCLC patients with higher TRM infiltration exhibited enhanced T-cell immunity, nature killer cell activation, and other TIME immune responses related pathways, indicating a more active immune profile benefitting from immunotherapy. However, the TRM signature revealed low TRM abundance and a lack of prognostic association among lung squamous cell carcinoma patients in contrast to adenocarcinoma, indicating that the two NSCLC subtypes are driven by distinct TIMEs. Altogether, this study provides valuable insights into the complex interactions between TRM and TIME and their impact on NSCLC patient prognosis. The development of a simplified 18-gene risk score provides a practical prognostic marker for risk stratification.

Humans↗
PubMed1979

Collaborative United Kingdom-Australasian study of cancer in patients treated with immunosuppressive drugs.

A collaborative study including centres in the United Kingdom, Australia, and New Zealand was instituted in 1970 to determine the incidence of cancer in patients treated for at least three months with azathioprine, cyclophosphamide, or chlorambucil. Follow-up of 3823 renal transplant recipients showed an almost 60-fold increase of non-Hodgkin's lymphoma together with an excess of squamous-cell skin cancer and mesenchymal tumours. A series of 1349 patients without transplants showed an excess of the same tumours, though to a less extent. These preliminary findings provide no clear evidence that immunosuppressive drugs produce the increased risk of most of the common cancers that might be expected from the simplest interpretation of impaired "immunosurveillance."

Adolescent↗
PubMed1979

Immunosurveillance in pre-malignant occupational bladder disease.

A population of workers exposed to bladder carcinogens has been studied by comparing their immunoreactivity against bladder cancer cells and against a control cancer cell with that found in normal individuals and in patients with bladder cancer. Data are presented which indicate equivalent increases in specific reactivity against bladder cancer cells in clinically normal carcinogen-exposed workers and in patients with bladder cancer. Increases in reactivity are related to degree of exposure and also to early malignant changes in the urothelium. This indicates that immune recognition of tumour antigens does occur before development of overt malignancy.

1-Naphthylamine↗
PubMed1979

Modulatory effects of oestrogen on immunological responsiveness. II. Suppression of tumour-associated immunity in patients with prostatic cancer.

The effect of oestrogen (diethylstilboesterol diphosphate, DES-P) on immunity to tumour-associated antigens in patients with prostatic cancer was evaluated by leucocyte adherence inhibition, a suggested in vitro correlate of cellular immunity. Significant (P smaller than 0.05) suppression of immunity to malignant prostate was observed in thirty out of thirty-one patients following pre-incubation of their leucocytes with therapeutically significant levels of DES-P. Suppression of tumour-associated immunity by exogenous oestrogen provides further evidence to earlier studies demonstrating oestrogenic suppression of non-specific cellular responsiveness evaluated by mitogen-induced lymphocytic blastogenesis, and for concern over the efficacy of oestrogenic therapy and its adverse effect in the treatment of patients with hormone-dependent tumours and responsive diseases. The reduced efficiency of immunosurveillance of tumours and underlying infectious agents may contribute to the exacerbation of disease. While speculative, these observations may also be relevant to the possible assocition between uterine cancer and prolonged administration of DES and the development of vaginal tumours in offspring found in association with maternal ingestion during pregnancy.

Aged↗
PubMed1975

Chronic antigenic stimulation, herpesvirus infection, and cancer in transplant recipients.

An increased incidence of malignancy has been reported in transplant recipients. The pathogenesis of this increase was originally attributed to immunosuppressive therapy. However, not all tumours are increased in proportion to their occurrence in the general population-75% of reported tumours are lymphorproliferative or carcinoma of the skin, lip, or cervix. This cannot be explained by impaired immunosurveillance, and alternative hypotheses must be considered. 90% of transplant recipients develop clinical or serological evidence of herpesvirus infection. Herpesviruses have been implicated in the pathogenesis of lymphorproliferative tumours and carcinoma of the skin and cervix. They can remain in latent form and be reactivated by allogeneic stimulation and/or immunosuppression. These viruses localise to skin, cervix, and neural tissue-i.e., exactly those sites where cancer develops in transplant patients. Herpesvirus infections in association with the presence of an allogeneic graft in an immunosuppressed patient may be responsible for the increased incidence of both lymphoproliferative tumours and carcinoma of the skin, lip, and cervix in the transplant recipient.

Antibodies, Viral↗
PubMed1979

A critical examination of the foundations of immunotherapy for cancer.

It is argued that immunotherapy (IMTH) for cancer, as well as the theory of cancer immunogenicity on which it rests, derives no secure foundation either from clinical observations or from experimental study of valid animal tumour models. Discouraging clinical observations include: the long history of failure of IMTH; the rejection of IMTH for choriocarcinoma--a true allograft in the patient; the extreme rarity of spontaneous regression, and progressive discrediting of the theory of immunosurveillance; the high frequency of nodal metastasis; and the failure to demonstrate a tumour-specific antigen in man. The great majority of animal tumours used for experimental studies of IMTH display artefactual immunogenicity associated with their mode of induction or conditions of transplantation and cannot be accepted as valid models of clinical cancer. The author reviews his total failure to demonstrate immunogenicity or successful IMTH using a wide range of animal tumours from which known laboratory artefacts have been strictly excluded. The inordinate promotion of tumour immunology and IMTH in recent years is attributed to unfortunate sociological influences encouraging premature assertion of clinical relevance from experimental research.

Animals↗