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. 2025 Sep 4;8(9):e71208. doi: 10.1002/hsr2.71208

Investigation of ESR Values in the Diagnosis of Malignancies: A Cross‐Sectional Study

Omid Abdollahi 1,2, Tina Vosoughi 1,2,, Afshin Talebi 1,2, Hossein Karimpourian 2, Mohammadhossein Rastegar 2, Elham Farhadi 3
PMCID: PMC12411560  PMID: 40918030

ABSTRACT

Background and Aim

Cancer is currently recognized as one of the leading causes of mortality worldwide. Given the limited understanding of the association between elevated erythrocyte sedimentation rate (ESR) and solid tumors (STs), this study aimed to examine ESR values at the time of malignancy diagnosis.

Methods

This cross‐sectional study utilized data extracted from the medical records of cancer patients at Shahid Baghaei‐2 Hospital and Shafa Hospital in Ahvaz, Iran, from February 2020 to October 2021. Patients diagnosed with leukemia, lymphoma, or multiple myeloma (MM) were excluded from the analysis. The ESR values, measured during the first hour at the onset of ST diagnosis, were documented. This is because in Iranian laboratories, ESR is checked during the first hour. Subsequently, patients were categorized based on age, gender, type of malignancy, and disease stage.

Results

Of the 428 cancer patients included, 259 (60.5%) were female. One‐way analysis of variance (ANOVA) revealed a statistically significant difference between the type of malignancy and ESR values at the time of ST diagnosis (p = 0.02). Notably, ESR levels were significantly elevated in patients with gastric and ovarian cancers compared to other cancer types. Additionally, a significant association was observed between ESR values and disease stage (p = 0.004).

Conclusion

This study demonstrated that ESR levels at the time of diagnosis were significantly associated with both the type and stage of STs. Higher ESR values were particularly evident in patients with gastric and ovarian cancers, as well as those in advanced disease stages, suggesting ESR may serve as a useful prognostic indicator in cancer assessment.

Keywords: erythrocyte sedimentation rate, ESR, inflammatory marker, malignancy, prognosis

1. Introduction

Cancer remains one of the foremost causes of mortality across human societies globally. According to data from the National Center for Health Statistics in the United States, ~1,858,460 new cancer cases were diagnosed, and 614,460 individuals succumbed to this complex disease in 2021 [1]. In Iran, cancer ranks as the third leading cause of death, following cardiovascular diseases and accidents. It accounts for a substantial proportion of mortality, ~14%, with an estimated 98 cancer‐related deaths occurring daily within the Iranian population [2].

The profound implications of cancer, including severe physical suffering, diminished physical capacity, and the substantial direct and indirect costs it imposes, underscore the urgent need for increased attention and enhanced understanding of this disease. Notably, solid tumors (STs) constitute over 85% of human cancers, characterized as abnormal tissue masses devoid of cysts or liquid components. These tumors, encompassing sarcomas, carcinomas, and lymphomas, may be classified as either benign (noncancerous) or malignant (cancerous) [3, 4].

The staging of cancer is a critical process typically conducted at two junctures: prior to the initiation of treatment, termed the clinical stage, and following surgical intervention, if surgery constitutes the sole treatment, known as the pathological stage [5, 6]. Concurrently, the grade of cancer, which indicates the tumor's growth rate on a scale from 1 to 3, is determined through microscopic examination of tumor cell samples. Grade 1, or low‐grade tumors, exhibit a growth rate marginally above that of normal cells [7, 8], while Grade 2 (intermediate‐grade) and Grade 3 (high‐grade) tumors demonstrate progressively faster proliferation, with higher grades often indicating a greater likelihood of requiring chemotherapy. Despite their distinct meanings, the concepts of stage and grade are frequently conflated. A widely adopted framework for staging is the Tumor, Node, Metastasis system, which employs three scores: the T score, assessing the primary tumor's size and growth; the N score, evaluating lymph node involvement; and the M score, indicating the presence or absence of distant metastases. Furthermore, extensive research has established a link between chronic inflammation and carcinogenesis, suggesting that even subclinical inflammation may contribute significantly to the risk, development, and progression of cancer by inducing excessive cellular proliferation and initiating a cascade of events that promote tumor growth [9, 10, 11]. Furthermore, tumor progression can activate the host immune response, ultimately leading to inflammation. The erythrocyte sedimentation rate (ESR) is a commonly employed test to measure the rate at which red blood cells (RBCs) settle in plasma within vertical tubes. An elevated ESR does not specify a particular disease but signals an underlying condition. Key determinants of increased ESR include RBC aggregation and hematocrit levels, primarily driven by fibrinogen and other acute‐phase proteins. Consequently, ESR elevations are associated with infectious diseases, inflammatory processes, and vascular collagen diseases. Immunoglobulins (Ig), alongside acute‐phase proteins, further enhance RBC aggregation. The presence of cancer cells may similarly stimulate an immune response, elevating acute‐phase proteins and Ig levels. Clinicians occasionally encounter patients with unexplained high ESR [12, 13]. Persistently elevated ESR of unknown origin is associated with malignancy in a notable proportion of cases. For instance, Holoğlu and colleagues reported that 31.5% of patients with extremely elevated ESR were diagnosed with malignancies, including STs, highlighting the importance of thorough diagnostic evaluation in this population [14]. However, cohort studies from Kiel to Stockholm, involving asymptomatic Swedish women, found that no more than 6% of cases with unexplained high ESR were diagnosed with cancer over 5‐, 6‐, and 10‐year follow‐ups, suggesting variability in this association depending on population and study design [15]. While some studies suggest a link between elevated ESR and malignancy, data on the prognosis of cancer patients hospitalized with unexplained elevated ESR remain limited. For example, Tas and Erturk found that elevated ESR was associated with worse survival in melanoma patients, but specific prognostic data for patients with unexplained ESR elevations are scarce, warranting further investigation [16]. Against this backdrop, the present study seeks to examine ESR values at the time of malignancy diagnosis, with a particular emphasis on STs.

2. Materials and Methods

This cross‐sectional study aimed to assess and compare the frequency of ESR values at the time of diagnosis of STs. Data were collected from the medical records of male and female cancer patients at Shahid Baghaei‐2 Hospital and Shafa Hospital in Ahvaz, Iran, from February 2020 to October 2021. Exclusion criteria included patients diagnosed with leukemia, lymphoma, or multiple myeloma (MM), as well as those with anemia at the time of malignancy diagnosis, active infections, or hemoglobin (Hb) levels below 9 g/dL. The first‐hour ESR values, measured at the onset of ST diagnosis, were documented. This is because in Iranian laboratories, ESR is checked during the first hour. Patients were subsequently categorized based on age, gender, type of malignancy, and disease stage. Additionally, Hb levels were documented in a checklist. Ultimately, 428 individuals were enrolled in the study, and their data were subjected to statistical analysis. The G*Power software was utilized to determine the required sample size for ESR evaluation, with a 95% confidence interval (CI) and 95% test power, yielding a minimum sample size of 428 patients.

For quantitative variables, central tendency was described using the mean and/or median, while data dispersion was expressed through standard deviation (SD) and/or interquartile range. Qualitative variables were summarized using frequency and percentage. The normality of the data was assessed via the Kolmogorov–Smirnov test and Q2–Q3 box plots. Statistical analyses included an independent‐samples t‐test to examine the relationship between gender and ESR values, one‐way analysis of variance (ANOVA) to assess associations between ESR values and age groups, malignancy type, and disease stage, and χ 2 tests to explore relationships between disease stage and malignancy type, as well as between malignancy type and ESR values. All statistical analyses were conducted using the SPSS Statistics software package (version 22).

This study adhered to the principles outlined in the Declaration of Helsinki. Ethical approval was obtained from the Medical Ethics Committee of the Affiliated Hospital of Jundishapur University of Medical Sciences (IR.AJUMS.HGOLESTAN.REC.1401.104). All participants were informed about the potential use of their health data for scientific research and provided written informed consent prior to inclusion in the study.

3. Results

Of the 428 patients enrolled in this study, 259 (60.5%) were female and 169 (39.5%) were male. The mean age of the cancer patients was 59.20 ± 14.19 years (mean ± SD), with ages ranging from a minimum of 17 to a maximum of 92 years. The highest frequency of patients was observed in the 61–70 age group, while the lowest was in the 10–20 age group. The overall mean ESR value was 38.65 ± 27.87 mm/h, with values ranging from 0 to 125 mm/h. An independent‐samples t‐test was employed to examine the relationship between gender and ESR values, revealing that ESR levels were significantly lower in female patients compared to their male counterparts, indicating a statistically significant gender difference (p < 0.05). One‐way ANOVA was used to assess the association between elevated ESR values at the time of ST diagnosis and age groups, demonstrating a significant difference (p < 0.05). Specifically, the highest mean ESR values were observed in the 10–20 age group (68.00 ± 50.30 mm/h), while the lowest were recorded in the 81–90 age group (22.04 ± 37.05 mm/h).

Further analysis using one‐way ANOVA revealed a significant relationship between ESR values at the time of ST diagnosis and the type of malignancy (p = 0.02) (Table 1). The association between disease stage and ESR was also evaluated through one‐way ANOVA. Among the 428 patients, the mean ESR values were 34.80 mm/h at Stage 1, 33.67 mm/h at Stage 2, 32.19 mm/h at Stage 3, and 42.64 mm/h at Stage 4, with a statistically significant difference observed across disease stages (p = 0.004) (Table 2). The χ 2 test was applied to explore the relationship between disease stage and malignancy type, providing the frequency distribution of malignancy types by stage and confirming a significant association (p < 0.001) (Table 3). Similarly, the χ 2 test was used to investigate the relationship between malignancy type and ESR values, with the frequency distribution of malignancy types relative to ESR levels indicating a significant correlation (p < 0.05) (Table 4). Hb levels were also analyzed, with a mean Hb value of 12.63 g/dL for ESR values below 25 mm/h and 11.81 g/dL for ESR values above 25 mm/h; however, this difference was not statistically significant (p = 0.12) (Table 5).

Table 1.

Relationship between elevated ESR values amid the diagnosis of STs and type of malignancy.

Type N Mean ESR ± SD p
Ovarian cancer 44 68 ± 50.30 0.002
Skin malignancy 6 52.13 ± 41.66
Colorectal and small intestine carcinoma 78 35.68 ± 29.49
Breast cancer 125 43.24 ± 29.49
Renal cell carcinoma and bladder cancer 18 31.54 ± 23.46
Gastric cancer 43 40.95 ± 28.65
Liver and bile ducts and pancreas malignancy 25 36.03 ± 27.70
Lung cancer 62 22.04 ± 37.05
Head and neck tumors 6 38.75 ± 15.71
Soft tissue sarcoma 19 25.43 ± 30.21
Germ cell tumor 1 90.00 ± 0.00

Table 2.

Relationship between elevated ESR values amid the diagnosis of STs and stage of disease.

Stage N Mean ESR ± SD p
1 5 34.80 ± 15.48 0.004
2 40 33.67 ± 22.19
3 129 32.19 ± 25.22
4 253 42.64 ± 29.42

Table 3.

Relationship between type of malignancy and stage of disease.

Type Stage p
1 2 3 4
(%) N (%) N (%) N (%) N
Ovarian cancer (0) 0 (0) 0 (9.3) 12 (12.6) 32 < 0.001
Skin malignancy (0) 0 (16.7) 1 (66.7) 4 (16.7) 1
Colorectal and small intestine carcinoma (0) 0 (20.5) 16 (35.9) 28 (43.6) 34
Breast cancer (1.6) 2 (10.3) 13 (33.3) 42 (54.8) 69
Renal cell carcinoma and bladder cancer (16.7) 1 (5.1) 2 (3.1) 4 (4.3) 11
Gastric cancer (4.7) 2 (9.3) 4 (25.6) 11 (60.5) 26
Liver and bile ducts and pancreas malignancy (0) 0 (8) 2 (0) 0 (92) 23
Lung cancer (1.6) 1 (0) 0 (24.2) 15 (74.2) 46
Head and neck tumors (0) 0 (0) 0 (50) 3 (50) 3
Soft tissue sarcoma (0) 0 (5.3) 1 (47.4) 9 (47.4) 9
Germ cell tumor (0) 0 (0) 0 (100) 1 (0) 0

Note:N (%)” represents the total number of individuals (N) and their corresponding percentage (%) in the respective category.

Table 4.

Relationship between type of malignancy and ESR values.

Type ESR p
< 25 > 25
(%) N (%) N
Ovarian cancer (25) 11 (75) 33 0.002
Skin malignancy (33.3) 2 (66.7) 4
Colorectal and small intestine carcinoma (37.2) 22 (62.8) 49
Breast cancer (53.6) 67 (46.4) 58
Renal cell carcinoma and bladder cancer (27.8) 5 (72.2) 13
Gastric cancer (39.5) 17 (60.5) 26
Liver and bile ducts and pancreas malignancy (36) 9 (64) 16
Lung cancer (21) 13 (79) 49
Head and neck tumors (50) 3 (50) 3
Soft tissue sarcoma (52.6) 10 (47.4) 9
Germ cell tumor (100) 1 0 (0)

Note:N (%)” represents the total number of individuals (N) and their corresponding percentage (%) in the respective category.

Table 5.

Relationship between ESR values and Hb levels.

Type Mean SD p
ESR < 25 12.63 1.64 0.16
> 25 11.81 7.55

Figure 1 illustrates the frequency of cancer types across different stages. Figure 2 depicts the frequency of cancer types in relation to ESR values below and above 25 mm/h, while Figure 3 presents the frequency of ESR values below and above 25 mm/h across various disease stages.

Figure 1.

Figure 1

Frequency of cancer types according to different stages.

Figure 2.

Figure 2

Frequency of cancer types according to ESR < 25 and ESR > 25.

Figure 3.

Figure 3

Frequency of ESR types < 25 and > 25 for different stages.

4. Discussion

Previous research has consistently demonstrated an association between chronic inflammation and carcinogenesis, suggesting that subclinical or even undetectable inflammation may play a role as significant as chronic inflammation in elevating the risk, development, and progression of cancer [17, 18, 19, 20]. Chronic inflammation is hypothesized to induce excessive cellular proliferation, triggering a cascade of cellular events that promote tumor growth. Additionally, tumor progression itself activates the host immune response, further amplifying inflammation [21, 22, 23, 24]. Several studies have also established a link between elevated ESR values and reduced survival rates across various malignancies, including colorectal cancer, renal cell carcinoma (RCC), head and neck cancer, soft tissue sarcoma, breast cancer, glioma, and prostate cancer, with patients exhibiting higher ESR values demonstrating shorter survival compared to those with normal levels [25].

Building on this foundation, the present study investigated ESR values at the time of malignancy diagnosis, focusing on STs. Among the 428 patients, 5 were classified at Stage 1, 40 at Stage 2, 129 at Stage 3, and 253 at Stage 4, underscoring a notable escalation in ESR with advancing disease stage. These findings align with those of Tas and Erturk, who identified ESR > 15 mm/h as a significant prognostic factor associated with shorter survival and linked elevated ESR to metastasis [16]. Although prior studies, often limited by small sample sizes (< 100 patients), have reported similar trends [26, 27, 28], the current study's larger cohort strengthens the evidence of ESR's association with malignancy type and stage.

Watson and colleagues' investigation into the prognostic utility of inflammatory markers in primary care settings demonstrated that such markers, including CRP and ESR, are not effective as rule‐out tests for cancer diagnosis, with nearly half of cancer patients exhibiting normal levels [17].

Similarly, Shibuya and colleagues noted that elevated ESR is associated with advanced disease stages in colorectal cancer, consistent with our observation of a significant association between ESR and disease stage [29].

In this study, among 428 patients with various STs, mean ESR values were significantly lower in women than in men, reflecting a gender disparity in the cohort's overall ESR average. This contrasts with Shibuya and colleagues' context‐specific findings, where gender differences in ESR thresholds were noted for specific cancers [29]. For instance, a gastric cancer study applied cut‐offs of 10 mm/h for men and 20 mm/h for women, linking these to survival [30]. These higher thresholds for women pertain to prognostic benchmarks rather than mean values and are specific to gastric cancer, unlike the broader trend observed here. Conversely, in RCC, abnormal ESR was defined differently for men and women [31], while a meta‐analysis reported cancer‐specific ESR cut‐offs ranging from 20 to 50 mm/h [32]. These findings align with the present study, illustrating that while mean ESR may differ by gender in a general cohort, diagnostic thresholds vary by cancer type and often indicate higher values for women.

Notably, no significant correlation was observed between ESR and Hb levels in this study, differing from Tas and Erturk's report of a significant ESR–Hb relationship in malignant melanoma patients [16]. This discrepancy may reflect differences in study populations. However, a significant association was identified between ESR and malignancy type, with over 79% of gastric cancer patients and 75% of ovarian cancer patients exhibiting ESR > 25 mm/h. Pradjatmo and colleagues similarly noted that ESR varies by cancer type and stage due to the body's immune response, corroborating these results [33]. Furthermore, the association between elevated ESR and malignancy is supported by Holoğlu and colleagues, who found that 31.5% of patients with extremely elevated ESR had malignancies, including STs, emphasizing the need for comprehensive diagnostic workup in such cases [14]. While ESR, a nonspecific marker, may remain within normal ranges (0–20 mm/h for men, 0–25 mm/h for women) in some cases, it can exceed 100 mm/h in aggressive or advanced cancers. Here, ESR's significant association with disease stage was evident, with higher levels in Stage 3 and Stage 4 patients—indicative of metastatic disease—compared to earlier stages. Consistent with this, Tas and Erturk linked elevated ESR to disease severity and metastasis in cancer patients, noting its negative prognostic impact on survival in melanoma [16]. Although our study did not specifically evaluate the prognosis of cancer patients hospitalized with unexplained elevated ESR, existing literature suggests that elevated ESR may be associated with poorer outcomes in certain malignancies. For instance, Tas and Erturk reported that elevated ESR was linked to worse survival in melanoma patients, and Shibuya and colleagues noted similar trends in colorectal cancer [16, 29]. However, specific prognostic data for patients with unexplained ESR elevations remain limited, highlighting a gap that future studies should address.

5. Conclusion

This study observed differences in ESR values among various types of malignancies, with notably higher levels in gastric and ovarian cancers. ESR levels also varied according to disease stage, with patients in advanced stages showing increased values compared to those in earlier stages. These observations suggest that elevated ESR at the time of diagnosis may negatively impact prognosis across different cancer types and might serve as an indicator of reduced survival rates, positioning ESR as a potential prognostic risk factor alongside other established markers. Despite its limited sensitivity and specificity, ESR remains a straightforward, cost‐effective, and widely accessible test, although it does not replace more advanced and expensive prognostic methods. The study's cross‐sectional design and relatively small sample size are limitations, indicating the need for further research. Future studies should use prospective designs with larger, more diverse patient groups to confirm these findings and evaluate ESR's applicability across a wider range of malignancies. Additionally, further research is needed to explore the prognostic implications of unexplained elevated ESR in hospitalized cancer patients, as current evidence suggests a potential link to poorer outcomes but lacks comprehensive data specific to this subgroup. Combining ESR with other inflammatory markers, such as C‐reactive protein or novel biomarkers, could enhance its prognostic value and support its integration into routine clinical practice for personalized cancer care and management.

Author Contributions

Omid Abdollahi: investigation, writing – original draft, methodology. Tina Vosoughi: supervision, conceptualization, writing – review and editing, validation. Afshin Talebi: methodology, investigation, writing – original draft. Hossein Karimpourian: writing – original draft, writing – review and editing. Mohammadhossein Rastegar: data curation, writing – original draft, investigation. Elham Farhadi: formal analysis, software. All authors have read and approved the final version of the manuscript.

Ethics Statement

This study was approved by the Medical Ethics Committee of the Affiliated Hospital of Jundishapur University of Medical Sciences (Ethical Code: IR.AJUMS.HGOLESTAN.REC.1401.104). This study was performed in line with the principles of the Declaration of Helsinki.

Consent

All patients and control subjects were included in the study with complete information and after obtaining consent. All consent forms are available upon request. All individual participants included in the study were written informed and consented to the possible use of relevant health data for scientific research and signed written informed consent.

Conflicts of Interest

The authors declare no conflicts of interest.

Transparency Statement

The lead author, Tina Vosoughi, affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Acknowledgments

The authors of the article express their gratitude to Jundishapur University of Medical Sciences, Shafa and Bagai 2 Hospital. The authors received no specific funding for this work.

Data Availability Statement

The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Corresponding author Tina Vosoughi had full access to all of the data in this study and takes complete responsibility for the integrity of the data and the accuracy of the data analysis.

References

  • 1. Siegel R. L., Miller K. D., Wagle N. S., and Jemal A., “Cancer Statistics, 2023,” CA: A Cancer Journal for Clinicians 73, no. 1 (2023): 17–48. [DOI] [PubMed] [Google Scholar]
  • 2. Torfi E., Bahreiny S. S., Saki N., et al., “Evaluation of Pro‐BNP Biomarker in Heart Failure Patients and Its Relationship With Complete Blood Count Parameters: A Case–Control Study,” Health Science Reports 7, no. 9 (2024): e70083. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3. National Academies of Sciences Engineering, and Medicine; Health and Medicine Division, Board on Health Care Services, Committee on Childhood Cancers and Disability , Aiuppa L., Cartaxo T., Spicer C. M., and Volberding P. A., eds., Childhood Cancer and Functional Impacts Across the Care Continuum (National Academies Press, 2020). [PubMed]
  • 4. Soleimani Samarkhazan H., Zehtabcheh S., Seraji H. R., et al., “Unveiling the Potential of CLL‐1: A Promising Target for AML Therapy,” Biomarker Research 13, no. 1 (2025): 28. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Ferlay J., Colombet M., Soerjomataram I., et al., “Cancer Statistics for the Year 2020: An Overview,” International Journal of Cancer 149, no. 4 (2021): 778–789. [DOI] [PubMed] [Google Scholar]
  • 6. Rajabi L., Ebrahimdoost M., Mohammadi S. A., Soleimani Samarkhazan H., Khamisipour G., and Aghaei M., “Aqueous and Ethanolic Extracts of Moringa oleifera Leaves Induce Selective Cytotoxicity in Raji and Jurkat Cell Lines by Activating the P21 Pathway Independent of P53,” Molecular Biology Reports 52, no. 1 (2025): 102. [DOI] [PubMed] [Google Scholar]
  • 7. Wang Y., Acs B., Robertson S., et al., “Improved Breast Cancer Histological Grading Using Deep Learning,” Annals of Oncology 33, no. 1 (2022): 89–98. [DOI] [PubMed] [Google Scholar]
  • 8. Aghapour S. A., Torabizadeh M., Bahreiny S. S., et al., “Investigating the Dynamic Interplay Between Cellular Immunity and Tumor Cells in the Fight Against Cancer: An Updated Comprehensive Review,” Iranian Journal of Blood and Cancer 16, no. 2 (2024): 84–101. [Google Scholar]
  • 9. Aghaei M., Khademi R., Far M. A. J., Bahreiny S. S., Mahdizade A. H., and Amirrajab N., “Genetic Variants of Dectin‐1 and Their Antifungal Immunity Impact in Hematologic Malignancies: A Comprehensive Systematic Review,” Current Research in Translational Medicine 72, no. 4 (2024): 103460. [DOI] [PubMed] [Google Scholar]
  • 10. Okada F., “Inflammation‐Related Carcinogenesis: Current Findings in Epidemiological Trends, Causes and Mechanisms,” Yonago Acta Medica 57, no. 2 (2014): 65–72. [PMC free article] [PubMed] [Google Scholar]
  • 11. Aghaei M., Khademi R., Bahreiny S. S., and Saki N., “The Need to Establish and Recognize the Field of Clinical Laboratory Science (CLS) as an Essential Field in Advancing Clinical Goals,” Health Science Reports 7, no. 8 (2024): e70008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12. Ramsay E. S. and Lerman M. A., “How to Use the Erythrocyte Sedimentation Rate in Paediatrics,” Archives of Disease in Childhood ‐ Education & Practice Edition 100, no. 1 (2015): 30–36. [DOI] [PubMed] [Google Scholar]
  • 13. Eftekhar Z., Aghaei M., and Saki N., “DNA Damage Repair in Megakaryopoiesis: Molecular and Clinical Aspects,” Expert Review of Hematology 17, no. 10 (2024): 705–712. [DOI] [PubMed] [Google Scholar]
  • 14. Holoğlu E. N., Uzunlulu M., and Torun C., “Extremely Elevated Erythrocyte Sedimentation Rates: Associations With Patients' Diagnoses and Clinical Characteristics,” Romanian Journal of Internal Medicine 63, no. 1 (2025): 70–78. [DOI] [PubMed] [Google Scholar]
  • 15. Åkerstedt T., Knutsson A., Narusyte J., Svedberg P., Kecklund G., and Alexanderson K., “Night Work and Breast Cancer in Women: A Swedish Cohort Study,” BMJ Open 5, no. 4 (2015): e008127. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Tas F. and Erturk K., “Elevated Erythrocyte Sedimentation Rate Is Associated With Metastatic Disease and Worse Survival in Patients With Cutaneous Malignant Melanoma,” Molecular and Clinical Oncology 7, no. 6 (2017): 1142–1146. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17. Watson J., Salisbury C., Banks J., Whiting P., and Hamilton W., “Predictive Value of Inflammatory Markers for Cancer Diagnosis in Primary Care: A Prospective Cohort Study Using Electronic Health Records,” British Journal of Cancer 120, no. 11 (2019): 1045–1051. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18. Grivennikov S. I., Greten F. R., and Karin M., “Immunity, Inflammation, and Cancer,” Cell 140 (2010): 883–899. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19. Ishizuka M., Nagata H., Takagi K., Iwasaki Y., and Kubota K., “Inflammation‐Based Prognostic System Predicts Postoperative Survival of Colorectal Cancer Patients With a Normal Preoperative Serum Level of Carcinoembryonic Antigen,” Annals of Surgical Oncology 19 (2012): 3422–3431. [DOI] [PubMed] [Google Scholar]
  • 20. Torabizadeh M., Aghaei M., Saki N., Vahid M. A., Bitaraf S., and Bandar B., “The Association of Nasal and Blood Eosinophils With Serum IgE Level in Allergic Rhinitis and Asthma: A Case‐Control Study,” Health Science Reports 7, no. 11 (2024): e70191. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21. Seong M.‐K., “Prognostic Inflammation Score in Surgical Patients With Colorectal Cancer,” Journal of Korean Medical Science 30, no. 12 (2015): 1793. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Saki N., Haybar H., and Aghaei M., “Subject: Motivation Can Be Suppressed, But Scientific Ability Cannot and Should Not Be Ignored,” Journal of Translational Medicine 21, no. 1 (2023): 520. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23. Bastani M.‐N., Jalilian S., Bahreiny S. S., et al., “Update Prognostic Potency of Surfactant Protein D (SP‐D) in the COVID‐19 Landscape: An In‐Depth Meta‐Analytical Exploration,” Biomarkers in Medicine 18, no. 24 (2024): 1135–1148. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Karimi F., Aghaei M., and Saki N., “Impact of Genetic Polymorphisms on Treatment Outcomes of Proteasome Inhibitors and Immunomodulatory Drugs in Multiple Myeloma,” Current Treatment Options in Oncology 26, no. 3 (2025): 197–212. [DOI] [PubMed] [Google Scholar]
  • 25. Strojnik T., Smigoc T., and Lah T. T., “Prognostic Value of Erythrocyte Sedimentation Rate and C‐Reactive Protein in the Blood of Patients With Glioma,” Anticancer Research 34, no. 1 (2014): 339–347. [PubMed] [Google Scholar]
  • 26. Tas F., Karabulut S., Bilgin E., Tastekin D., and Duranyildiz D., “Clinical Significance of Serum Fibronectin and Vitronectin Levels in Melanoma Patients,” Melanoma Research 24, no. 5 (2014): 475–479. [DOI] [PubMed] [Google Scholar]
  • 27. Tas F., Bilgin E., Erturk K., and Duranyildiz D., “Clinical Significance of Serum Claudin‐1 Levels in Melanoma Patients,” Melanoma Research 26, no. 4 (2016): 377–381. [DOI] [PubMed] [Google Scholar]
  • 28. Tas F., Karabulut S., Serilmez M., et al., “Clinical Significance of Serum M30 and M65 Levels in Melanoma,” Melanoma Research 23, no. 5 (2013): 390–395. [DOI] [PubMed] [Google Scholar]
  • 29. Shibuya N., Ishizuka M., Takagi K., et al., “Relationship Between Preoperative Erythrocyte Sedimentation Rate and Survival After Surgery in Patients With Colorectal Cancer,” Anticancer Research 38, no. 12 (2018): 6783–6788. [DOI] [PubMed] [Google Scholar]
  • 30. Lee D. Y., Hong S. W., Chang Y. G., Lee W. Y., and Lee B., “Clinical Significance of Preoperative Inflammatory Parameters in Gastric Cancer Patients,” Journal of Gastric Cancer 13, no. 2 (2013): 111–116. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31. Sengupta S., Lohse C. M., Cheville J. C., et al., “The Preoperative Erythrocyte Sedimentation Rate Is an Independent Prognostic Factor in Renal Cell Carcinoma,” Cancer 106, no. 2 (2006): 304–312. [DOI] [PubMed] [Google Scholar]
  • 32. Wu Y., Fu X., Zhu X., et al., “Prognostic Role of Systemic Inflammatory Response in Renal Cell Carcinoma: A Systematic Review and Meta‐Analysis,” Journal of Cancer Research and Clinical Oncology 137 (2011): 887–896. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Pradjatmo H., Nugroho K. A., and Pasala M., “Analysis of Erythrocyte Sedimentation Rate Order in Epithelial Ovarian Cancer,” Journal of Cancer 14, no. 12 (2023): 2173–2180. [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Corresponding author Tina Vosoughi had full access to all of the data in this study and takes complete responsibility for the integrity of the data and the accuracy of the data analysis.


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