Radiation Therapy Weaken Immune System – For many patients undergoing radiation therapy, their immune systems are not affected by radiation therapy. That’s because radiation is aimed at specific targets in the body and can be designed to avoid the bone marrow, where cells make up the immune system.
However, there are some patients who receive radiation therapy who may be at risk of infection due to a weakened immune system. It is more common in patients receiving concurrent chemotherapy or radiation treatment regimens that require large amounts of bone marrow to be exposed to radiation.
Radiation Therapy Weaken Immune System
Here we provide information on how radiotherapy affects the immune system and tips on how to improve your immunity during and after treatment.
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Radiotherapy uses high doses of radiation to target cancer cells. Although treatment is usually localized, healthy cells near cancerous areas can sometimes be damaged.
If stem cells in the bone marrow are damaged by radiotherapy, the body struggles to produce white blood cells (WBCs). Also known as leukocytes, WBCs are responsible for attacking disease-causing organisms such as bacteria, viruses, parasites, and fungi.
When the number of white blood cells is low – a condition called leukopenia – the body can be vulnerable to infection.
Radiation that targets large areas of bone is also likely to suppress the immune system, because the production of white blood cells in the bone marrow is inhibited.
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However, patients who receive radiation to their entire body (called total body radiation) are at the highest risk of immune suppression. This treatment is used only in very special cases, usually in preparation for a bone marrow transplant.
The skin forms a physical barrier against pathogens. In some cases, high doses of radiation can damage the skin by creating breaks or wounds in the skin through which microbes enter the body. A radiation oncologist may prescribe topical treatments to reduce the risk of infection if you develop skin breakdown during treatment.
Like radiation therapy, chemotherapy targets and destroys cancer cells. However, there are important differences between the two treatment options.
While radiotherapy is placed in the cancer treatment area, chemotherapy enters the bloodstream to reach the entire body, including the bone marrow. In some cases, chemotherapy can affect the production of white blood cells. Because of this, chemotherapy is often more likely to weaken the immune system than radiotherapy. However, if your cancer care team offers a combination of both chemotherapy and radiation therapy, the risk of immune system suppression may increase.
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Your cancer care team may also prescribe medications that help your brain produce more white blood cells, which helps reduce the risk of infection.
For most patients undergoing radiation therapy, the effect on the bone marrow will be minimal. However, for patients whose immune systems have been compromised by treatment, it may take several weeks for the bone marrow to return to normal, and in rare cases, the weakness may be permanent.
At SERO, our expert radiation oncologists and care teams are here to help guide you through your cancer journey, from diagnosis to remission. This will help you understand how radiotherapy can affect your immune system.
Whether you have questions about increasing your white blood cell count or reducing your risk of infection during treatment, we are here to provide compassionate and compassionate care.
Md Radiotherapy And Oncology Course
We use cookies to give you the best experience on our website – by continuing to use our website, you accept the terms set out in our privacy policy Okay Radiotherapy (RT) is key in many types of cancer Healing is and works through mediation. Various forms of cancer cell death, although increasing the effectiveness of treatment is still a major problem. Radiation resistance is a major cause of cancer growth, so overcoming treatment resistance is now one of the biggest challenges for doctors. Growing evidence suggests that the immune response plays a role in reprogramming the radiation-induced tumor microenvironment (TME). Interestingly, radiation immunosuppression can enhance the immune system’s ability to destroy tumor cells. This creates an immune balance that we hypothesize allows the radiosensitizer to work. Vitamin D has been reported to act synergistically with RT by potentiating treatment-induced antiproliferative effects. In addition, vitamin D may regulate the TME and may also induce immunostimulation by preventing immunosuppression after radiation. Previous reviews have focused on vitamin D metabolism and epidemiological trials, but the synergistic effects of vitamin D and current treatments are unknown. This review summarizes vitamin D radiosensitivity, radiation resistance, and vitamin D-regulated TME that may contribute to successful vitamin D-adjuvant radiotherapy.
Radiotherapy (RT) is commonly the definitive treatment for many types of tumors, including colorectal cancer, nasal carcinoma, and cervical cancer (Chen et al., 2019; Cohen et al., 2019; Decker et al., 2019). ) are included. Radiation resistance is considered an important cause of tumor recurrence and local failure, is involved in various cellular molecular mechanisms and achieves therapeutic resistance of cancer cells. Although some strategies, such as radiosensitizers, have recently been investigated, sensitizers have been limited to preclinical studies due to the toxic effects of these agents.
Vitamin D, a fat-soluble steroid that mediates many physiological functions (Maurya et al., 2020), has been shown to be involved in anti-tumor activity in several cancers (Kem et al., 2019). In addition, accumulating data indicate that vitamin D utilizes multiple mechanisms to enhance radiation-induced tumor cell elimination (Sundaram and Gewirtz, 1999; Chowdhury et al., 2001; Bristol et al., 2012; Sharma et al., 2014). ). Thus, a deeper understanding of how vitamin D interacts with RT in cancer may aid in the development of effective sensitizers to overcome radioresistance.
It should be noted that the immune system plays an important role in the response to RT (Chen et al., 2019). Radiation can lead to both positive and negative regulation of the immune response, and this has been observed not only in tumor cells, but also in the tumor microenvironment (TME). Importantly, vitamin D is also involved in the immune microenvironment (Cheroengam and Holick, 2020), although the underlying mechanism has not been clearly elucidated.
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Although there is a growing awareness of the importance of vitamin D in the response of tumor cells to radiation, there are few reviews reporting the underlying mechanism. In this review, we briefly present the mechanisms influencing vitamin D and radiosensitivity. In addition, we discuss how the immune response is regulated in response to RT. Finally, we present the modulation of the TME by vitamin D and illustrate the complex relationship between vitamin D, radiation, and antitumor immunity.
Vitamin D is produced from 7-dehydrocholesterol in human skin after exposure to ultraviolet rays in sunlight, so it is affected by climate, latitude, skin pigmentation and cultural habits. In addition, dietary habits and supplements may also affect vitamin D levels (Amrin et al., 2020). Cytochrome P450-mediated two-step catalysis is an important process in the production of the steroid hormone calcitriol (the organic form of vitamin D) ( Jones et al., 2014 ). The less active form of vitamin D, 25(OH)D
, is produced in the liver after the first hydroxylation by vitamin D 25-hydroxylase (CYP2R1 and CYP27A1) (Baikal, 2014). 25(OH)D
It is known that the main form of circulation of vitamin D is in the blood, but there is no general consensus about the threshold level. Recently, 25(OH)D levels of 75–150 nmol/L (30–60 ng/mL) have been suggested to be the optimal vitamin D threshold ( Bischoff-Ferrari et al., 2016 ). An association between 25(OH)D levels and cancer risk has been reported in several solid cancers (Yao et al., 2017; Ramakrishnan et al., 2019; Yuan et al., 2019) and higher circulating 25(OH)D levels. has been described. . level contributes to a better prognosis of colon cancer (Markotic et al., 2019). Next, kidney 25 (OH) d
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As a substrate and convert it to 1, 25-dihydroxy-vitamin D3, which is hydroxylated by CYP27B1 (Jones et al., 2014).
(Jones et al., 2012). Interestingly, either activation of the catabolic enzyme CYP24A1 by calcidol or calcitriol or inactivation of CYP27B1 by calcitriol may lead to a negative feedback loop for vitamin D regulation and the role of CYP24A1 as an important mediator rather than a rate limiter. can increase Vitamin D production, but hormone autoregulation, likely corrects hypercalcemia. Hypercalcemia due to increased concentration of calcitriol or decreased blood concentration due to its instability may certainly limit its clinical use. This eventually led to the investigation of calcitriol analogues that may have equal or enhanced anticancer activities with fewer side effects (Jones, 2010).
Able to regulate the expression of multiple genes depending on tissues, cell types and context (Karlberg and Muñoz, 2020). By binding to the vitamin D receptor (VDR), 1, 25 (OH).
Dimerization with the retinoid X receptor (RXR), which promotes nuclear translocation of this complex and drives vitamin D response elements (VDREs) to target genes, is followed by recruitment of co-modulators. Therefore, calcitriol may interfere with the expression of target genes in the genomic pathway (Karlberg and Munoz, 2020). It acts genomically, through which 1, 25 (OH)
Radiation Therapy And The Innate Immune Response: Clinical Implications For Immunotherapy Approaches
It is a VDR-RXR complex
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