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Journal articles on the topic 'Cancer immunity'

Author: Grafiati

Published: 14 December 2024

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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Pinto, Joseph A., Jhajaira M. Araujo, and Henry L. Gómez. "Sex, immunity, and cancer." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1877, no. 1 (January 2022): 188647. http://dx.doi.org/10.1016/j.bbcan.2021.188647.

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12

Hong, Hong, Qi Wang, Jing Li, Hans Liu, Xin Meng, and Haiyan Zhang. "Aging, Cancer and Immunity." Journal of Cancer 10, no. 13 (2019): 3021–27. http://dx.doi.org/10.7150/jca.30723.

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13

IV, Edmund T. Anderson. "Depression, Immunity and Cancer." Science News 127, no. 15 (April 13, 1985): 227. http://dx.doi.org/10.2307/3969687.

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Kelly, Priscilla N. "Phages and cancer immunity." Science 369, no. 6506 (August 20, 2020): 930.5–931. http://dx.doi.org/10.1126/science.369.6506.930-e.

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15

Burns, Edith A., and Elaine A. Leventhal. "Aging, Immunity, and Cancer." Cancer Control 7, no. 6 (November 2000): 513–22. http://dx.doi.org/10.1177/107327480000700603.

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16

Borsig, Lubor. "Selectins in cancer immunity." Glycobiology 28, no. 9 (January 17, 2018): 648–55. http://dx.doi.org/10.1093/glycob/cwx105.

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17

Singh, Rajesh, Manoj Kumar Mishra, and Himanshu Aggarwal. "Inflammation, Immunity, and Cancer." Mediators of Inflammation 2017 (2017): 1. http://dx.doi.org/10.1155/2017/6027305.

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18

Martín-Sierra, C., P. Laranjeira, M. R. Domingues, and A. Paiva. "Lipoxidation and cancer immunity." Redox Biology 23 (May 2019): 101103. http://dx.doi.org/10.1016/j.redox.2019.101103.

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19

Clifford, Gary, and Silvia Franceschi. "Immunity, infection, and cancer." Lancet 370, no. 9581 (July 2007): 6–7. http://dx.doi.org/10.1016/s0140-6736(07)61023-x.

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20

Núñez, Marı́a J., Paula Mañá, David Liñares, Marı́a P. Riveiro, José Balboa, Juan Suárez-Quintanilla, Mónica Maracchi, Manuel Rey Méndez, José M. López, and Manuel Freire-Garabal. "Music, immunity and cancer." Life Sciences 71, no. 9 (July 2002): 1047–57. http://dx.doi.org/10.1016/s0024-3205(02)01796-4.

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21

Hakim, Frances T., Francis A. Flomerfelt, Michael Boyiadzis, and Ronald E. Gress. "Aging, immunity and cancer." Current Opinion in Immunology 16, no. 2 (April 2004): 151–56. http://dx.doi.org/10.1016/j.coi.2004.01.009.

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22

Derhovanessian, Evelyna, Rafael Solana, Anis Larbi, and Graham Pawelec. "Immunity, ageing and cancer." Immunity & Ageing 5, no. 1 (2008): 11. http://dx.doi.org/10.1186/1742-4933-5-11.

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23

Ma, Ruixia, Bin Yi, Adam I. Riker, and Yaguang Xi. "Metformin and cancer immunity." Acta Pharmacologica Sinica 41, no. 11 (August 31, 2020): 1403–9. http://dx.doi.org/10.1038/s41401-020-00508-0.

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24

Stokes, G. "Oral cancer: Overall immunity." British Dental Journal 216, no. 1 (January 2014): 3. http://dx.doi.org/10.1038/sj.bdj.2013.1243.

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25

Grivennikov, Sergei I., Florian R. Greten, and Michael Karin. "Immunity, Inflammation, and Cancer." Cell 140, no. 6 (March 2010): 883–99. http://dx.doi.org/10.1016/j.cell.2010.01.025.

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26

Trainin, N. "Cellular immunity and cancer." European Journal of Cancer 29 (January 1993): S2. http://dx.doi.org/10.1016/0959-8049(93)90631-o.

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27

Rainsford, K. D. "Alcohol immunity and cancer." Inflammopharmacology 3, no. 1 (March 1995): 24. http://dx.doi.org/10.1007/bf02659107.

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28

Blomberg, Bonnie, Daniela Frasca, Alain Diaz, and Michael B. Antoni. "Aging, Immunity and Cancer." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 88.13. http://dx.doi.org/10.4049/jimmunol.210.supp.88.13.

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Abstract Our studies have shown that breast cancer patients receiving CBSM (Cognitive Behavioral Stress Management) have less stress and inflammation and better immune response, e.g. antibody response to influenza vaccine. More recently immune (B lymphocyte, antibodies) and metabolic (higher) conditions were characterized. We previously showed the stress reduction group had better long term (11 year) survival. Currently we are further analyzing negative and positive contributors to immune response in cancer patients including age and body mass. Supported by grants from NIH (R01 AI)", Florida Breast Cancer and SCCC

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29

Giampazolias, Evangelos, Mariana Pereira da Costa, Khiem C. Lam, Kok Haw Jonathan Lim, Ana Cardoso, Cécile Piot, Probir Chakravarty, et al. "Vitamin D regulates microbiome-dependent cancer immunity." Science 384, no. 6694 (April 26, 2024): 428–37. http://dx.doi.org/10.1126/science.adh7954.

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A role for vitamin D in immune modulation and in cancer has been suggested. In this work, we report that mice with increased availability of vitamin D display greater immune-dependent resistance to transplantable cancers and augmented responses to checkpoint blockade immunotherapies. Similarly, in humans, vitamin D–induced genes correlate with improved responses to immune checkpoint inhibitor treatment as well as with immunity to cancer and increased overall survival. In mice, resistance is attributable to the activity of vitamin D on intestinal epithelial cells, which alters microbiome composition in favor of Bacteroides fragilis , which positively regulates cancer immunity. Our findings indicate a previously unappreciated connection between vitamin D, microbial commensal communities, and immune responses to cancer. Collectively, they highlight vitamin D levels as a potential determinant of cancer immunity and immunotherapy success.

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30

Li, Mengyuan, Zhixian Liu, and Xiaosheng Wang. "Exploration of the Combination of PLK1 Inhibition with Immunotherapy in Cancer Treatment." Journal of Oncology 2018 (December 2, 2018): 1–13. http://dx.doi.org/10.1155/2018/3979527.

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Background. PLK1 overexpression is oncogenic and is associated with poor prognosis in various cancers. However, the current PLK1 inhibitors have achieved limited clinical successes. On the other hand, although immunotherapies are demonstrating efficacy in treating many refractory cancers, a substantial number of patients do not respond to such therapies. The potential of combining PLK1 inhibition with immunotherapy for cancer treatment is worthy of exploration. Methods. We analyzed the associations of PLK1 expression with tumor immunity in 33 different cancer types. Moreover, we analyzed the associations of the drug sensitivities of PLK1 inhibitors with tumor immunity in cancer cell lines. Furthermore, we explored the mechanism underlying the significant associations between PLK1 and tumor immunity. Finally, we experimentally verified some findings from bioinformatics analysis. Results. The cancers with higher PLK1 expression levels tended to have lower immune activities, such as lower HLA expression and decreased B cells, NK cells and tumor-infiltrating lymphocytes infiltration. On the other side, elevated tumor immunity likely increased the sensitivity of cancer cells to PLK1 inhibitors. The main mechanism underlying the associations between PLK1 and tumor immunity may lie in the aberrant cell cycle and p53 pathways in cancers. Conclusions. Our findings implicate that the PLK1 inhibition and immunotherapy combination may achieve a synergistic antitumor efficacy.

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31

Wang, Xiaoping, and Qiaoxia Wang. "Alpha-Fetoprotein and Hepatocellular Carcinoma Immunity." Canadian Journal of Gastroenterology and Hepatology 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/9049252.

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Hepatocarcinoma is one of the most prevalent gastroenterological cancers in the world with less effective therapy. As an oncofetal antigen and diagnostic marker for liver cancer, alpha-fetoprotein (AFP) possesses a variety of biological functions. Except for its diagnosis in liver cancer, AFP has become a target for liver cancer immunotherapy. Although the immunogenicity of AFP is weak and it could induce the immune escapes through inhibiting the function of dendritic cells, natural killer cells, and T lymphocytes, AFP has attracted more attention in liver cancer immunotherapy. By in vitro modification, the immunogenicity and immune response of AFP could be enhanced. AFP-modified immune cell vaccine or peptide vaccine has displayed the specific antitumor immunity against AFP-positive tumor cells and laid a better foundation for the immunotherapy of liver cancer.

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32

Tiri, Alessandra, Riccardo Masetti, Francesca Conti, Anna Tignanelli, Elena Turrini, Patrizia Bertolini, Susanna Esposito, and Andrea Pession. "Inborn Errors of Immunity and Cancer." Biology 10, no. 4 (April 9, 2021): 313. http://dx.doi.org/10.3390/biology10040313.

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Inborn Errors of Immunity (IEI) are a heterogeneous group of disorders characterized by a defect in the function of at least one, and often more, components of the immune system. The aim of this narrative review is to discuss the epidemiology, the pathogenesis and the correct management of tumours in patients with IEI. PubMed was used to search for all of the studies published over the last 20 years using the keywords: “inborn errors of immunity” or “primary immunodeficiency” and “cancer” or “tumour” or “malignancy”. Literature analysis showed that the overall risk for cancer in children with IEI ranges from 4 to 25%. Several factors, namely, age of the patient, viral infection status and IEI type can influence the development of different cancer types. The knowledge of a specific tumour risk in the presence of IEI highlights the importance of a synergistic effort by immunologists and oncologists in tracking down the potential development of cancer in known IEI patients, as well as an underlying IEI in patients with newly diagnosed cancers. In the current genomic era, the creation of an international registry of IEI cases integrated with malignancies occurrence information is fundamental to optimizing the diagnostic process and to evaluating the outcomes of new therapeutic options, with the hope to obtain a better prognosis for these patients.

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33

H Tan, Peng, Mingrui Xie, and Eleftherios Sfakianakis. "Complex interaction of adipokines in breast cancer and anti-tumour immunity; a new paradigm for cancer treatment." Cancer Research and Cellular Therapeutics 5, no. 2 (June 9, 2021): 01–16. http://dx.doi.org/10.31579/2640-1053/077.

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Obesity and its related complications have been the pressing disease pandemic affecting the developed world. It is well-established that the direct consequence of obesity in the cardiovascular system resulting in many diseases. However, its implications in carcinogenesis, cancer treatment and one’s anti-tumour immunity are gradually unfolding. To understand how fat cells can affect these, one needs to explore how the fat cell affects epithelial and immune cells. To this end, we explore the way how the adipocytes, via its production of adipokines, influence these cells, resulting in early epithelial cell transformation into cancer cells and influencing anti-tumour immunity once the cancer is established. In order to simplify our discussion, we focus this review on breast cancer. We propose that to have an effective therapy for cancer treatment, we need to intervene at the adipokine interaction with epithelial cells, cancer cells, and immune cells. In this review we also decipher the potential therapeutic targets in controlling carcinogenesis and disease progression.

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Singh, Dr Ravi Pratap. "HLA A24 Associated Tumor Immunity in HER2/neu Positive Breast Cancer." Recent Advances in Pathology & Laboratory Medicine 3, no. 2 (August 21, 2017): 13–16. http://dx.doi.org/10.24321/2454.8642.201702.

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35

Badia-Ramentol, Jordi, Jenniffer Linares, Andrea Gómez-Llonin, and Alexandre Calon. "Minimal Residual Disease, Metastasis and Immunity." Biomolecules 11, no. 2 (January 20, 2021): 130. http://dx.doi.org/10.3390/biom11020130.

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Progression from localized to metastatic disease requires cancer cells spreading to distant organs through the bloodstream. Only a small proportion of these circulating tumor cells (CTCs) survives dissemination due to anoikis, shear forces and elimination by the immune system. However, all metastases originate from CTCs capable of surviving and extravasating into distant tissue to re-initiate a tumor. Metastasis initiation is not always immediate as disseminated tumor cells (DTCs) may enter a non-dividing state of cell dormancy. Cancer dormancy is a reversible condition that can be maintained for many years without being clinically detectable. Subsequently, late disease relapses are thought to be due to cancer cells ultimately escaping from dormant state. Cancer dormancy is usually associated with minimal residual disease (MRD), where DTCs persist after intended curative therapy. Thus, MRD is commonly regarded as an indicator of poor prognosis in all cancers. In this review, we examine the current understanding of MRD and immunity during cancer progression to metastasis and discuss clinical perspectives for oncology.

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36

Prendeville, Hannah, and Lydia Lynch. "Diet, lipids, and antitumor immunity." Cellular & Molecular Immunology 19, no. 3 (January 5, 2022): 432–44. http://dx.doi.org/10.1038/s41423-021-00781-x.

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AbstractTumour growth and dissemination is largely dependent on nutrient availability. It has recently emerged that the tumour microenvironment is rich in a diverse array of lipids that increase in abundance with tumour progression and play a role in promoting tumour growth and metastasis. Here, we describe the pro-tumorigenic roles of lipid uptake, metabolism and synthesis and detail the therapeutic potential of targeting lipid metabolism in cancer. Additionally, we highlight new insights into the distinct immunosuppressive effects of lipids in the tumour microenvironment. Lipids threaten an anti-tumour environment whereby metabolic adaptation to lipid metabolism is linked to immune dysfunction. Finally, we describe the differential effects of commondietary lipids on cancer growth which may uncover a role for specific dietary regimens in association with traditional cancer therapies. Understanding the relationship between dietary lipids, tumour, and immune cells is important in the context of obesity which may reveal a possibility to harness the diet in the treatment of cancers.

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37

Krishnamoorthy, Mithunah, John G. Lenehan, Jeremy P. Burton, and Saman Maleki Vareki. "Immunomodulation in Pancreatic Cancer." Cancers 12, no. 11 (November 12, 2020): 3340. http://dx.doi.org/10.3390/cancers12113340.

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Pancreatic cancer has a high mortality rate, and its incidence is increasing worldwide. The almost universal poor prognosis of pancreatic cancer is partly due to symptoms presenting only at late stages and limited effective treatments. Recently, immune checkpoint blockade inhibitors have drastically improved patient survival in metastatic and advanced settings in certain cancers. Unfortunately, these therapies are ineffective in pancreatic cancer. However, tumor biopsies from long-term survivors of pancreatic cancer are more likely to be infiltrated by cytotoxic T-cells and certain species of bacteria that activate T-cells. These observations suggest that T-cell activation is essential for anti-tumor immunity in pancreatic cancers. This review discusses the immunological mechanisms responsible for effective anti-tumor immunity and how immune-based strategies can be exploited to develop new pancreatic cancer treatments.

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38

Li, Mengyuan, Yuxiang Ma, You Zhong, Qian Liu, Canping Chen, Lei Qiang, and Xiaosheng Wang. "KALRN mutations promote antitumor immunity and immunotherapy response in cancer." Journal for ImmunoTherapy of Cancer 8, no. 2 (October 2020): e000293. http://dx.doi.org/10.1136/jitc-2019-000293.

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Backgroundkalirin RhoGEF kinase (KALRN) is mutated in a wide range of cancers. Nevertheless, the association between KALRN mutations and the pathogenesis of cancer remains unexplored. Identification of biomarkers for cancer immunotherapy response is crucial because immunotherapies only show beneficial effects in a subset of patients with cancer.MethodsWe explored the correlation between KALRN mutations and antitumor immunity in 10 cancer cohorts from The Cancer Genome Atlas program by the bioinformatics approach. Moreover, we verified the findings from the bioinformatics analysis with in vitro and in vivo experiments. We explored the correlation between KALRN mutations and immunotherapy response in five cancer cohorts receiving immune checkpoint blockade therapy.ResultsAntitumor immune signatures were more enriched in KALRN-mutated than KALRN-wildtype cancers. Moreover, KALRN mutations displayed significant correlations with increased tumor mutation burden and the microsatellite instability or DNA damage repair deficiency genomic properties, which may explain the high antitumor immunity in KALRN-mutated cancers. Also, programmed cell death 1 ligand (PD-L1) expression was markedly upregulated in KALRN-mutated versus KALRN-wildtype cancers. The increased antitumor immune signatures and PD-L1 expression in KALRN-mutated cancers may favor the response to immune checkpoint blockade therapy in this cancer subtype, as evidenced in five cancer cohorts receiving antiprogrammed cell death protein 1 (PD-1)/PD-L1/cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) immunotherapy. Furthermore, the significant association between KALRN mutations and increased antitumor immunity was associated with the fact that KALRN mutations compromised the function of KALRN in targeting Rho GTPases for the regulation of DNA damage repair pathways. In vitro and in vivo experiments validated the association of KALRN deficiency with antitumor immunity and the response to immune checkpoint inhibitors.ConclusionsThe KALRN mutation is a useful biomarker for predicting the response to immunotherapy in patients with cancer.

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Maiorino, Laura, Juliane Daßler-Plenker, Lijuan Sun, and Mikala Egeblad. "Innate Immunity and Cancer Pathophysiology." Annual Review of Pathology: Mechanisms of Disease 17, no. 1 (January 24, 2022): 425–57. http://dx.doi.org/10.1146/annurev-pathmechdis-032221-115501.

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Chronic inflammation increases the risk of several cancers, including gastric, colon, and hepatic cancers. Conversely, tumors, similar to tissue injury, trigger an inflammatory response coordinated by the innate immune system. Cellular and molecular mediators of inflammation modulate tumor growth directly and by influencing the adaptive immune response. Depending on the balance of immune cell types and signals within the tumor microenvironment, inflammation can support or restrain the tumor. Adding to the complexity, research from the past two decades has revealed that innate immune cells are highly heterogeneous and plastic, with variable phenotypes depending on tumor type, stage, and treatment. The field is now on the cusp of being able to harness this wealth of data to ( a) classify tumors on the basis of their immune makeup, with implications for prognosis, treatment choice, and clinical outcome, and ( b) design therapeutic strategies that activate antitumor immune responses by targeting innate immune cells.

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40

Cullen, S. P., M. Brunet, and S. J. Martin. "Granzymes in cancer and immunity." Cell Death & Differentiation 17, no. 4 (January 15, 2010): 616–23. http://dx.doi.org/10.1038/cdd.2009.206.

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41

Rani, Aradhana, and John J. Murphy. "STAT5 in Cancer and Immunity." Journal of Interferon & Cytokine Research 36, no. 4 (April 2016): 226–37. http://dx.doi.org/10.1089/jir.2015.0054.

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42

Cohen, Sheldon, and Bruce S. Rabin. "Psychologic Stress, Immunity, and Cancer." JNCI: Journal of the National Cancer Institute 90, no. 1 (January 7, 1998): 3–4. http://dx.doi.org/10.1093/jnci/90.1.3.

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43

Pence, Barbara C., and Dale M. Dunn. "Vitamin D, Cancer and Immunity." Journal of Nutritional Immunology 2, no. 1 (July 13, 1993): 109–25. http://dx.doi.org/10.1300/j053v02n01_10.

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44

Good, Robert A., and Ellen Lorenz. "Nutrition, Immunity, Aging, and Cancer." Nutrition Reviews 46, no. 2 (April 27, 2009): 62–67. http://dx.doi.org/10.1111/j.1753-4887.1988.tb05388.x.

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45

Lim, Raymond J., Bin Liu, Kostyantyn Krysan, and Steven M. Dubinett. "Lung Cancer and Immunity Markers." Cancer Epidemiology Biomarkers & Prevention 29, no. 12 (August 20, 2020): 2423–30. http://dx.doi.org/10.1158/1055-9965.epi-20-0716.

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46

Van Epps, Heather L. "Boosting innate immunity in cancer." Journal of Experimental Medicine 201, no. 9 (May 2, 2005): 1353. http://dx.doi.org/10.1084/jem2019iti3.

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47

Knuth, Alexander. "Cancer immunity hits multiple myeloma." Blood 105, no. 10 (May 15, 2005): 3765–66. http://dx.doi.org/10.1182/blood-2005-03-0868.

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48

Valdés-Ramos, Roxana, and Alejandra D. Benítez-Arciniega. "Nutrition and immunity in cancer." British Journal of Nutrition 98, S1 (October 2007): S127—S132. http://dx.doi.org/10.1017/s0007114507833009.

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Abstract:

The purpose of this article is to give a general overview of the effects of nutrition on the development of cancer as well as part of a therapeutic approach. There is much evidence that diet and lifestyle can alter the risk of cancer development as is the case for many other chronic diseases. This may be through a direct action on the immune system, either by enhancing or suppressing it, as well as on the development of the tumour itself, by modulating gene expression or by antioxidant activity. Protective effects can be achieved by adequate intakes of vitamins A and C, β-carotene, selenium and n-3 fatty acids among others, while negative effects are found mainly with high intakes of n-6 and saturated fatty acids. Weight gain, obesity and lack of regular physical activity have also been associated with an increased risk of cancer. The protective effects are best observed when adequate diet and lifestyle are present together. With respect to the therapeutic role of nutrition in cancer, it has been observed that the use of pre- or post-operative enteral or parenteral nutrition may improve patients' survival rates and quality of life; however, more research is needed in this particular area. Breast, colon, rectum, prostate, stomach and lung are the types of cancer most commonly associated with diet or dietary components.

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Tan, Ting-Ting, and Lisa M. Coussens. "Humoral immunity, inflammation and cancer." Current Opinion in Immunology 19, no. 2 (April 2007): 209–16. http://dx.doi.org/10.1016/j.coi.2007.01.001.

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Maruyama, Kouji, Zohair Selmani, Hidee Ishii, and Ken Yamaguchi. "Innate immunity and cancer therapy." International Immunopharmacology 11, no. 3 (March 2011): 350–57. http://dx.doi.org/10.1016/j.intimp.2010.09.012.

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