Relevant bibliographies by topics / Cancer immunity

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cancer immunity'

Author: Grafiati
Published: 14 December 2024

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Journal articles on the topic "Cancer immunity"

1

Michael, J. Dochniak. "Maladaptive Immunity and Metastasizing Cancer." Cancer Medicine Journal 3, no. 1 (June 30, 2020): 31–34. http://dx.doi.org/10.46619/cmj.2020.3-1017.

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The ability of innate immunity to inhibit metastatic cells is limited, based on Stage IV cancer survival rates. The dysregulation of the immune system through acquired immunity may result in pathological conditions that alter metastatic cells. Immunoglobulin-E (IgE) antibodies developed by the humoral immune system are a significant contributor to maladaptive immunity. Hypersensitivities are maladaptive immune reactions against harmless allergens. Forced allergen-specific immune responses may provide immediate-type allergies that affect the incidence and prevalence of endogenous proteins essential for metastasizing cells. Furthermore, allergies may shift the body’s resource allocation away from metastasizing cells to IgE-primed effector-cell proliferation. Therefore, research efforts need to explore if hyper-allergenic skin creams can be used to starve-out metastatic cells, wherever they are in the body, to determine if maladaptive immunotherapy is a viable treatment for Stage IV cancer.
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Persing, David H., and Franklyn G. Prendergast. "Infection, Immunity, and Cancer." Archives of Pathology & Laboratory Medicine 123, no. 11 (November 1, 1999): 1015–22. http://dx.doi.org/10.5858/1999-123-1015-iiac.

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Abstract A significant percentage of human cancers worldwide are associated with infections due to known viruses, including human papillomaviruses (cervical cancer and other skin cancers), human T-lymphotropic viruses (adult T-cell leukemias and lymphomas in endemic areas), hepatitis B virus (liver cancer), and Epstein-Barr virus (Burkitt lymphoma and nasopharyngeal carcinoma). The fraction of human cancers attributable to infection may now need to be revised in light of the fact that new viral associations have been discovered and other nonviral associations have been identified. This article addresses the increasingly recognized role of infectious agents as precipitants of human neoplasia and the possibility that novel diagnostic, therapeutic, and chemopreventive strategies may emanate directly from research directed at identifying and understanding these agents.
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Kazbarienė, Birutė. "Tumor and immunity." Medicina 45, no. 2 (February 10, 2009): 162. http://dx.doi.org/10.3390/medicina45020021.

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System of organism defense is an important complex of interrelated cellular, molecular, genetic, and other components, which regulate homeostasis of host. Experimental and clinical data show that immune system functions are significant, but also a complicated question in cancer development. It is very important to investigate and understood how immune system coordinates the response to cancer cells. Our understanding about innate and adaptive immunity functions and interaction with transformed cells is constantly changing. Different responses of these system components can promote, reduce, or inhibit tumor development. It is established that malignant cells develop into invasive cancer with interaction with tumor microenvironment, which is influenced by inflammation. Clinical and experimental studies have revealed the link between inflammation and cancer risk. Many cancers develop in the sites of inflammation. Activation of humoral and cellular immunity may predispose to neoplastic or cancer development. Despite the scientific progress, understanding of the immune system mechanisms responding to malignance remains insufficient.
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Urushizaki, Ichiro, and Yutaka Kohgo. "Cancer and immunity." Japanese Journal of Clinical Immunology 8, no. 1 (1985): 1–14. http://dx.doi.org/10.2177/jsci.8.1.

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Steinle, Alexander, and Adelheid Cerwenka. "MULT1plying cancer immunity." Science 348, no. 6230 (April 2, 2015): 45–46. http://dx.doi.org/10.1126/science.aaa9842.

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Bekeschus, Sander, Thomas von Woedtke, Klaus-Dieter Weltmann, and Hans-Robert Metelmann. "Plasma, Cancer, Immunity." Clinical Plasma Medicine 9 (February 2018): 13–14. http://dx.doi.org/10.1016/j.cpme.2017.12.021.

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Heidari, Alireza, Katrina Schmitt, Maria Henderson, and Elizabeth Besana. "Hereditary immunity in cancer." International Journal of Advanced Chemistry 8, no. 1 (April 28, 2020): 94. http://dx.doi.org/10.14419/ijac.v8i1.30607.

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Cancer is one of the malignant diseases and millions of people worldwide die from cancer annually. Breast cancer diagnosis requires the analysis of images and attributes as well as collecting many clinical and mammography variables. In diagnosis of breast cancer, it is im-portant to determine whether a tumor is benign or malignant. The information about breast cancer risk prediction along with the type of tu-mor are crucial for patients and effective medical decision making. An ideal diagnostic system could effectively distinguish between benign and malignant cells; however, such a system has not been created yet. In this study, a model is developed to improve the prediction probabil-ity of breast cancer. It is necessary to have such a prediction model as the survival probability of breast cancer is high when patients are diagnosed at early stages.
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Hiam-Galvez, Kamir J., Breanna M. Allen, and Matthew H. Spitzer. "Systemic immunity in cancer." Nature Reviews Cancer 21, no. 6 (April 9, 2021): 345–59. http://dx.doi.org/10.1038/s41568-021-00347-z.

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Rathmell, Jeffrey C. "Obesity, Immunity, and Cancer." New England Journal of Medicine 384, no. 12 (March 25, 2021): 1160–62. http://dx.doi.org/10.1056/nejmcibr2035081.

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Orzołek, Izabela, Jan Sobieraj, and Joanna Domagała-Kulawik. "Estrogens, Cancer and Immunity." Cancers 14, no. 9 (April 30, 2022): 2265. http://dx.doi.org/10.3390/cancers14092265.

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Sex hormones are included in many physiological and pathological pathways. Estrogens belong to steroid hormones active in female sex. Estradiol (E2) is the strongest female sex hormone and, with its receptors, contributes to oncogenesis, cancer progression and response to treatment. In recent years, a role of immunosurveillance and suppression of immune response in malignancy has been well defined, forming the basis for cancer immunotherapy. The interplay of sex hormones with cancer immunity, as well as the response to immune checkpoint inhibitors, is of interest. In this review, we investigate the impact of sex hormones on natural immune response with respect to main active elements in anticancer immune surveillance: dendritic cells, macrophages, lymphocytes and checkpoint molecules. We describe the main sex-dependent tumors and the contribution of estrogen in their progression, response to treatment and especially modulation of anticancer immune response.
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Dissertations / Theses on the topic "Cancer immunity"

1

Zunino, Barbara. "Dialogue entre le métabolisme et l’immunité dans le traitement des cancers." Thesis, Nice, 2014. http://www.theses.fr/2014NICE4113.

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Il est connu depuis de nombreuses années que le métabolisme des cellules cancéreuses diffère de celui des cellules saines. La Restriction Calorique (RC) est connue pour prolonger la durée de vie et pour limiter l’oncogenèse. Ainsi, il a été montré que la RC et ses mimétiques comme le 2-deoxyglucose (2DG) augmentent l’efficacité de la chimiothérapie et peuvent aussi induire une immunité anti-tumorale. J’ai pu montrer qu’en régulant le métabolisme via la restriction calorique (ou des mimétiques) nous pouvions moduler l’expression de la protéine anti-apoptotique Mcl-1. Ainsi nous avons établi in vivo et in vitro que la RC restaure la sensibilité des cellules de lymphome à l’apoptose induite par un inhibiteur de Bcl-2/XL, l’ABT-737. Nous avons aussi établi que ces effets sont indépendants de la protéine p53 et/ou des « protéines BH3-only ». La deuxième partie de mon travail a été d’élucider les mécanismes moléculaires mis en place lors de la Chimiothérapie Hyperthermique Intra péritonéale (CHIP) pouvant expliquer les effets bénéfiques observés chez les patients atteints d’une carcinose péritonéale (CP). Une partie de ces bénéfices sont dus à la mise en place d’une immunité anti-tumorale. En utilisant des modèles in vivo et in vitro j’ai mis en évidence l’implication de la protéine du choc thermique 90 (Hsp90) dans l’effet observé. Ainsi, l’inhibition spécifique de la Hsp90 réverse les effets protecteurs de la CHIP, soulignant l’importance de cette protéine dans notre modèle d’immunité anti-tumorale
The link between cell metabolism and cancer at the cellular level has long been known. Caloric restriction (CR) is known to prolong lifespan and to protect from cancer incidence. The molecular mechanisms involved in these benefic effects have been evaluated and may offer new opportunities for therapeutic intervention. Moreover, CR and CR-mimetics such as 2-deoxyglucose (2DG) has been shown to enhance chemotherapy efficiency and to induce an anti-cancer immune response. During the period of my PhD I demonstrated how the modulation of metabolism through caloric restriction or through its mimetics could significantly reduce the expression of the anti-apoptotic protein Mcl-1 and sensitize lymphoma-bearing mice to apoptosis induced by a Bcl-2/XL inhibitor, ABT-737. We have demonstrated that CR can control Mcl-1 translation and sensitize cells to ABT-737-induced death regardless of the presence or absence of p53 and/or of the main “BH3-only proteins”. Then, I focused on deciphering the molecular mechanisms allowing the Hyper-thermic Intra-Peritoneal Chemotherapy (HIPEC) to be beneficial to patients suffering from peritoneal carcinomatosis. Part of the protective effect was mediated through the induction of an efficient anti-cancer immune response. Next, I showed the involvement of heat shock proteins 90 (Hsp90) in the observed effect. Indeed, when Hsp90 was blocked we lost the protection induced by the HIPEC-treated cells, therefore underling the role of Hsp90 in this HIPEC-dependent induction of anti-cancer immune response
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They, Laetitia. "Renforcement des effets immunomodulateurs d’un anticorps monoclonal anti-tumoral : étude des effets potentialisateurs de thérapies combinées et analyse des mécanismes impliqués." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT076/document.

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Le mélanome est la forme la plus agressive des cancers de la peau. Si sa prise en charge à des stades précoces est de bon pronostic, l’espérance de vie des patients chute dramatiquement pour les stades métastatiques. Malgré les avancées thérapeutiques spectaculaires récentes, le problème majeur réside dans la résistance aux traitements et la récidive et le défi principal est désormais de tendre vers un contrôle efficace et durable. Les anticorps monoclonaux (AcM) ont la capacité de cibler et éliminer spécifiquement la cellule tumorale tout en recrutant des cellules du système immunitaire, permettant de développer et/ou renforcer l’immunité de l’hôte avec le développement d’une réponse immune anti-tumorale de type vaccinale. Dans un modèle de tumeur solide de mélanome murin après greffe sous-cutanée des cellules B16F10, nous avons étudié le potentiel immunomodulateur de l’AcM TA99 qui cible un antigène de surface TYRP-1 surexprimé dans les mélanocytes tumoraux. Nos résultats montrent qu’environ 30% des souris sont protégées sur le long-terme et présentent une réponse immunitaire humorale et cellulaire mémoire. Par ailleurs, l’analyse de l’infiltrat immunitaire chez les souris qui échappent au traitement par l’AcM TA99 et qui développent une tumeur à plus ou moins long terme, montre une surexpression de PD-1 et Tim3 associée à une perte de fonctionnalité des cellules effectrices au sein de la tumeur. Ce même phénotype a été observé sur des biopsies de patients atteints de mélanome métastatique. Nous montrons aussi dans le cadre de ce travail que, le blocage de l’axe PD1/PD-L1 par inoculation d’un AcM anti-PD1 au moment de l’échappement, potentialise la réponse immunitaire anti-tumorale et entraîne une augmentation de la survie. Cependant, l’absence de régression complète suggère la mise en place d’autres voies immunosuppressives. En effet nous avons observé une surexpression des ectonucleotidases CD39 et CD73 dans le micro-environnement tumoral suggérant l’implication de l’adénosine dans la résistance au traitement de l’AcM TA99 plus l’α-PD-1. Ce résultat ouvre des perspectives intéressantes pour le blocage concomitant la voie de l’adénosine et de l’axe PD1/PD-L1. Une autre stratégie a consisté à améliorer les effets immunomodulateurs précoces de l’AcM TA99 en le combinant avec l’oxaliplatine, chimiothérapie favorisant la mort immunogénique. Bien que les combinaisons thérapeutiques testées dans cette étude montrent des effets in vivo encourageants avec un délai significatif dans la survie globale, aucune augmentation significative de la réponse anti-tumorale sur le long terme n’a pu être observée, suggérant la mise en place d’autres voies immunosuppressives non redondantes ou des stratégies de combinaisons non adaptées. Une analyse dynamique approfondie, tant phénotypique que fonctionnelle, des différents acteurs cellulaires du micro-environnement tumoral sera une étape clé dans la mise en place de combinaisons pertinentes en association avec l’AcM TA99. Ce travail prend d’autant plus d’intérêt qu’un essai clinique de phase I (IMC-20D7S) utilisant le flanvotumab (équivalent humain de l’AcM TA99) réalisé chez 27 patients atteints de mélanome métastatique, montre des effets cliniques intéressants sans effets secondaires sévères, ouvrant la voie au développement de combinaisons thérapeutiques associées à cet AcM
Melanoma is the most aggressive form of skin cancer. Although early management is of good prognosis, the survival of patients decrease dramatically for metastatic stages. Despite the recent spectacular therapeutic advances, the major problem lies in resistance to treatment and relapse and the main challenge now is to develop an effective and sustainable control. Monoclonal antibodies (mAbs) have the ability to specifically target and eliminate tumor cells while recruiting cells from the immune system, to develop and / or enhance the immunity of the host with the development of a vaccinal immune response. In a solid tumor model of murine melanoma after subcutaneous transplantation of B16F10 cells, we investigated the immunomodulatory effect of TA99 mAb targeting a TYRP-1 surface antigen overexpressed in tumor melanocytes. Our results showed that about 30% of mice are protected in the long term and have an antitumoral humoral and cellular immune response. Moreover, the analysis of the immune infiltrate in mice that escape to the treatment with TA99 mAb and develop a tumor, shows an overexpression of PD-1 and Tim3 associated with a loss of effector cell functions within the tumor. This same phenotype has been observed in biopsies of patients with metastatic melanoma. Thus, blocking the PD-1 / PDL-1 axis by inoculation of an anti-PD1 mAb at the time of tumor escape potentiates the anti-tumor immune response and results in increased survival. However, the absence of complete regression suggests the establishment of other immunosuppressive pathways. Indeed we have observed an overexpression of CD39 and CD73 ectonucleotidases in the tumor microenvironment suggesting the involvement of adenosine in the resistance mechanisms observed and opening interesting perspectives for the concomitant blocking of this pathway and the PD1 / PDL-1 axis. Another strategy has been to improve the early immunomodulatory effects of TA99 mAb by combining it with oxaliplatin, a chemotherapy that promotes immunogenic death. Although the therapeutic combinations tested in this study showed encouraging in vivo effects with a significant delay in overall survival, no significant increase in the long-term anti-tumor response was observed, suggesting the establishment of other non-redundant immunosuppressive mechanisms or unsuitable combinations strategies. Both phenotypic and functional analysis of the different cellular actors of the tumor microenvironment will be a key step in the implementation of relevant combinations in association with the TA99 mAb. This work is highlighted by a phase I clinical trial (IMC-20D7S) using flanvotumab (human equivalent of mAb TA99) in 27 patients with metastatic melanoma that shows interesting clinical outcome without severe side effects, opening the way for the development of therapeutic combinations associated with this mAb
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3

Zunino, Barbara. "Dialogue entre le métabolisme et l’immunité dans le traitement des cancers." Electronic Thesis or Diss., Nice, 2014. http://www.theses.fr/2014NICE4113.

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Il est connu depuis de nombreuses années que le métabolisme des cellules cancéreuses diffère de celui des cellules saines. La Restriction Calorique (RC) est connue pour prolonger la durée de vie et pour limiter l’oncogenèse. Ainsi, il a été montré que la RC et ses mimétiques comme le 2-deoxyglucose (2DG) augmentent l’efficacité de la chimiothérapie et peuvent aussi induire une immunité anti-tumorale. J’ai pu montrer qu’en régulant le métabolisme via la restriction calorique (ou des mimétiques) nous pouvions moduler l’expression de la protéine anti-apoptotique Mcl-1. Ainsi nous avons établi in vivo et in vitro que la RC restaure la sensibilité des cellules de lymphome à l’apoptose induite par un inhibiteur de Bcl-2/XL, l’ABT-737. Nous avons aussi établi que ces effets sont indépendants de la protéine p53 et/ou des « protéines BH3-only ». La deuxième partie de mon travail a été d’élucider les mécanismes moléculaires mis en place lors de la Chimiothérapie Hyperthermique Intra péritonéale (CHIP) pouvant expliquer les effets bénéfiques observés chez les patients atteints d’une carcinose péritonéale (CP). Une partie de ces bénéfices sont dus à la mise en place d’une immunité anti-tumorale. En utilisant des modèles in vivo et in vitro j’ai mis en évidence l’implication de la protéine du choc thermique 90 (Hsp90) dans l’effet observé. Ainsi, l’inhibition spécifique de la Hsp90 réverse les effets protecteurs de la CHIP, soulignant l’importance de cette protéine dans notre modèle d’immunité anti-tumorale
The link between cell metabolism and cancer at the cellular level has long been known. Caloric restriction (CR) is known to prolong lifespan and to protect from cancer incidence. The molecular mechanisms involved in these benefic effects have been evaluated and may offer new opportunities for therapeutic intervention. Moreover, CR and CR-mimetics such as 2-deoxyglucose (2DG) has been shown to enhance chemotherapy efficiency and to induce an anti-cancer immune response. During the period of my PhD I demonstrated how the modulation of metabolism through caloric restriction or through its mimetics could significantly reduce the expression of the anti-apoptotic protein Mcl-1 and sensitize lymphoma-bearing mice to apoptosis induced by a Bcl-2/XL inhibitor, ABT-737. We have demonstrated that CR can control Mcl-1 translation and sensitize cells to ABT-737-induced death regardless of the presence or absence of p53 and/or of the main “BH3-only proteins”. Then, I focused on deciphering the molecular mechanisms allowing the Hyper-thermic Intra-Peritoneal Chemotherapy (HIPEC) to be beneficial to patients suffering from peritoneal carcinomatosis. Part of the protective effect was mediated through the induction of an efficient anti-cancer immune response. Next, I showed the involvement of heat shock proteins 90 (Hsp90) in the observed effect. Indeed, when Hsp90 was blocked we lost the protection induced by the HIPEC-treated cells, therefore underling the role of Hsp90 in this HIPEC-dependent induction of anti-cancer immune response
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4

Decque, Adrien. "Etude de la SUMOylation dans l’immunité innée et l’oncogenèse." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066312/document.

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La SUMOylation est une modification post-traductionnelle réversible permettant de diversifier les fonctions de centaines de substrats. Elle est impliquée dans des processus essentiels à la cellule et à l'organisme, tels que la réparation de l'ADN, la mitose, la transcription. A l'aide de modèles murins génétiquement modifiés déficients pour l'unique enzyme E2 de SUMOylation, UBC9, nous avons caractérisé les conséquences de la réduction de la SUMOylation sur l'immunité innée et l'oncogenèse.Nous révélons un rôle majeur de la SUMOylation dans la régulation négative du gène codant pour l'IFN- . La dérégulation de ce gène par l'absence d'Ubc9 a des conséquences importantes sur l'immunité innée, avec une augmentation de l'expression du programme transcriptionnel inflammatoire, une hypersensibilité au choc endotoxique, et une protection contre les infections virales. L'étude du profil chromatinien de SUMO autour du gène Ifnb1 a révélé trois nouveaux domaines à potentiel régulateur. Enfin, la SUMOylation régule l'expression de rétrovirus endogènes, potentiellement déclencheurs d'une réponse interféron.Le second axe de recherche a permis de caractériser les conséquences de la réduction de la SUMOylation sur la transformation cellulaire et l'oncogenèse colorectale. Nous montrons une sensibilité accrue des cellules transformées à la perte de SUMOylation comparées aux cellules primaires. De plus, les souris hétérozygotes pour Ubc9 présentent une réduction du nombre de polypes intestinaux dans un modèle d'oncogenèse colorectale.Ces résultats permettent d'affiner nos connaissances sur le rôle de la SUMOylation dans l'oncogenèse et l'immunité innée
SUMOylation is a reversible post-translational modification modifying the functions of hundreds ofproteins. It is implicated in essential cellular and organismal processes, such as nuclear shuttling, DNArepair, mitosis, transcription. Using genetically modified models, deficient for the uniqueSUMOylation E2 enzyme UBC9, we characterized the consequences of a decrease in globalSUMOylation in two processes: innate immunity and oncogenesis.We reveal a major role for SUMOylation in the negative regulation of the gene coding for IFN-.Deregulation of this gene in the absence of Ubc9 has dramatic consequences on innate immunity, withincreased inflammatory transcriptional program expression, endotoxic shock hypersensitivity, andprotection against viral infection. Chromatin binding profile analysis of SUMO surrounding the Ifnb1gene revealed three new putative regulatory domains. Finally, SUMOylation regulates endogenousretroviruses expression, potential triggers for interferon response.Our second research axis allowed the characterization of the consequences of global SUMOylationdecrease on cellular transformation and colorectal oncogenesis. Our results show increased sensitivityof transformed cells to SUMOylation loss, when compared to primary cells. Furthermore, decreasingUBC9 levels by half causes a two-fold decrease in intestinal polyp numbers developing in the colon ofmice, in a chemically-induced model of colorectal oncogenesis.Altogether, these results helped increasing our knowledge of the role of SUMOylation in majorcellular processes implicated in oncogenesis and innate immunity
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Meyer, Andrea Michael. "Ro52 in innate immunity, proliferation control and cancer /." Zürich : ETH, 2009. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18198.

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Al, Khathami Ali Gaithan. "Towards gastric cancer immunotherapy : assessment of cancer immunity and potential immune targets." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8855/.

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Gastric cancer (GC), the fourth most common malignancy worldwide, has poor prognosis and treatment innovation is needed. The aims of this project were to investigate immune targets and treatment strategies for GC. I identified new T-cell epitopes in three Epstein-Barr virus (EBV) tumor antigens, LMP1, LMP2 and BARF1, expressed in the 10% of GC cases positive for EBV. T-cell clones showed that a BARF1-specific CD4 T-cell epitope restricted by HLA-DR51, an allele common in the population, was presented by an EBV-positive epithelial cancer cell line. Analysing blood and fresh tumor from newly diagnosed GC patients, I detected T-cell responses to MAGEA1, MAGEA4 and NY-ESO-1 tumour antigens in blood but not tumor. Compared to healthy donors, patients had: higher frequencies of LAG3 or CTLA4 positive CD8 T-cells, TIM-3 or CTLA4 CD4+ T-cells, T-regs, NKT-cells and gamma-delta T-cells in blood and tissue. Patients also had high granulocytic MDSC frequencies in PBMC. The CD4:CD8 ratio was low in some patients' blood, potentially indicating immunosenesence, but was always higher in tumor tissue. I successfully generated tumour infiltrating lymphocytes (TILs) from nine patients' tumors. These comprised high T-cells and NK-cells and low T-reg and MDSC. LAG-3 was increased, but PD1, was decreased on TIL T-cells. Using 3-dimensional organoids established from two patients, I showed that TIL NK-cells, but not TIL T-cells, recognized autologous tumor organoids. My results are the first proof of principle that TILs can readily be generated from gastric tumors, can target tumors cells and therefore be used to treat gastric cancer.
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Titu, Liviu. "Specific cytotoxic lymphocyte immunity against telomerase in colorectal cancer." Thesis, University of Hull, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273656.

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Gajurel, Damodar. "Boosting Anti-Cancer Immunity with a Novel Chimeric Molecule." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/370742.

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High mortality, second only to cardiovascular causes, and high morbidity (physical as well as psychological) from cancer are unacceptable. Despite many years of multi-modality (conventional) treatment with surgery, radiotherapy, and chemotherapy, the status of cancer management, especially lung cancer, is still not satisfactory and alternate management strategies need to be developed. Anti-tumour immunotherapy is being explored as a potential new form of cancer therapies. Cancer vaccines, as forms of immunotherapy, have been developed and tested in clinical trials. Unfortunately, almost all of them did not achieve expected clinical responses. One of the reasons for this failure has been attributed to the poor immunogenicity/antigenicity of those vaccines. It has been suggested that whole tumour cells, harbouring all known and unknown cancer antigens, would better serve as vaccine antigens by circumventing the probability of tumour antigen loss due to tumour immune editing than selected single antigens used in most of those failed trials. The fact that even histologically similar types of tumours can harbour divergent antigens in different patients also explains the failure of clinical trials using allogeneic cancer cell vaccines suggesting that personalized tumour vaccines using autologous whole tumour cells would most likely ensure clinical success of cancer vaccines. But, at the same time, studies have shown that, in contrast to isolated single antigens, whole cancer cells also contain self-antigens that could lead, if not to outright immune tolerance, then to poor immune response, necessitating the use of immune-potentiating adjuvants to garner sufficient anti-tumour immune stimulation, i.e. enhanced immunogenicity. Therefore, combining autologous whole cancer cells with the appropriate immune-potentiating adjuvant in various novel ways could ensure a highly immunogenic and clinically effective vaccine. Considering the above facts, this study has been initiated to design a lung cancer vaccine with improved immunogenicity by conjugating a known strong and safe immune-potentiating adjuvant, i.e. unmethylated cytosine-phosphate-guanine oligodeoxynucleotide (CpG ODN) to whole A549 human lung cancer cell (as vaccine antigens) with the help of cross-linker bis-sulfosuccinimidyl suberate (BS3) in a novel way. Studies have shown that bi-directionally active NHS-ester moiety of BS3 covalently attach to the surface of the cancer cell membrane on one side and to one end of CpG ODN on the other side forming a novel chimeric molecule with 100-fold enhanced immune-potentiating capacity compared to their use in physical and temporal isolation. The formation of this covalently stable chimeric molecule using A549 whole lung cancer cells with CpG ODN, for the first time, was confirmed using fluorescein molecule tagged CpG ODNs and a scanning laser confocal microscope. The immunogenicity of this novel chimeric molecule was tested in vitro by measuring the level of the cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α) released after exposure to U937 differentiated macrophages. The results of the level of the cytokines confirm that quantitatively more IL-6 and TNF-α, as surrogate markers for anti-cancer immune response, were released with the incorporation of the novel chimeric molecule than its control. The chimeric molecule induced the release of about 4500 pg/ml of TNF-α. This was very close to the amount of TNF-α (about 5000 pg/ml) released by 100 ng/ml of lipopolysaccharide (LPS) used as positive control. The negative control i.e. unconjugated CpG ODN and macrophages, released only around 500-600 pg/ml of TNF-α (i.e. our novel chimeric molecule induced nine times more cytokine release than its control. The difference in means of the cytokines released by them was also statistically significant (p < 0.05). The results indicated that this novel chimeric molecule is highly immunogenic and could be further tested in animal models as the next step towards the development of a personalized anti-lung clinical cancer vaccine.
Thesis (Masters)
Master of Medical Research (MMedRes)
School of Medical Science
Griffith Health
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Lemay, Chantal. "Harnessing Oncolytic Virus-mediated Anti-tumour Immunity." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23318.

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Treatment of permissive tumours with the oncolytic virus (OV) VSV-Δ51 leads to a robust anti-tumour T cell response, which contributes to efficacy; however, many tumours are not permissive to in vivo treatment with VSV-Δ51. In an attempt to channel the immune stimulatory properties of VSV-Δ51 and broaden the scope of tumours that can be treated by an OV, a potent oncolytic vaccine platform was developed, consisting of tumour cells infected with VSV-Δ51. I demonstrate that prophylactic immunization with this infected cell vaccine (ICV) protected mice from subsequent tumour challenge, and expression of GM-CSF by the virus (VSVgm-ICV) increased efficacy. Immunization with VSVgm-ICV in the VSV-resistant B16-F10 model induced maturation of dendritic cells, natural killer (NK) cells, and T cells. I demonstrate that this approach is robust enough to control the growth of established and spontaneous tumours. This strategy is broadly applicable because of VSV’s extremely broad tropism, allowing nearly all cell types to be infected at high MOIs in vitro, where the virus replication kinetics outpace the cellular IFN response. It is also personalized to the unique tumour antigen(s) displayed by the cancer cell. Histone deacetylase inhibitors (HDIs) can augment viral replication, making them particularly interesting complements to OV therapy. However, the impact of HDIs on the generation and re-stimulation of immune responses remains to be clearly elucidated. Along with my collaborators at McMaster University, I demonstrate that MS-275, but not SAHA, selectively depletes naïve and regulatory lymphocytes. Memory lymphocytes that are being boosted remain unscathed and even have enhanced cytokine production, potentially as a consequence of the depleted lymphocyte compartment. This leads to a delay in anti-VSV neutralizing antibodies and T cell responses. Interestingly, HDI treatment of B16-F10 cells appears to inhibit VSV replication but allows for a longer persistence within the tumour. When used in an oncolytic prime/boost vaccination model, MS-275 potently enhanced survival. Though the anti-tumour immune response is enhanced, a near complete reduction in autoimmune vitiligo is observed with MS-275 administration. Therefore, this HDI uniquely modulates the immune response to enhance anti-tumour immunity and decrease the anti-viral response, while also decreasing autoimmune sequelae.
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Aloulou, Nijez. "Rôle de la leptine dans le cancer colorectal humain." Thesis, Paris Est, 2008. http://www.theses.fr/2008PEST0027.

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Par sa fréquence et sa gravité, le CCR représente un réel problème de santé publique. Avec 37000 nouveaux cas par an et 15% des décès, il constitue la 2ème cause de mortalité par cancer en France. Malgré d'importants progrès thérapeutiques durant cette dernière décennie, il rest un cancer de mauvais pronostic. Des facteurs génétiques et environnementaux ont été impliqués dans la genèse de ce cancer. La caractérisation moléculaire du CCR a permis d'identifier les tumeurs par instabiblité génique, appelées MSI (Microsatelite Instability) possédant des anomalies de réparation d'appariement d'ADN (MMR mismatch repair). Celles-ci sont fréquemment retrouvées (80%) dans les CCRs familiaux et rarement (15%) dans les cancers sporadiques. Les tumeurs avec phénotype MSI sont de bon pronostic. Le rôle possible de l'alimentation et particulièrement celui du fuel énergétique sur la survenue d'anomalies d'appariement d'ADN a été suggéré. De nombreuses hormones et en particulier la leptine ont été rapportées comme facteur de promotion tumorale. De plus, la leptine possède de nombreuses propriétés immunrégulatrices. Son effet sur l'immunité colique tiendrait autant à sa capacité à initier la production de cytokines à partir des cellules épithéliales digestives qu'à sa capacité à contrôler la prolifération des lymphocytes. Nous avons formulé l'hypothèse que la leptine pouvait réguler des fonctions immunes dans le microenvironnement tumoral. L'ensemble de ces données souligne l'importance de l'étude chez l'homme. L'analyse des données prospectives de 171 patients avec CCR permet de noter une surexpression du récepteur de la leptine dans un sous groupe de tumeurs. Les relations entre le récpteur de la leptine et la réponse immunitaire ont été analysées dans le microenvironnement tumoral humain, par des modèles cellulaires in vitro et animaux in vivo. Nous avons découvert que l'effet pro immunitaire de leptine dépendait du niveau d'expression de sonrécepteur et du degré d'instabilité microsatellitaire dans la cellule tumorale. L'expression du récepteur de la leptine pourrait être considérée comme un marqueur pronostique dans le CCR humain
Cancer of the colon and rectum (CRC) is a real challenge in Western countries because of the prevalence, cost and bad prognosis. With they 37,000 new cases each year and 15% of mortality it is currently the 2nd cause of cancer death in France. Despite significant advances in diagnosis and treatment over the past decade, it remains with bad prognosis. Genetic and environmental factors were involved in the genesis of this cancer. Molecular characterization of CRC leaded to the identification of gene instability (MSI) in tumors with mismatch repair (MMR) abnormalities. This is found frequently (80%) the CRC hereditary no polyposis colon cancer family (HNPCC) and rarely (15%) in sporadic cancers. Those tumors with MSI phenotype are considered to be of good prognosis. The possible role of food and particulary energy balance on the occurrence of MMR abnormalities has been suggested. Several hormones including leptin have been reported to promote tumour growth. In addition, leptin may regulate immune response tin GIT. Its pro immunogenic effect results from cytokines production by gastrointestinal epithelial cells as well as its ability to control the proliferation of lymphocytes. We hypothesised that leptin might regulate anti tumour immune response. The analysis of prospective data from 171 patients with CRC showed that overexpression of leptin receptor in subset of tumours. Relationships between leptin recptor and tumour immune response have been studied in the tumour microenvironment in human tissues, and in culture cells in vitro as well as in animal models in vivo. Results showed intensity of immune response was depended on the level of leptin receptor expression and MSI in colon tumour cells. Thus leptin receptor expression may be considered as a prognostic marker in colon and rectal cancer in human
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Books on the topic "Cancer immunity"

1

E, Reif Arnold, Mitchell Malcolm S, and Biological Response Modifier Program (U.S.), eds. Immunity to cancer. Orlando: Academic Press, 1985.

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Bo, Dupont, ed. Immunity to cancer. Copenhagen: Munksgaard, 2002.

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E, Macher, and Sorg Clemens, eds. Local immunity in cancer. Münster: Wissenschaftliche Verlagsgesellschaft Regensberg & Biermann, 1986.

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Raz, Yirmiya, and Taylor Anna N, eds. Alcohol, immunity, and cancer. Boca Raton: CRC Press, 1993.

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Orentas, Rimas, James W. Hodge, and Bryon D. Johnson, eds. Cancer Vaccines and Tumor Immunity. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470170113.

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Seya, Tsukasa, Misako Matsumoto, Keiko Udaka, and Noriyuki Sato, eds. Inflammation and Immunity in Cancer. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55327-4.

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Orentas, Rimas. Cancer vaccines and tumor immunity. Hoboken, N.J: Wiley-Interscience, 2008.

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Rimas, Orentas, Hodge James W, and Johnson Bryon D, eds. Cancer vaccines and tumor immunity. Hoboken, N.J: John Wiley & Sons, 2008.

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Ray, P. K., ed. Advances in Immunity and Cancer Therapy. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-9558-4.

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Ray, P. K. Advances in Immunity and Cancer Therapy. New York, NY: Springer New York, 1985. http://dx.doi.org/10.1007/978-1-4612-5068-5.

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Book chapters on the topic "Cancer immunity"

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Mora, Javier, Warner Alpízar-Alpízar, and Andreas Weigert. "Cancer Immunity." In Nijkamp and Parnham's Principles of Immunopharmacology, 191–208. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-10811-3_12.

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Tu, Shi-Ming. "Cancer Immunity." In Cancer Treatment and Research, 147–59. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5968-3_14.

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Carlberg, Carsten, and Eunike Velleuer. "Cancer Immunity." In Cancer Biology: How Science Works, 129–46. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75699-4_10.

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Huang, Gonghua. "Innate Immunity." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3064-6.

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Schwab, Manfred. "Adaptive Immunity." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_74-2.

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Huang, Gonghua. "Innate Immunity." In Encyclopedia of Cancer, 2282–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3064.

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Gratama, Jan W., Cor H. J. Lamers, and Reno Debets. "A10 Cancer immunity." In Principles of Immunopharmacology, 151–78. Basel: Birkhäuser Basel, 2011. http://dx.doi.org/10.1007/978-3-0346-0136-8_10.

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Sharifi, Laleh. "Nutrition and Cancer." In Nutrition and Immunity, 283–300. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16073-9_13.

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Silva, Lindsey M., and Jae U. Jung. "Autophagy and Immunity." In Autophagy and Cancer, 145–65. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6561-4_8.

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Abolhassani, Hassan, Niyaz Mohammadzadeh Honarvar, Terezie T. Mosby, and Maryam Mahmoudi. "Nutrition, Immunity, and Cancers." In Cancer Immunology, 533–44. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_24.

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Conference papers on the topic "Cancer immunity"

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Pittet, Mikael. "Abstract IA04: Cancer-promoting immunity." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-ia04.

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Leslie, Christina S. "Decoding Epigenomic Programs in Immunity and Cancer." In BCB '19: 10th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3307339.3342129.

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Zou, Weiping. "Abstract IA18: Metabolic impact on cancer immunity." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-ia18.

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Isaeva, O. G., and V. A. Osipov. "Photodynamic therapy influence on anti-cancer immunity." In Saratov Fall Meeting 2009, edited by Valery V. Tuchin and Elina A. Genina. SPIE, 2009. http://dx.doi.org/10.1117/12.853588.

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Ouni, Rim, Ying Henderson, Yunyun Chen, Naimah Turner, William Padron, Ali Dadbin, Elena McBeath Fujiwara, et al. "Characterization of Altered immunity in Anaplastic Thyroid Cancer." In Leading Edge of Cancer Research Symposium. The University of Texas at MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00072.

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Milani, Valeria, Veit Buecklein, and Rolf Dieter Issels. "Abstract B11: Hyperthermia and antitumor immunity." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-b11.

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Kudo-Saito, Chie, Masayoshi Toyoura, Yuji Shoya, Akiko Ishida, and Ryoko Kon. "Abstract 3224: Blocking FSTL1 reprograms cancer-caused abnormal immunity." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3224.

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Khan, Mohammad W., Shingo Tsuji, MengXi Tian, Nairika Meshgin, Shea Grenier, Matthew J. Giacalone, and Kathleen L. McGuire. "Abstract A05: Immunity, the colonic environment, and colon cancer." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-a05.

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Stromnes, Ingunn M., Scott Brockenbrough, Thomas M. Schmitt, Jennifer D. Hotes, Markus A. Carlson, Carlos Cuevos, Philip D. Greenberg, and Sunil R. Hingorani. "Abstract PR10: Re-engineering immunity to treat pancreas cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-pr10.

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Mittendorf, Elizabeth A., Gheath Alatrash, Na Qiao, Haile Xiao, Pariya Sukhumalchandra, Kathryn Quintanilla, Karen Clise-Dwyer, and Jeffrey Molldrem. "Abstract 801: Uptake of exogenous neutrophil elastase by breast cancer cells: A novel link between innate immunity, inflammation and breast cancer immunity." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-801.

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Reports on the topic "Cancer immunity"

1

Andersen, Barbara L. Stress and Immunity Breast Cancer Project. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada398948.

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Andersen, Barbara L. Stress and Immunity Breast Cancer Project. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada334925.

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Eck, Stephen, and Heike Boxhorn. Gene Therapy Mediated Breast Cancer Immunity. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada335064.

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Nesbit, Heike K. Gene Therapy Mediated Breast Cancer Immunity. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382694.

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Weinberg, Andrew D. Enhancing Anti-Prostate Cancer Immunity through OX40 Engagement. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada437192.

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Vieweg, Johannes. Enhancement of Anti-Telomerase Immunity Against Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada485726.

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Vieweg, Johannes W. Enhancement of Anti-Telomerase Immunity Against Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada444923.

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Weinberg, Andrew D. Enhancing Anti-Prostate Cancer Immunity Through OX40 Engagement. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada455612.

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Ioannides, Constantin G. Epitope Specific T Cell Immunity to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada414361.

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Weinberg, Andrew D. Enhancing Anti-Prostate Cancer Immunity Through OX40 Engagement. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada422213.

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