Survival Time Of Cancer Patients Research Articles

[Exploration and practice of cardio-oncology].

With the improvement of oncology diagnosis and treatment, the survival time of cancer patients has been significantly prolonged, and the cancer therapy-related cardiovascular toxicity such as radiotherapy, chemotherapy, immunotherapy, and surgery are becoming more and more prominent, and it is in this context that the germ of Cardio-Oncology exploration has come into being. The multidisciplinary Cardio-Oncology team aims to establish a multidisciplinary prevention and control system to assess patients' baseline risk factors, individualized monitoring, and weighing the risk-benefit ratio of cancer therapy. At present, the connotation of the discipline of Cardio-Oncology has been expanded horizontally and deepened vertically in China, and Cardio-Oncology treatment centers have blossomed all over the country. Moreover, international and domestic scholars continue to improve Cardio-Oncology guidelines and consensus through their own practice, and develop artificial intelligence software to help the development of the discipline. It is believed that in the future, with the training of Cardio-Oncologists and the output of high-quality clinical research evidence, cardiovascular safety of cancer patients can be ensured more scientifically and effectively.

The role of ferroptosis in cardio-oncology.

With the rapid development of new generations of antitumor therapies, the average survival time of cancer patients is expected to be continuously prolonged. However, these therapies often lead to cardiotoxicity, resulting in a growing number of tumor survivors with cardiovascular disease. Therefore, a new interdisciplinary subspecialty called "cardio-oncology"has emerged, aiming to detect and treat cardiovascular diseases associated with tumors and antitumor therapies. Recent studies have highlighted the role of ferroptosis in both cardiovascular and neoplastic diseases. The balance between intracellular oxidative stress and antioxidant defense is crucial in regulating ferroptosis. Tumor cells can evade ferroptosis by upregulating multiple antioxidant defense pathways, while many antitumor therapies rely on downregulating antioxidant defense and promoting ferroptosis in cancer cells. Unfortunately, these ferroptosis-inducing antitumor therapies often lack tissue specificity and can also cause injury to the heart, resulting in ferroptosis-induced cardiotoxicity. A range of cardioprotective agents exert cardioprotective effects by inhibiting ferroptosis. However, these cardioprotective agents might diminish the efficacy of antitumor treatment due to their antiferroptotic effects. Most current research on ferroptosis only focuses on either tumor treatment or heart protection but rarely considers both in concert. Therefore, further research is needed to study how to protect the heart during antitumor therapies by regulating ferroptosis. In this review, we summarized the role of ferroptosis in the treatment of neoplastic diseases and cardiovascular diseases and also attempted to propose further research directions for ferroptosis in the field of cardio-oncology.

A weighted distance-based dynamic ensemble regression framework for gastric cancer survival time prediction

Accurate prediction of gastric cancer patient survival time is essential for clinical decision-making. However, unified static models lack specificity and flexibility in predictions owing to the varying survival outcomes among gastric cancer patients. We address these problems by using an ensemble learning approach and adaptively assigning greater weights to similar patients to make more targeted predictions when predicting an individual’s survival time. We treat these problems as regression problems and introduce a weighted dynamic ensemble regression framework. To better identify similar patients, we devise a method to measure patient similarity, considering the diverse impacts of features. Subsequently, we use this measure to design both a weighted K-means clustering method and a fuzzy K-means sampling technique to group patients and train corresponding base regressors. To achieve more targeted predictions, we calculate the weight of each base regressor based on the similarity between the patient to be predicted and the patient clusters, culminating in the integration of the results. The model is validated on a dataset of 7791 patients, outperforming other models in terms of three evaluation metrics, namely, the root mean square error, mean absolute error, and the coefficient of determination. The weighted dynamic ensemble regression strategy can improve the baseline model by 1.75%, 2.12%, and 13.45% in terms of the three respective metrics while also mitigating the imbalanced survival time distribution issue. This enhanced performance has been statistically validated, even when tested on six public datasets with different sizes. By considering feature variations, patients with distinct survival profiles can be effectively differentiated, and the model predictive performance can be enhanced. The results generated by our proposed model can be invaluable in guiding decisions related to treatment plans and resource allocation. Furthermore, the model has the potential for broader applications in prognosis for other types of cancers or similar regression problems in various domains.

Synergistic effects of immune checkpoints and checkpoint inhibitors in inflammatory neuropathies: Implications and mechanisms.

Immune checkpoint molecules play pivotal roles in the regulation of immune homeostasis. Disruption of the immune checkpoints causes autoimmune/inflammatory as well as malignant disorders. Over the past few years, the immune checkpoint molecules with inhibitory function emerged as potential therapeutic targets in oncological conditions. The inhibition of the function of these molecules by using immune checkpoint inhibitors (ICIs) has brought paradigmatic changes in cancer therapy due to their remarkable clinical benefits, not only in improving the quality of life but also in prolonging the survival time of cancer patients. Unfortunately, the ICIs soon turned out to be a "double-edged sword" as the use of ICIs caused multiple immune-related adverse effects (irAEs). The development of inflammatory neuropathies such as Guillain-Barré syndrome (GBS) and Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) as the secondary effects of immunotherapy appeared very challenging as these conditions result in significant and often permanent disability. The underlying mechanism(s) through which ICIs trigger inflammatory neuropathies are currently not known. Compelling evidence suggests autoimmune reaction and/or inflammation as the independent risk mechanism of inflammatory neuropathies. There is a lack of understanding as to whether prior exposure to the risk factors of inflammatory neuropathies, the presence of germline genetic variants in immune function-related genes, genetic variations within immune checkpoint molecules, the existence of autoantibodies, and activated/memory T cells act as determining factors for ICI-induced inflammatory neuropathies. Herein, we highlight the available pieces of evidence, discuss the mechanistic basis, and propose a few testable hypotheses on inflammatory neuropathies as irAEs of immunotherapy.

Driver gene KRAS aggravates cancer-associated stroke outcomes

The incidence of cancer-associated stroke has increased with the prolonged survival times of cancer patients. Recent genetic studies have led to progress in cancer therapeutics, but relationships between oncogenic mutations and stroke remain elusive. Here, we focused on the driver gene KRAS, which is the predominant RAS isoform mutated in multiple cancer types, in cancer associated stroke study. KRASG13D/− and parental human colorectal carcinoma HCT116 cells were inoculated into mice that were then subjected to a photochemically-induced thrombosis model to establish ischemic stroke. We found that cancer inoculation exacerbated neurological deficits after stroke. Moreover, mice inoculated with KRASG13D/− cells showed worse neurological deficits after stroke compared with mice inoculated with parental cells. Stroke promoted tumor growth, and the KRASG13D/− allele enhanced this growth. Brain RNA sequencing analysis and serum ELISA showed that chemokines and cytokines mediating pro-inflammatory responses were upregulated in mice inoculated with KRASG13D/− cells compared with those inoculated with parental cells. STAT3 phosphorylation was promoted following ischemic stroke in the KRASG13D/− group compared with in the parental group, and STAT3 inhibition significantly ameliorated stroke outcomes by mitigating microglia/macrophage polarization. Finally, we compared the prognosis and mortality of colorectal cancer patients with or without stroke onset between 1 January 2007 and 31 December 2020 using a hospital-based cancer registry and found that colorectal cancer patients with stroke onset within 3 months after cancer diagnosis had a worse prognosis. Our work suggests an interplay between KRAS and ischemic stroke that may offer insight into future treatments for cancer-associated stroke.

Restoration of p53 functions by suppression of mortalin-p53 sequestration: an emerging target in cancer therapy.

Functional inactivation of wild-type p53 is a major traitof cancerous cells. In many cases, such inactivation occurs by either TP53 gene mutations or due to overexpression of p53 binding partners. This review focuses on an overexpressed p53 binding partner called mortalin, a mitochondrial heat shock protein that sequesters both wild-type and mutant p53 in malignant cells due to changes in subcellular localization. Clinical evidence suggestsa drastic depletion of the overall survival time of cancer patients with high mortalin expression. Therefore, mortalin-p53 sequestration inhibitors could begame changers in improving overall survival rates. This review explores the consequences of mortalin overexpression and challenges, statusand strategies for accelerating drug discovery to suppress mortalin-p53 sequestration.

KITENIN promotes aerobic glycolysis through PKM2 induction by upregulating the c-Myc/hnRNPs axis in colorectal cancer

PurposeThe oncoprotein KAI1 C-terminal interacting tetraspanin (KITENIN; vang-like 1) promotes cell metastasis, invasion, and angiogenesis, resulting in shorter survival times in cancer patients. Here, we aimed to determine the effects of KITENIN on the energy metabolism of human colorectal cancer cells.Experimental designThe effects of KITENIN on energy metabolism were evaluated using in vitro assays. The GEPIA web tool was used to extrapolate the clinical relevance of KITENIN in cancer cell metabolism. The bioavailability and effect of the disintegrator of KITENIN complex compounds were evaluated by LC–MS, in vivo animal assay.ResultsKITENIN markedly upregulated the glycolytic proton efflux rate and aerobic glycolysis by increasing the expression of GLUT1, HK2, PKM2, and LDHA. β-catenin, CD44, CyclinD1 and HIF-1A, including c-Myc, were upregulated by KITENIN expression. In addition, KITENIN promoted nuclear PKM2 and PKM2-induced transactivation, which in turn, increased the expression of downstream mediators. This was found to be mediated through an effect of c-Myc on the transcription of hnRNP isoforms and a switch to the M2 isoform of pyruvate kinase, which increased aerobic glycolysis. The disintegration of KITENIN complex by silencing the KITENIN or MYO1D downregulated aerobic glycolysis. The disintegrator of KITENIN complex compound DKC1125 and its optimized form, DKC-C14S, exhibited the inhibition activity of KITENIN-mediated aerobic glycolysis in vitro and in vivo.ConclusionsThe oncoprotein KITENIN induces PKM2-mediated aerobic glycolysis by upregulating the c-Myc/hnRNPs axis.

Current progress of immunotherapy based on NK cell in cancer therapy

Cancer generally refers to malignant tumor, including carcinoma, sarcoma and carcinosarcoma. This disease is caused by malignant cell hyperplasia. It is invasive and metastable. It is manifested by the continuous growth of a local mass of the body that destroys the normal tissue structure and can be transferred to other sites. It has been reported that there will be about 20 million new cases of cancer in 2020 and half of all cancer patients will die. Surgery, chemotherapy and radiotherapy, as the three standard treatment methods for cancer, plays an vital role in improving the survival rate and prolonging the survival time of cancer patients. In recent years, researchers have focused on the immune mechanism of tumors to explore the treatment of malignant tumors. Driven by the rapid development of modern molecular biology and gene engineering technology, immunotherapy has been paid more and more attention, showing good effect and application prospects, has become the world's recognized malignancy of the fourth treatment mode. Among these, natural killer cells (NK) fight cancer through their cytolytic function and the production of IFN-γ. One of the primary clinical objectives is to use their abilities for tumour immunotherapy. This article looks at advances in NK cell-based tumor therapy.

Effects of the Intake of Deuterium Depleted Water During Cancer Therapy: A Narrative Review

Drinking water has a deuterium (2H) concentration of 150 ppm. The intake of deuteriumdepleted water (DDW) provides a series of effects on the improvement of the state of health, contributing to the prevention of various diseases, as well as the delay in the evolution of certain types of cancer. The objective of this review is to verify the influence of DDW intake on the regression and survival rate of different types of cancer in living beings. The intake of DDW in patients with chronic lymphocytic leukemia, lung, prostate and breast cancer, as well as the antitumor effects of the intake of DDW in living beings, were analyzed. In conclusion, commenting that the intake of DDW has beneficial effects on the increase in the average survival time of cancer patients, favors the inhibition of cancer cell growth, increases the probability of total or partial regression of malignant tumors, as well as the delay in the multiplication of various types of tumor cells (PC-3, MDA, HT-29 and M14) and contributes to the decrease in PSA values in patients with prostate cancer.

A review on CRISPR/Cas: a versatile tool for cancer screening, diagnosis, and clinic treatment.

Cancer is one of the leading causes of death worldwide and it has the trend of increase incidence. However, in the past decades, as quickly developed new technologies and modified old techniques for cancer screening, diagnosis, and treatment, the cancer-caused mortality rates dropped quickly, and the survival times of cancer patients are enhanced. However, the current death rate is still about 50% and the survival patients always suffer from the side effect of current cancer treatments. Recently developed Nobel Prize-winning CRISPR/Cas technology provides new hope on cancer screening, early diagnosis, and clinic treatment as well as new drug development. Currently, four major CRISPR/Cas9-derived genome editors, CRISPR/Cas9 nucleotide sequence editor, CRISPR/Cas base editor(BE), CRISPR prime editor(PE), and CRISPR interference (CRISPRi) (including both CRISPRa and CRISPRr), were well developed and used to various research and applications, including cancer biology study and cancer screening, diagnosis, and treatment. Additionally, CRISPR/Cas12 and CRISPR/Cas13 genome editors were also widely used in cancer-related basic and applied research as well as treatment. Cancer-associated SNPs and genetic mutations as well as both oncogenes and tumor suppressor genes are perfect targets for CRISPR/Cas-based gene therapy for cancer treatment. CRISPR/Cas is also employed to modify and generate new Chimeric antigen receptor (CAR) T-cells for improving its safety, efficiency, and longer-time last for treating various cancers. Currently, there are many clinic trails of CRISPR-based gene therapy for cancer treatments. Although all CRISPR/Cas-derived genome and epigenome tools are promising methods for cancer biology study and treatment, the efficiency and long term-safety are still the major concerns for CRISPR-based gene therapy. Developing new CRISPR/Cas delivery methods and reducing the potential side effects, including off-target impacts, will enhance CRISPR/Cas application in cancer-related research, diagnosis, and therapeutical treatment.

Histone H3 phospho-regulation by KimH3 in both interphase and mitosis.

Histone H3 is phosphorylated at Ser10 by multiple kinases, and many of them are anti-cancer targets. Here, we report the first kinase that can phosphorylate H3Ser10 in both interphase and mitosis, which we named KimH3 (kinase of interphase and mitotic Histone H3). Meta-analysis indicates that KimH3 is upregulated in a broad spectrum of human cancers and its high expression is correlated with reduced the median survival time of cancer patients. In mitosis, CDK1 phosphorylates KimH3, which then phosphorylates H3Ser10 to regulate cell cycle procession. In interphase, EGF induces KimH3 activation and H3Ser10 phosphorylation, which is involved in MAPK-ERK1/2 signaling pathway to activate immediate-early genes transcription. Consequently, a small molecule inhibitor of KimH3 significantly inhibited tumor growth in mice. This is not only consistent with the dual roles of KimH3 in both interphase and mitotic Histone H3 phosphorylation, but also reveals it as an important potential anti-cancer target.

Survival Times of Lung, Breast, Cervical, and Prostate Cancer Patients in Africa

Cancer is a leading cause of death and disability in Africa, and addressing this disease remains a significant challenge for many African countries. This paper examines the survival times of cancer in Africa through a critical review of 38 publications that comprise 27,795 samples with lung, breast, cervical, and prostate cancer. The overall survival time at one year was 77.4%, and the loco-regional rate of survival at three years was 71.8%. For cervical, breast, lung, and prostate cancer, the five-month survival time was 73.1-79.9%. The mean survival times for lung cancer patients at one year was 78.2%, and the mean annual survival times at three years was 52.8%. The mean age at the time of the study was 57.6 years. Total estimated pooled survival times for cancer patients in Africa was 60.66% (95% CI: 56.27, 65.06). And, the survival times of cancer patients in Southern Africa is 14.30%, 26.21% in Eastern Africa, 24.51% in Western Africa, and 41.06% in Central Africa. To improve survival times of lung, breast, cervical, and prostate cancer patients in Africa, it is important to increase awareness about cancer and its risk factors. And consortia should be promoted, whereby regions in Africa that have better resources can serve as mentors.

Predictors of cognitive failures in cancer survivors.

Progress in cancer dia-gnostic and treatment increases the probability of survival and survival time in cancer patients. Current research focuses on the quality of life of cancer survivors and the late effects of treatment, which can take the form of cognitive failures in daily life. The aim of the presented research was to examine the relationships between subjectively-reported cognitive failures and selected socio-demographic, clinical, and psychological characteristics (age, hormonal treatment, depression, anxiety, fatigue, sleep satisfaction). The research sample consisted of 102 cancer survivors aged 25-79 years and a mean time since the end of the last treatment was 17.4 months (standard deviation = 15.4). The largest part of the sample consisted of breast cancer survivors (62.4%). The level of cognitive errors and failures was measured by the Cognitive Failures Questionnaire. The PHQ-9 Patient Health Questionnaire, the GAD-7 General Anxiety Disorder Scale, and the WHOQOL-BREF Quality of Life Questionnaire were used to measure depression, anxiety, and selected aspects of quality of life. An increased level of cognitive failures in daily life was found in approximately one-third of cancer survivors. The overall cognitive failures score is strongly related to the level of depression and anxiety. Decreasing levels of energy and sleep satisfaction are associated with increasing cognitive failures in everyday life. The age and hormonal therapy do not significantly differentiate the level of cognitive failures. In the regression model, which explained 34.4% of the variance of subjectively-reported cognitive functioning, depression was the only significant predictor. The study results mention relationship between subjective evaluation of cognitive functioning and emotional experience in cancer survivors. The administration of self-reported methods for measuring cognitive failures can be helpful in clinical practice in identifying psychological distress.

Diagnosing and Prognosing Bone Metastasis in Prostate Cancer: Clinical Utility of Blood Biomarkers.

Bone metastasis (BM) may occur in any type of cancer. The diagnosis of patients with BM has increased due to improved imaging technologies and advances in cancer drug therapy that have prolonged the survival time of cancer patients. BM may be asymptomatic in the early stages; however, as the disease progresses, it causes pain, fracture, neurological symptoms associated with spinal cord compression, hypercalcemia, and other specific symptoms that significantly impair the patient's quality of life (QOL). Imaging modalities have disadvantages, such as high cost, radiation exposure, and bone pain associated with holding posture for imaging test; further, they are time-consuming. Hence, patients with BM require convenient and useful biomarkers. However, no blood biomarkers generally useful for diagnosis and therapeutic monitoring of BM are established. Prostate cancer (PC) and breast cancer, in particular, are among the most prone to BM because BM occurs in approximately 70% of patients with advanced disease. Herein, we reviewed various potential bone turnover markers and liquid biopsy for diagnosis and prognosis prediction in patients with BM of PC based on PubMed literature search. The usefulness of conventional bone turnover markers of BM in PC is limited, and cut-off values vary. In the future, the creation of algorithms using these conventional markers and multiple tests, such as liquid biopsy and imaging tests, will help to develop highly accurate techniques for the diagnosis of BM.

A network medicine approach for identifying diagnostic and prognostic biomarkers and exploring drug repurposing in human cancer

Cancer is a heterogeneous disease mainly driven by abnormal gene perturbations in regulatory networks. Therefore, it is appealing to identify the common and specific perturbed genes from multiple cancer networks. We developed an integrative network medicine approach to identify novel biomarkers and investigate drug repurposing across cancer types. We used a network-based method to prioritize genes in cancer-specific networks reconstructed using human transcriptome and interactome data. The prioritized genes show extensive perturbation and strong regulatory interaction with other highly perturbed genes, suggesting their vital contribution to tumorigenesis and tumor progression, and are therefore regarded as cancer genes. The cancer genes detected show remarkable performances in discriminating tumors from normal tissues and predicting survival times of cancer patients. Finally, we developed a network proximity approach to systematically screen drugs and identified dozens of candidates with repurposable potential in several cancer types. Taken together, we demonstrated the power of the network medicine approach to identify novel biomarkers and repurposable drugs in multiple cancer types. We have also made the data and code freely accessible to ensure reproducibility and reusability of the developed computational workflow.

Data-driven intelligent decision for multimedia medical management

Since medical diagnosis runs through the whole journey of human health, the traditional medical diagnosis methods cannot ensure the diagnosis accurate due to the interference of multiple external factors. In response, this paper proposes a multimedia medical management method supported by the data-driven intelligent decision (MMD-DI). This method can be used to predict the survival time of cancer patients under the help of gradient boosting decision tree (GBDT) and hybrid neural network model. First, the feature factors were scanned to match the conditions by GBDT, according to the set value domain; Then the factors were inputted into the neural network. The hybrid neural network was employed to predict the survival time of cancer patients, and it was constructed by combining the convolutional neural network (CNN) and the long short-term memory (LSTM) model. Finally, the stability of the proposed MMD-DI was analyzed, and performance was compared with a series of commonly exploited baseline methods: the mean of cross-validated RMSE (Root Mean Squared Error) evaluation results is 0.183, the mean of cross-validated MAE (Mean Absolute Error) evaluation results is 0.147, the two indicators are both much lower than the commonly exploited baseline methods. A series of experiments proved that MMD-DI has excellent performance and can be used in the multimedia medical management systems.

The Application of CRISPR/Cas9 Technology for Cancer Immunotherapy: Current Status and Problems.

Cancer is one of the main causes of disease-related deaths in the world. Although cancer treatment strategies have been improved in recent years, the survival time of cancer patients is still far from satisfied. Cancer immunotherapy, such as Oncolytic virotherapy, Immune checkpoints inhibition, Chimeric antigen receptor T (CAR-T) cell therapy, Chimeric antigen receptor natural killer (CAR-NK) cell therapy and macrophages genomic modification, has emerged as an effective therapeutic strategy for different kinds of cancer. However, many patients do not respond to the cancer immunotherapy which warrants further investigation to optimize this strategy. The clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9 (CRISPR/Cas9), as a versatile genome engineering tool, has become popular in the biology research field and it was also applied to optimize tumor immunotherapy. Moreover, CRISPR-based high-throughput screening can be used in the study of immunomodulatory drug resistance mechanism. In this review, we summarized the development as well as the application of CRISPR/Cas9 technology in the cancer immunotherapy and discussed the potential problems that may be caused by this combination.

Constructing a Cancer Patient-Specific Network Based on Second-Order Partial Correlations of Gene Expression and DNA Methylation.

Typically patient-specific gene networks are constructed with gene expression data only. Such networks cannot distinguish direct gene interactions from indirect interactions via others such as the effect of epigenetic events to gene activity. There is an increasing evidence of inter-individual variations not only in gene expression but also in epigenetic events such as DNA methylation. In this paper we propose a new method for constructing a cancer patient-specific gene correlation network using both gene expression and DNA methylation data. We derive a patient-specific network from differential second-order partial correlations of gene expression and DNA methylation between normal samples and the patient sample. The network represents direct interactions between genes by controlling the effect of DNA methylation. Using this method, we constructed 4,000 patient-specific networks for 10 types of cancer. The networks are highly effective in classifying different types of cancer and in deriving potential prognostic gene pairs. In particular, potential prognostic gene pairs derived from the networks were powerful in predicting the survival time of cancer patients. This approach will help identify patient-specific gene correlations and predict prognosis of cancer patients.

Virtual Screening for Potential Phytobioactives as Therapeutic Leads to Inhibit NQO1 for Selective Anticancer Therapy.

NAD(P)H:quinone acceptor oxidoreductase-1 (NQO1) is a ubiquitous flavin adenine dinucleotide-dependent flavoprotein that promotes obligatory two-electron reductions of quinones, quinonimines, nitroaromatics, and azo dyes. NQO1 is a multifunctional antioxidant enzyme whose expression and deletion are linked to reduced and increased oxidative stress susceptibilities. NQO1 acts as both a tumor suppressor and tumor promoter; thus, the inhibition of NQO1 results in less tumor burden. In addition, the high expression of NQO1 is associated with a shorter survival time of cancer patients. Inhibiting NQO1 also enables certain anticancer agents to evade the detoxification process. In this study, a series of phytobioactives were screened based on their chemical classes such as coumarins, flavonoids, and triterpenoids for their action on NQO1. The in silico evaluations were conducted using PyRx virtual screening tools, where the flavone compound, Orientin showed a better binding affinity score of −8.18 when compared with standard inhibitor Dicumarol with favorable ADME properties. An MD simulation study found that the Orientin binding to NQO1 away from the substrate-binding site induces a potential conformational change in the substrate-binding site, thereby inhibiting substrate accessibility towards the FAD-binding domain. Furthermore, with this computational approach we are offering a scope for validation of the new therapeutic components for their in vitro and in vivo efficacy against NQO1.

Survival Time among Young and Old Breast Cancer Patients in Relation to Circulating Blood-Based Biomarkers, Acute Radiation Skin Reactions, and Tumour Recurrence

Introduction: It has been suggested that age could influence the treatment-induced side effects and survival time of cancer patients. The influence of age on blood-based biomarkers, acute radiation skin reactions (ARSRs), and survival time of breast cancer patients was analysed. Materials and Methods: Two hundred ninety-three individuals, 119 breast cancer patients, and 174 healthy blood donors were included. Results: Before radiotherapy (RT), decreased levels of lymphocytes, interleukin 2, platelet-derived growth factors, and tumour necrosis factor but increased levels of monocyte-to-lymphocyte ratio, neutrophil-to-lymphocyte ratio, C-reactive protein, and macrophage inflammatory protein 1b (MIP1b) were detected in the patient group. All of the patients developed ARSRs and intensity of ARSRs was inversely related to the MIP1b level before RT. Fifteen out of 119 (13%) patients deceased during follow-up time. No influence of age (≤50 compared to >50 years) on survival time was detected (p = 0.442). Tumour recurrence, found in 11 out of 119 (9%) patients, had impact on survival time of these patients (p < 0.001). Conclusions: The level of circulating MIP1b before RT was associated with intensity of ARSRs. Tumour recurrence, but not age, was associated with poor survival time. Analysis of circulating MIP1b was low cost, rapid, and could be done in routine laboratory facility. Since RT almost always induces ARSRs, the possibility of using MIP1b as a prognostic biomarker for ARSRs is of interests for further investigation.