Research ArticleClinical Studies
Open Access

PRDX4 Potentially Serves as an Independent Marker for Early Recurrence of Oral Squamous Cell Carcinoma

TAIJIRO HASHIMOTO, TAKERU OYAMA, YANGXIAN ZHANG, YUKINOBU ITO, JIA HAN, YAO LIU, MITSUAKI YOSHIDA, AKIHIRO SHIOYA, MASASHI OKURO, MORIMASA KITAMURA and SOHSUKE YAMADA
Anticancer Research May 2026, 46 (5) 2583-2597; DOI: https://doi.org/10.21873/anticanres.18139

Abstract

Background/Aim: Oral squamous cell carcinoma (OSCC), a main histological subtype of oral cavity cancer, remains one of the most prevailing tumors worldwide with the increasing incidence and mortality. Since a high rate of early local recurrence is one of the major risk factors for poor outcome of OSCC, its prognostic biomarkers are urgently needed. Peroxiredoxin 4 (PRDX4), a member of PRDXs, which are involved in the antioxidant defense, is a unique secreted subtype of PRDXs. A certain number of previous studies have disclosed that the overexpression of the PRDX4 protein has a clear relationship with tumor initiation and progression in many cancers. Furthermore, recent studies have revealed that PRDX4 promotes tumor development through the Wnt/β-catenin signaling pathway.

Materials and Methods: To assess the status of the PRDX4/β-catenin expression and its association with clinical outcomes, including early local recurrence in OSCC, we immunohistochemically examined PRDX4 expression levels and cytoplasmic β-catenin protein accumulation levels in a total of 72 postoperative OSCC samples.

Results: The immunohistochemically high expression of PRDX4 was significantly correlated with poorer early phase 2-year recurrence-free survival (RFS), associated closely with higher PRDX4 expression levels especially the OSCC nests of invasive fronts or perineural invasion. In addition, a multivariate Cox regression analysis revealed that PRDX4 was an independent prognostic factor for 2-year RFS. Moreover, high β-catenin accumulation is significantly associated with distant metastasis. A comparison of the combination of a high expression of PRDX4 and high β-catenin protein accumulation groups with the other groups only showed a significant predominance among men.

Conclusion: The increased expression of PRDX4 may be a useful independent prognostic biomarker for recurrence of OSCC, especially in the early postoperative phase.

Keywords:

Introduction

Oral squamous cell carcinoma (OSCC) is the main histological subtype of oral cavity cancer, accounting for approximately 90% of all cancer cases (1). Globally, the incidence of OSCC in 2022 was 389,846, with 188,438 associated deaths (Global Cancer Observatory), and the rate is constantly increasing (2). Despite easy access to clinical examinations, the majority of OSCCs are diagnosed at an advanced stage because the early stages of the tumor are frequently asymptomatic (3, 4). OSCC is primarily treated with radical surgery with postoperative radiation and/or chemotherapy (5). Approximately one-third of patients experience postoperative recurrence, with the most common pattern being local recurrence (5), which is a major risk factor for poor outcomes (6). Recurrence usually occurs within the first 18 months after surgery, leading to poor overall survival (OS) (7, 8). Moreover, patients with early recurrence have a significantly worse prognosis than those with late recurrence (5, 9-11). However, the identification of early recurrence in the postoperative state can be a clinical challenge until large and symptomatic tumors emerge (5). Because of the detrimental properties of early recurrence, prognostic and predictive biomarkers are urgently needed.

We focused on peroxiredoxins (PRDXs) as candidate biomarkers for the early recurrence of OSCC. PRDXs protect organisms against oxidative stress caused by the accumulation of reactive oxygen species (ROS) by catalyzing peroxide reduction to remove excessive hydroxyperoxide (12). PRDX4 is the only secreted subtype of PRDX localized in the endoplasmic reticulum (ER) and contributes to oxidative protein folding and the antioxidant function (12-14). In the ER, PRDX4, in collaboration with endoplasmic reticulum oxidoreductin 1 (ERO1) via protein disulfide isomerase (PDI), acts as a sulfhydryl oxidase to introduce disulfide bonds into nascent proteins that are transferred to the Golgi body for secretion (12). Decreased capacity for oxidative protein folding by PRDX4 leads to a large amount of ER stress, resulting in a number of diseases, including delayed wound healing (15), osteonecrosis of the femoral head (16), fatty liver disease (17-19), atherosclerosis (20), diabetes (21, 22) and metabolic syndrome (13, 22).

Moreover, aberrations in the expression of PRDX4 have been detected in a large number of solid and hematopoietic neoplasms, and the majority of them were significantly upregulated, including lung cancer (lung adenocarcinoma) (23-26), liver cancer (hepatocellular carcinoma and hepatoblastoma) (27-29), pancreatic cancer (30), gastric cancer (31), colorectal cancer (32, 33), renal cancer (renal papillary carcinoma) (34), prostate cancer (32, 35, 36), breast cancer (32, 37), ovarian cancer (32), brain tumor (glioma) (38, 39), multiple myeloma (40), and acute myeloid and promyelocytic leukemia (32, 41). High PRDX4 expression levels showed a significantly close association with tumor initiation and progression, resulting in a poor prognosis. More recently, the overexpression of PRDX4 predicted shortened survival in hepatoblastoma (28), and the strong immunohistochemical expression of PRDX4 predicted poorer survival in pancreatic ductal adenocarcinoma (30).

Aberrations in the expression of PRDX4 have also been reported in squamous cell carcinomas including OSCC (42, 43). The overexpression of PRDX4 has been reported in human OSCC tissues and cell lines, based on an immunohistochemical analysis and a meta-analysis, and is associated with increased cell proliferation, migration, and invasion through the reduced expression of adhesion molecules in vitro (42, 44). Furthermore, elevated expression levels of PRDX4 mRNA were detected using the Gene Expression Array based on quantitative reverse transcription PCR (qRT-PCR) in human OSCC tissue (45). In the lung, high expression of PRDX4 was observed in squamous cell carcinoma by immunostaining, which was significantly correlated with higher recurrence rates and shorter recurrence-free survival (RFS) (43). These studies revealed that PRDX4 is significantly over-expressed in squamous cell carcinomas from various organ types.

One of the major mechanisms by which the over-expression of PRDX4 contributes to malignancy is activation of the Wnt/β-catenin signaling pathway (46, 47). In fact, knockdown of PRDX4 by short hairpin RNA (shRNA) inhibited the Wnt/β-catenin signaling pathway in two renal cell carcinoma cell lines (46). The degradation of PRDX4 inactivated the Wnt/β-catenin signaling pathway in hepatocellular carcinoma cells (47). These studies have shown that PRDX4 can promote cell growth, invasion, and migration through the Wnt/β-catenin signaling pathway, which plays a crucial role in the initiation and progression of malignant neoplasms. However, to our knowledge, no previous studies have disclosed the relationship between increased PRDX4 expression and recurrence, especially early recurrence, after surgical treatment of OSCC and its underlying mechanisms, including the Wnt/β-catenin signaling pathway. The detection of increased PRDX4 expression levels in postsurgical lesions might indicate the need for immediate therapeutic interventions for recurrent OSCC.

Our aim was to assess the potential application of the expression of PRDX4 and β-catenin as a biomarker, especially for the early recurrence after surgical treatment of OSCC. We investigated PRDX4/β-catenin expression levels and their association with the clinical characteristics and outcomes, including early local recurrence after surgical treatment of OSCC in 72 patients, based on an immunohistochemical analysis of PRDX4 and β-catenin.

Materials and Methods

Ethics approval and consent to participate. All intended procedures in the present study, including the use of specimens obtained from human subjects, were approved by the Medical Ethics Committee of Kanazawa Medical University (permission number: C133). All patients provided informed written consent according to the guidelines of the Japanese Society of Pathology. All patients provided informed written consent for publication.

Samples. A total of 85 cases of formalin-fixed paraffin-embedded (FFPE) tissue blocks were retrieved from archives of the Pathological Department of Kanazawa Medical University Hospital. Corresponding clinicopathological information was also collected from hospital electronic records. Thirteen cases were excluded from the analysis because of a lack of either FFPE tissue blocks or clinicopathological information.

Immunohistochemistry. Immunohistochemical staining was performed using the antibody-linked dextran polymer method for antibody-bridge labelling with hematoxylin counterstaining (EnVision; Dako Cytomation Corporation, Glostrup, Denmark). Antibodies against PRDX4 (Life Technologies Corporation, Carlsbad, CA, USA), β-catenin (Life Technologies Corporation), and S-100 protein (Dako Cytomation Corporation) were used at 1:200, 1:1,000, and 1:100 dilutions, respectively. Human PRDX4 transgenic mice pancreatic tissues (especially, islets of Langerhans) were used as positive controls for PRDX4 (20-25), and post-surgical well-differentiated tubular colorectal adenocarcinomas archived in our hospital, for β-catenin (48). The 3-mm-thick unstained sections were deparaffinized with xylene, hydrated using a graded ethanol series (100, 90, and 80%) for 1 min each, and washed with PBS three times. The sections were unmasked in citrate buffer using Pascal (Agilent Technologies Japan, Ltd., Tokyo, Japan), incubated in 10% H2O2 in methanol for 5 min to block endogenous peroxidase activity, and washed with PBS. The slides were then incubated with 1% serum for 1 h. First, the antibodies were applied and incubated overnight at 4°C. The second antibody-peroxidase linked polymers were then applied and the sections were incubated with a solution consisting of 20 mg of 3.3′-diaminobenzidine tetrahydrochloride, 65 mg of sodium azide, and 20 ml of 30% H2O2 in 100 ml of Tris-HCl (50 mM, pH 7.6). After counterstaining with Meyer’s hematoxylin, sections were observed under a light microscope. The sections were first scanned at low power for all fields (original magnification: ×40) with tumor and non-tumor tissues to account for the heterogeneity of distribution.

Immunohistochemical analysis. In each case, PRDX4 and β-catenin immunoreactivity was assessed semi-quantitatively by evaluating the proportion of cells with clearly higher expression levels in the total neoplastic OSCC cells in comparison to the adjacent non-tumor squamous cells, which presented very weak or negative expression levels of both proteins. The cutoff values for immunohistochemical staining of PRDX4 (10%) and β-catenin (10%) were selected and validated based on a receiver operating characteristic (ROC) curve analysis (Figure 1). All patients were divided into two groups based on the expression of PRDX4 as follows: high when PRDX4 staining was ≥10% and low when staining was <10%. All histological and immunohistochemical slides were evaluated by two independent observers (certified surgical pathologists in our department, A.S. and T.O.) using a blinded protocol design (observers were blinded to the clinicopathological data).

Figure 1.
Figure 1.

Receiver operating characteristic (ROC) curves for determining cutoff values of Peroxiredoxin 4 (PRDX4) (A) and β-catenin (B) expression levels using immunostaining in oral squamous cell carcinoma. The cutoff values of PRDX4 and β-catenin were both 10% each [area under the ROC curve (AUC), 58% and 53%; sensitivity, 33% and 58%; specificity, 93% and 60%, respectively).

The interobserver agreement, as measured by the interclass correlation coefficient, was excellent (>99%) for all antibodies investigated. For the few (<1%) instances of disagreement, a consensus score was determined by a third board-certified pathologist (S.Y.) in our department.

Statistical analysis. The correlations between the PRDX4 and/or β-catenin expression status and clinicopathological characteristics were analyzed using the chi-squared test. Statistical significance was set at p<0.05. Survival curves were generated using the Kaplan-Meier method. Log-rank and generalized Wilcoxon tests were used for the statistical comparison of RFS between a cohort with high PRDX4 expression levels and a cohort with low expression levels, using GraphPad Prism 10 (GraphPad software, Tokyo, Japan). Statistical significance was set at p<0.05.

Results

Clinicopathological characteristics of the cases. A total of 72 patients who underwent surgery at Kanazawa Medical University Hospital were included in the present study. Table I describes the detailed clinicopathological characteristics of the patients. Subsequently, the cases were dichotomized into two groups according to clinicopathological characteristics (e.g., sex, age, tumor differentiation, maximum diameter, T-category of TNM staging system, and lymph node or distant metastasis) (Table II). The patients included 44 men and 28 women. The average age of the patients was 62.5 years (range=26-93 years). Fourteen of 72 (19%) of the tumors were ≥30 mm in maximal diameter. Lymphatic, venous, and perineural invasion were observed in 24% (17/72), 25% (18/72), and 22% (16/72) of the tumors, respectively. The majority of tumors (96%; 69/72) were classified as well-to-moderately differentiated, while the remainder were poorly differentiated squamous cell carcinomas. Based on the TNM classification, 56% (40/72) of cases were classified as pathological T category ≥2 (pT2 to pT4). Lymph node metastasis (pN1 or higher) was observed in 29% (21/72) of the tumors. Distant metastasis (M1) was observed in 7% (5/72) of the tumors; metastases were detected in the lung (3/5), liver (2/5), and spine (2/5). Local recurrence developed in 21% (15/72) of the patients. A smoking history was present in 60% (43/72) of the cases, and a drinking history was present in 64% (46/72).

View this table:
Table I.

The detailed relationships among the PRDX4 expression, beta-catenin accumulation, and each patients’ variables.

View this table:
Table II.

The clinicopathological characteristics of the oral squamous cell carcinoma patients (n=72).

Association of the overexpression of PRDX4 and β-catenin accumulation with clinicopathological characteristics. Figure 2 shows representative images of OSCC in the high-PRDX4 and high-β-catenin protein accumulation groups (Figure 2A-C), and the low-PRDX4 and low-β-catenin protein accumulation groups (Figure 2D-F). The expression of PRDX4 and β-catenin protein accumulation were both higher, especially in the tumor cell nests of the invasive fronts (Figure 2B and C), in comparison to the low expression group (Figure 2E and F). Moreover, in the invasive fronts, tumors with the high PRDX4 expression levels and β-catenin protein accumulation formed smaller tumor cell nests, compared to those with low PRDX4 expression levels and β-catenin protein accumulation. Table III shows that 51 (71%) samples showed high PRDX4 expression levels and 41 (57%) samples showed high β-catenin protein accumulation. The high expression of PRDX4 was significantly associated with a history of smoking (p=0.003) and drinking (p=0.003). All patients with distant metastasis were in the high β-catenin expression group (p=0.044), and the group showed a significant male predominance (p=0.016).

Figure 2.
Figure 2.

Representative hematoxylin and eosin staining of tumors with high- Peroxiredoxin 4 (PRDX4) expression and high-β-catenin protein accumulation (A) and low-PRDX4 and low-β-catenin protein accumulation (D). In the invasive fronts, high-PRDX4 expression levels and high-β-catenin protein accumulation formed smaller tumor cell nests in comparison to those with low-PRDX4 expression levels and low-β-catenin protein accumulation. Immunostaining of PRDX4 in the high (B) and low (E) expression groups. Immunostaining of β-catenin in the high (C) and low (F) expression groups. Higher PRDX4 expression levels and β-catenin protein accumulation were frequently observed in tumor cell nests in the invasive fronts. Scale bar=100 μm.

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Table III.

Correlations between PRDX4 expression levels and clinicopathological variables.

Survival analysis. Figure 3 shows 2-year and 5-year RFS in the PRDX4-high and PRDX4-low groups (Figure 3A), β-catenin-high and β-catenin-low groups (Figure 3B), and the combination of PRDX4-high and β-catenin-high vs. the others (Figure 3C). These analyses were performed using the Kaplan-Meier method. Figure 3A shows that the high expression of PRDX4 was significantly associated with poorer 2-year (p=0.0433) and 5-year RFS (p=0.0471). However, Figure 3B showed no significant differences in 2-year (p=0.931) and 5-year RFS (p=0.948) according to the β-catenin expression status, and Figure 3C also exhibited no significant differences in 2-year (p=0.221) and 5-year RFS (p=0239) between the PRDX4-high-β-catenin-high groups and the others. The median RFS of the PRDX4-high and PRDX4-low groups was 772 and 1,396 days, respectively, that of the β-catenin-high and β-catenin-low groups was 1,567 and 685 days, and that of the PRDX4-high-β-catenin-high- and other groups was 772 and 1,396 days, respectively.

Figure 3.
Figure 3.

Kaplan-Meier curves for 2-year recurrence-free survival (RFS) (red vertical lines) and 5-year RFS (blue vertical lines) in the Peroxiredoxin 4 (PRDX4)-high and PRDX4-low expression groups (A), β-catenin-high and β-catenin-low protein accumulation groups (B), and PRDX4-high-β-catenin high and the other groups (C). yrs=Years.

Cox regression analysis. Multivariate Cox regression analyses were performed with sex, age, maximal tumor diameter, histological differentiation of SCC, pT category, lymph node and distant metastasis, perineural, lymphatic and venous invasion, and smoking and drinking history as covariates. Table IV shows that the high expression of PRDX4 (p=0.047), maximal tumor size ≥30 mm (p=0.029), and perineural invasion (p=0.023) were independent prognostic factors for 2-year RFS. Although perineural invasion was an independent prognostic factor for 2-year RFS and was not correlated with the high expression of PRDX4, we additionally investigated the tumor microenvironment around the peripheral nerves by immunohistochemical staining for S-100 protein. Figure 4 shows that tiny PRDX4-positive tumor nests were frequently observed around S-100 protein-positive peripheral nerves.

View this table:
Table IV.

The univariate analyses of RFS according to the clinicopathological variables and the expression of PRDX4 and β-catenin.

Figure 4.
Figure 4.

Perineural invasion in the microenvironment of a Peroxiredoxin 4 (PRDX4)-high tumor nests. Immunostaining for S-100 protein indicating peripheral nerves (red dashed circle) (A) and immunostaining of PRDX4 indicating tumor cell nests surrounding the peripheral nerves (red arrows) (B). Scale bar=100 μm.

Discussion

The present study revealed that the high expression of PRDX4 in OSCC is a significant prognostic factor, particularly for early recurrence. Indeed, Kaplan-Meier analyses showed that the recurrence-free survival rates of the PRDX4 high expression group rapidly decreased within one to two years and log-rank tests indicated the significant worse 2-year (p=0.0433) and 5-year RFS (p=0.0471) in the PRDX4 high expression group. Furthermore, univariate and multivariate analyses of the Cox proportional regression model revealed that the high expression of PRDX4 predicted significantly worse 2-year RFS in comparison to the low expression of PRDX4 (p=0.0469), indicating that an aberrantly increased PRDX4 expression level could be a candidate independent biomarker for early recurrence of OSCC. Therefore, detection of the early recurrence by the high expression of PRDX4 in postoperative specimens might indicate the possibility of therapeutic intervention to improve patient survival. Moreover, PRDX4 could be a candidate serum biomarker to detect early recurrence of OSCC after surgical treatment, since the protein is known to be the only soluble PRDX subtype (12, 13). In fact, the serum expression of PRDX4 can be detected in some tissues (e.g., pancreatic tissue), wherein protein secretion is critical for both exocrine and endocrine secretion (12, 13, 21).

The present study has some limitations. This was a retrospective study conducted within a single institution with a relatively small study population. In practice, among the clinicopathological characteristics listed in Table III, lymph node metastasis shows only a propensity to correlate with PRDX4 overexpression. Larger study population could determine whether there is any true association between PRDX4 overexpression and lymph node metastasis, and any contribution of lymph node metastasis to early recurrence. Thus, further follow-up with a larger cohort is needed to confirm our conclusions. Furthermore, we only evaluated histopathological sections (but not serum) and could not comprehensively analyze the critical roles or the underlying mechanisms of PRDX4 in the prognosis of OSCC. Therefore, the pivotal effects of the overexpression of PRDX4 on OSCC will be determined using human OSCC cell lines (SCC-4, 9, 15, available from American Type Culture Collection) and/or OSCC animal models in human PRDX4 transgenic mice as our future research. Finally, identical studies using other antibodies or other cutoff values may be necessary to validate the results of this study in the future, since OSCC could be a heterogeneous cancer where immunohistochemical expression might vary depending on its site of origin.

Intriguingly, the univariate and multivariate Cox regression analyses in the present study revealed that perineural invasion was an independent prognostic factor for 2-year RFS, although it was not associated with the increased expression of PRDX4 (Table IV). Perineural invasion has been recognized as one of the critical histopathological characteristics in various malignancies, including those of the breast, pancreas, colorectum, and prostate, and it correlates with higher tumor grade, increased risk of locoregional recurrence, and a potentially worse prognosis (49). As shown in Figure 4, tiny OSCC nests surrounding the peripheral nerves in the tumor microenvironment showed high PRDX4 expression levels. Accordingly, the localized overexpression of PRDX4 surrounding the peripheral nerves, instead of the overall expression of the tumor, might be closely associated with poor outcomes, including early recurrence. Further studies are needed to investigate the association between microenvironmentally localized high PRDX4 expression levels (e.g., perineural invasion and/or invasive fronts) and early recurrence.

In this study, we revealed that high PRDX4 expression was significantly associated with early recurrence, and high protein accumulation of β-catenin with distant metastasis of OSCC. However, the results of immunohistochemical analyses showed no association between them. This was inferred to be because distant metastasis is commonly a later event of tumor progression and the process in which PRDX4 affect Wnt/β-catenin signaling pathway might require long lead time. Nevertheless, the impacts of PRDX4 on Wnt/β-catenin have been disclosed in several studies. These studies have demonstrated that high PRDX4 levels could affect malignant characteristics by maintaining stem cell- like properties mainly activated by the Wnt/β-catenin signaling pathway (50-52). Such stem cell-like tumor cells have been reported to express splicing variant isoforms of CD44 (CD44v) (53, 54), a major Wnt target gene, leading to increased production of the antioxidant glutathione, which removes excessive ROS in the tumor microenvironment and may enhance malignant features (52). Similarly, the expression of the antioxidant PRDX4 can be up-regulated, especially in stem cell-like tumor cell populations within malignant neoplasms, including OSCC. Therefore, PRDX4 may be a candidate biomarker for stem cell-like tumor cells, which aggressively enhance the occurrence and growth of malignant neoplasms. Further in-depth studies will be required in the near future. Furthermore, since PRDX4 in the ER lumen mainly catalyzes oxidative protein folding, its decreased expression results in the accumulation of unfolded proteins, which causes cell apoptosis (12, 13, 19). In contrast, malignant cells including OSCC cells, as shown in Figure 2B (invasive fronts) and Figure 4B (perineural invasion), significantly upregulate PRDX4 to protect themselves from apoptosis caused by the accumulation of unfolded protein, which promotes tumor initiation and development. Thus, inhibiting the overexpression of PRDX4 could be an attractive therapeutic target for OSCC.

In conclusion, we demonstrated that high PRDX4 expression in OSCC is a significant and independent prognostic factor, particularly for early recurrence, and may serve as a useful biomarker for detecting early recurrence in postoperative histopathological specimens.

Acknowledgements

The Authors would like to thank Brian Quinn for editing the manuscript. We thank the members of the Department of Pathology, Kanazawa Medical University Hospital, for providing expert technical assistance.

Footnotes

  • Authors’ Contributions

    Taijiro Hashimoto, Yangxion Zhang, Takeru Oyama, Akihiro Shioya and Sohsuke Yamada conceptualized and designed the experiments. Mitsuaki Yoshida, Taijiro Hashimoto, Yangxion Zhang and Jia Han performed experiments. Taijiro Hashimoto, Jia Han, Yukinobu Ito and Takeru Oyama analyzed the data and drafted the manuscript. Masashi Okuro, Morimasa Kitamura and Sohsuke Yamada have reviewed and edited the manuscript. Sohsuke Yamada supervised the study. All authors have read and approved the final version of the manuscript.

  • Conflicts of Interest

    All Authors have no competing financial and/or non-financial interests to declare in relation to this study.

  • Funding

    This work was supported in part by Japan Society for the Promotion of Science (20K07454 to S. Y. and 23K06474 to T. O.), by Hokkoku Cancer Foundation (to S. Y.) and by Grant for Promoting Research from Kanazawa Medical University (S2023-A4 to T.O.)

  • Artificial Intelligence (AI) Disclosure

    No artificial intelligence (AI) tools, including large language models or machine learning software, were used in the preparation, analysis, or presentation of this manuscript.

  • Received February 10, 2026.
  • Revision received March 5, 2026.
  • Accepted March 10, 2026.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

References

  1. ↵
    1. Muralidharan S,
    2. Nikalje M,
    3. Subramaniam T,
    4. Koshy JA,
    5. Koshy AV,
    6. Bangera D
    : A narrative review on oral squamous cell carcinoma. J Pharm Bioallied Sci 17(Suppl 1): S204-S206, 2025. DOI: 10.4103/jpbs.jpbs_593_25
    OpenUrlCrossRefPubMed
  2. ↵
    1. Esperouz F,
    2. Ciavarella D,
    3. Lorusso M,
    4. Santarelli A,
    5. Lo Muzio L,
    6. Campisi G,
    7. Lo Russo L
    : Critical review of OCT in clinical practice for the assessment of oral lesions. Front Oncol 15: 1569197, 2025. DOI: 10.3389/fonc.2025.1569197
    OpenUrlCrossRefPubMed
  3. ↵
    1. Jagadeesan D,
    2. Sathasivam KV,
    3. Fuloria NK,
    4. Balakrishnan V,
    5. Khor GH,
    6. Ravichandran M,
    7. Solyappan M,
    8. Fuloria S,
    9. Gupta G,
    10. Ahlawat A,
    11. Yadav G,
    12. Kaur P,
    13. Husseen B
    : Comprehensive insights into oral squamous cell carcinoma: Diagnosis, pathogenesis, and therapeutic advances. Pathol Res Pract 261: 155489, 2024. DOI: 10.1016/j.prp.2024.155489
    OpenUrlCrossRefPubMed
  4. ↵
    1. Bagan J,
    2. Sarrion G,
    3. Jimenez Y
    : Oral cancer: Clinical features. Oral Oncol 46(6): 414-417, 2010. DOI: 10.1016/j.oraloncology.2010.03.009
    OpenUrlCrossRefPubMed
  5. ↵
    1. Hosni A,
    2. Huang SH,
    3. Chiu K,
    4. Xu W,
    5. Su J,
    6. Bayley A,
    7. Bratman SV,
    8. Cho J,
    9. Giuliani M,
    10. Kim J,
    11. O’Sullivan B,
    12. Ringash J,
    13. Waldron J,
    14. Spreafico A,
    15. Yu E,
    16. de Almeida JR,
    17. Monteiro E,
    18. Chepeha DB,
    19. Irish JC,
    20. Goldstein DP,
    21. Hope A
    : Predictors of early recurrence prior to planned postoperative radiation therapy for oral cavity squamous cell carcinoma and outcomes following salvage intensified radiation therapy. Int J Radiat Oncol Biol Phys 103(2): 363-373, 2019. DOI: 10.1016/j.ijrobp.2018.09.013
    OpenUrlCrossRefPubMed
  6. ↵
    1. Montero PH,
    2. Patel SG
    : Cancer of the oral cavity. Surg Oncol Clin N Am 24(3): 491-508, 2015. DOI: 10.1016/j.soc.2015.03.006
    OpenUrlCrossRefPubMed
  7. ↵
    1. Lyu WN,
    2. Lin MC,
    3. Shen CY,
    4. Chen LH,
    5. Lee YH,
    6. Chen SK,
    7. Lai LC,
    8. Chuang EY,
    9. Lou PJ,
    10. Tsai MH
    : An oral microbial biomarker for early detection of recurrence of oral squamous cell carcinoma. ACS Infect Dis 9(9): 1783-1792, 2023. DOI: 10.1021/acsinfecdis.3c00269
    OpenUrlCrossRefPubMed
  8. ↵
    1. Wang Y,
    2. Yang T,
    3. Gan C,
    4. Wang K,
    5. Sun B,
    6. Wang M,
    7. Zhu F
    : Temporal and spatial patterns of recurrence in oral squamous cell carcinoma, a single-center retrospective cohort study in China. BMC Oral Health 23(1): 679, 2023. DOI: 10.1186/s12903-023-03204-7
    OpenUrlCrossRefPubMed
  9. ↵
    1. Liao CT,
    2. Chang JT,
    3. Wang HM,
    4. Ng SH,
    5. Hsueh C,
    6. Lee LY,
    7. Lin CH,
    8. Chen IH,
    9. Huang SF,
    10. Cheng AJ,
    11. Yen TC
    : Salvage therapy in relapsed squamous cell carcinoma of the oral cavity: How and when? Cancer 112(1): 94-103, 2008. DOI: 10.1002/cncr.23142
    OpenUrlCrossRefPubMed
    1. Kernohan MD,
    2. Clark JR,
    3. Gao K,
    4. Ebrahimi A,
    5. Milross CG
    : Predicting the prognosis of oral squamous cell carcinoma after first recurrence. Arch Otolaryngol Head Neck Surg 136(12): 1235, 2010. DOI: 10.1001/archoto.2010.214
    OpenUrlCrossRefPubMed
  11. ↵
    1. Liu SA,
    2. Wong YK,
    3. Lin JC,
    4. Poon CK,
    5. Tung KC,
    6. Tsai WC
    : Impact of recurrence interval on survival of oral cavity squamous cell carcinoma patients after local relapse. Otolaryngol Head Neck Surg 136(1): 112-118, 2007. DOI: 10.1016/j.otohns.2006.07.002
    OpenUrlCrossRefPubMed
  12. ↵
    1. Fujii J,
    2. Ochi H,
    3. Yamada S
    : A comprehensive review of peroxiredoxin 4, a redox protein evolved in oxidative protein folding coupled with hydrogen peroxide detoxification. Free Radic Biol Med 227: 336-354, 2025. DOI: 10.1016/j.freeradbiomed.2024.12.015
    OpenUrlCrossRefPubMed
  13. ↵
    1. Yamada S,
    2. Guo X
    : Peroxiredoxin 4 (PRDX4): Its critical in vivo roles in animal models of metabolic syndrome ranging from atherosclerosis to nonalcoholic fatty liver disease. Pathol Int 68(2): 91-101, 2018. DOI: 10.1111/pin.12634
    OpenUrlCrossRefPubMed
  14. ↵
    1. Hanaka T,
    2. Kido T,
    3. Noguchi S,
    4. Yamada S,
    5. Noguchi H,
    6. Guo X,
    7. Nawata A,
    8. Wang KY,
    9. Oda K,
    10. Takaki T,
    11. Izumi H,
    12. Ishimoto H,
    13. Yatera K,
    14. Mukae H
    : The overexpression of peroxiredoxin-4 affects the progression of idiopathic pulmonary fibrosis. BMC Pulm Med 19(1): 265, 2019. DOI: 10.1186/s12890-019-1032-2
    OpenUrlCrossRefPubMed
  15. ↵
    1. Yamaguchi R,
    2. Guo X,
    3. Zheng J,
    4. Zhang J,
    5. Han J,
    6. Shioya A,
    7. Uramoto H,
    8. Mochizuki T,
    9. Yamada S
    : PRDX4 improved aging-related delayed wound healing in mice. J Invest Dermatol 141(11): 2720-2729, 2021. DOI: 10.1016/j.jid.2021.04.015
    OpenUrlCrossRefPubMed
  16. ↵
    1. Vu DA,
    2. Han J,
    3. Ichiseki T,
    4. Ueda S,
    5. Kumagai M,
    6. Shioya A,
    7. Oyama T,
    8. Liu Y,
    9. Yoshida M,
    10. Yamada S,
    11. Shimasaki M
    : Complementary roles of HMGB1 and PRDX4 in the pathophysiology of steroid-associated osteonecrosis of the femoral head: a histopathological and immunohistochemistry study. Virchows Arch, 2026. DOI: 10.1007/s00428-025-04371-4
    OpenUrlCrossRef
  17. ↵
    1. Zhang J,
    2. Guo X,
    3. Hamada T,
    4. Yokoyama S,
    5. Nakamura Y,
    6. Zheng J,
    7. Kurose N,
    8. Ishigaki Y,
    9. Uramoto H,
    10. Tanimoto A,
    11. Yamada S
    : Protective effects of peroxiredoxin 4 (PRDX4) on cholestatic liver injury. Int J Mol Sci 19(9): 2509, 2018. DOI: 10.3390/ijms19092509
    OpenUrlCrossRefPubMed
    1. Homma T,
    2. Kurahashi T,
    3. Lee J,
    4. Nabeshima A,
    5. Yamada S,
    6. Fujii J
    : Double knockout of peroxiredoxin 4 (Prdx4) and superoxide dismutase 1 (Sod1) in mice results in severe liver failure. Oxid Med Cell Longev 2018: 2812904, 2018. DOI: 10.1155/2018/2812904
    OpenUrlCrossRefPubMed
  19. ↵
    1. Nawata A,
    2. Noguchi H,
    3. Mazaki Y,
    4. Kurahashi T,
    5. Izumi H,
    6. Wang KY,
    7. Guo X,
    8. Uramoto H,
    9. Kohno K,
    10. Taniguchi H,
    11. Tanaka Y,
    12. Fujii J,
    13. Sasaguri Y,
    14. Tanimoto A,
    15. Nakayama T,
    16. Yamada S
    : Overexpression of peroxiredoxin 4 affects intestinal function in a dietary mouse model of nonalcoholic fatty liver disease. PLoS One 11(4): e0152549, 2016. DOI: 10.1371/journal.pone.0152549
    OpenUrlCrossRefPubMed
  20. ↵
    1. Guo X,
    2. Yamada S,
    3. Tanimoto A,
    4. Ding Y,
    5. Wang KY,
    6. Shimajiri S,
    7. Murata Y,
    8. Kimura S,
    9. Tasaki T,
    10. Nabeshima A,
    11. Watanabe T,
    12. Kohno K,
    13. Sasaguri Y
    : Overexpression of peroxiredoxin 4 attenuates atherosclerosis in apolipoprotein E knockout mice. Antioxid Redox Signal 17(10): 1362-1375, 2012. DOI: 10.1089/ars.2012.4549
    OpenUrlCrossRefPubMed
  21. ↵
    1. Ding Y,
    2. Yamada S,
    3. Wang KY,
    4. Shimajiri S,
    5. Guo X,
    6. Tanimoto A,
    7. Murata Y,
    8. Kitajima S,
    9. Watanabe T,
    10. Izumi H,
    11. Kohno K,
    12. Sasaguri Y
    : Overexpression of peroxiredoxin 4 protects against high-dose streptozotocin-induced diabetes by suppressing oxidative stress and cytokines in transgenic mice. Antioxid Redox Signal 13(10): 1477-1490, 2010. DOI: 10.1089/ars.2010.3137
    OpenUrlCrossRefPubMed
  22. ↵
    1. Nabeshima A,
    2. Yamada S,
    3. Guo X,
    4. Tanimoto A,
    5. Wang KY,
    6. Shimajiri S,
    7. Kimura S,
    8. Tasaki T,
    9. Noguchi H,
    10. Kitada S,
    11. Watanabe T,
    12. Fujii J,
    13. Kohno K,
    14. Sasaguri Y
    : Peroxiredoxin 4 protects against nonalcoholic steatohepatitis and type 2 diabetes in a nongenetic mouse model. Antioxid Redox Signal 19(17): 1983-1998, 2013. DOI: 10.1089/ars.2012.4946
    OpenUrlCrossRefPubMed
  23. ↵
    1. Shioya A,
    2. Guo X,
    3. Motono N,
    4. Mizuguchi S,
    5. Kurose N,
    6. Nakada S,
    7. Aikawa A,
    8. Ikeda Y,
    9. Uramoto H,
    10. Yamada S
    : The combination of weak expression of PRDX4 and very high MIB-1 labelling index independently predicts shorter disease-free survival in stage I lung adenocarcinoma. Int J Med Sci 15(10): 1025-1034, 2018. DOI: 10.7150/ijms.25734
    OpenUrlCrossRefPubMed
    1. Zheng J,
    2. Guo X,
    3. Nakamura Y,
    4. Zhou X,
    5. Yamaguchi R,
    6. Zhang J,
    7. Ishigaki Y,
    8. Uramoto H,
    9. Yamada S
    : Overexpression of PRDX4 modulates tumor microenvironment and promotes urethane-induced lung tumorigenesis. Oxid Med Cell Longev 2020: 8262730, 2020. DOI: 10.1155/2020/8262730
    OpenUrlCrossRefPubMed
  25. ↵
    1. Mizutani K,
    2. Guo X,
    3. Shioya A,
    4. Zhang J,
    5. Zheng J,
    6. Kurose N,
    7. Ishibashi H,
    8. Motono N,
    9. Uramoto H,
    10. Yamada S
    : The impact of PRDX4 and the EGFR mutation status on cellular proliferation in lung adenocarcinoma. Int J Med Sci 16(9): 1199-1206, 2019. DOI: 10.7150/ijms.36071
    OpenUrlCrossRefPubMed
  26. ↵
    1. Iwai S,
    2. Motono N,
    3. Oyama T,
    4. Shioya A,
    5. Yamada S,
    6. Uramoto H
    : The clinical relevance of the expression of SGLT2 in lung adenocarcinoma. Oncology 102(8): 710-719, 2024. DOI: 10.1159/000536060
    OpenUrlCrossRefPubMed
  27. ↵
    1. Guo X,
    2. Noguchi H,
    3. Ishii N,
    4. Homma T,
    5. Hamada T,
    6. Hiraki T,
    7. Zhang J,
    8. Matsuo K,
    9. Yokoyama S,
    10. Ishibashi H,
    11. Fukushige T,
    12. Kanekura T,
    13. Fujii J,
    14. Uramoto H,
    15. Tanimoto A,
    16. Yamada S
    : The association of peroxiredoxin 4 with the initiation and progression of hepatocellular carcinoma. Antioxid Redox Signal 30(10): 1271-1284, 2019. DOI: 10.1089/ars.2017.7426
    OpenUrlCrossRefPubMed
  28. ↵
    1. Liu Y,
    2. Han J,
    3. Shioya A,
    4. Zhang YX,
    5. Dung VA,
    6. Oyama T,
    7. Guo X,
    8. Yang Q,
    9. Ito T,
    10. Yamada S
    : The immunohistochemical combination of low SGLT2 expression and high PRDX4 expression independently predicts shortened survival in patients undergoing surgical resection for hepatoblastoma. Diagn Pathol 20(1): 2, 2025. DOI: 10.1186/s13000-025-01596-4
    OpenUrlCrossRefPubMed
  29. ↵
    1. Zheng J,
    2. Guo X,
    3. Shioya A,
    4. Yoshioka T,
    5. Matsumoto K,
    6. Hiraki T,
    7. Kusano H,
    8. Oyama T,
    9. Kurose N,
    10. Yamaguchi R,
    11. Uramoto H,
    12. Ieiri S,
    13. Okajima H,
    14. Kohno M,
    15. Yamada S
    : Peroxiredoxin 4 promotes embryonal hepatoblastoma cell migration but induces fetal cell differentiation. Am J Transl Res 12(6): 2726-2737, 2020.
    OpenUrlPubMed
  30. ↵
    1. Han J,
    2. Itoh T,
    3. Shioya A,
    4. Sakurai M,
    5. Oyama T,
    6. Kumagai M,
    7. Takamura H,
    8. Okuro M,
    9. Mukai T,
    10. Kitakata H,
    11. Inagaki M,
    12. Higashi M,
    13. Guo X,
    14. Yamada S
    : The combination of the low immunohistochemical expression of peroxiredoxin 4 and perilipin 2 predicts longer survival in pancreatic ductal adenocarcinoma with peroxiredoxin 4 possibly playing a main role. Histol Histopathol 38(12): 1415-1427, 2023. DOI: 10.14670/HH-18-666
    OpenUrlCrossRefPubMed
  31. ↵
    1. Park SY,
    2. Lee YJ,
    3. Park J,
    4. Kim TH,
    5. Hong SC,
    6. Jung EJ,
    7. Ju YT,
    8. Jeong CY,
    9. Park HJ,
    10. Ko GH,
    11. Song DH,
    12. Park M,
    13. Yoo J,
    14. Jeong SH
    : PRDX4 overexpression is associated with poor prognosis in gastric cancer. Oncol Lett 19(5): 3522-3530, 2020. DOI: 10.3892/ol.2020.11468
    OpenUrlCrossRefPubMed
  32. ↵
    1. Jia W,
    2. Chen P,
    3. Cheng Y
    : PRDX4 and its roles in various cancers. Technol Cancer Res Treat 18: 1533033819864313, 2019. DOI: 10.1177/1533033819864313
    OpenUrlCrossRef
  33. ↵
    1. Zhou H,
    2. Li L,
    3. Chen J,
    4. Hou S,
    5. Zhou T,
    6. Xiong Y
    : Expression and prognostic value of PRDX family in colon adenocarcinoma by integrating comprehensive analysis and in vitro and in vivo validation. Front Oncol 13: 1136738, 2023. DOI: 10.3389/fonc.2023.1136738
    OpenUrlCrossRefPubMed
  34. ↵
    1. Kocatürk B
    : In silico analysis reveals PRDX4 as a prognostic and oncogenic marker in renal papillary cell carcinoma. Gene 859: 147201, 2023. DOI: 10.1016/j.gene.2023.147201
    OpenUrlCrossRefPubMed
  35. ↵
    1. Basu A,
    2. Banerjee H,
    3. Rojas H,
    4. Martinez SR,
    5. Roy S,
    6. Jia Z,
    7. Lilly MB,
    8. De León M,
    9. Casiano CA
    : Differential expression of peroxiredoxins in prostate cancer: consistent upregulation of PRDX3 and PRDX4. Prostate 71(7): 755-765, 2011. DOI: 10.1002/pros.21292
    OpenUrlCrossRefPubMed
  36. ↵
    1. Ummanni R,
    2. Barreto F,
    3. Venz S,
    4. Scharf C,
    5. Barett C,
    6. Mannsperger HA,
    7. Brase JC,
    8. Kuner R,
    9. Schlomm T,
    10. Sauter G,
    11. Sültmann H,
    12. Korf U,
    13. Bokemeyer C,
    14. Walther R,
    15. Brümmendorf TH,
    16. Balabanov S
    : Peroxiredoxins 3 and 4 are overexpressed in prostate cancer tissue and affect the proliferation of prostate cancer cells in vitro. J Proteome Res 11(4): 2452-2466, 2012. DOI: 10.1021/pr201172n
    OpenUrlCrossRefPubMed
  37. ↵
    1. Jiang W,
    2. Wang M,
    3. Chen Q,
    4. Yu X,
    5. Liu G,
    6. He X,
    7. Mei C,
    8. Ou C
    : Immune infiltration related PRDX4 facilitates the malignant features and drug resistance of breast cancer. Sci Rep 15(1): 27507, 2025. DOI: 10.1038/s41598-025-13361-0
    OpenUrlCrossRefPubMed
  38. ↵
    1. Szeliga M
    : Comprehensive analysis of the expression levels and prognostic values of PRDX family genes in glioma. Neurochem Int 153: 105256, 2022. DOI: 10.1016/j.neuint.2021.105256
    OpenUrlCrossRefPubMed
  39. ↵
    1. Kim TH,
    2. Song J,
    3. Alcantara Llaguno SR,
    4. Murnan E,
    5. Liyanarachchi S,
    6. Palanichamy K,
    7. Yi JY,
    8. Viapiano MS,
    9. Nakano I,
    10. Yoon SO,
    11. Wu H,
    12. Parada LF,
    13. Kwon CH
    : Suppression of peroxiredoxin 4 in glioblastoma cells increases apoptosis and reduces tumor growth. PLoS One 7(8): e42818, 2012. DOI: 10.1371/journal.pone.0042818
    OpenUrlCrossRefPubMed
  40. ↵
    1. Demasi AP,
    2. Martinez EF,
    3. Napimoga MH,
    4. Freitas LL,
    5. Vassallo J,
    6. Duarte AS,
    7. Soares AB,
    8. Araujo NS,
    9. Araujo VC
    : Expression of peroxiredoxins I and IV in multiple myeloma: association with immunoglobulin accumulation. Virchows Arch 463(1): 47-55, 2013. DOI: 10.1007/s00428-013-1433-1
    OpenUrlCrossRefPubMed
  41. ↵
    1. Palande KK,
    2. Beekman R,
    3. van der Meeren LE,
    4. Beverloo HB,
    5. Valk PJ,
    6. Touw IP
    : The antioxidant protein peroxiredoxin 4 is epigenetically down regulated in acute promyelocytic leukemia. PLoS One 6(1): e16340, 2011. DOI: 10.1371/journal.pone.0016340
    OpenUrlCrossRefPubMed
  42. ↵
    1. Cao R,
    2. Zhang W,
    3. Zhang H,
    4. Wang L,
    5. Chen X,
    6. Ren X,
    7. Cheng B,
    8. Xia J
    : Comprehensive analysis of the PRDXs family in head and neck squamous cell carcinoma. Front Oncol 12: 798483, 2022. DOI: 10.3389/fonc.2022.798483
    OpenUrlCrossRefPubMed
  43. ↵
    1. Hwang JA,
    2. Song JS,
    3. Yu DY,
    4. Kim HR,
    5. Park HJ,
    6. Park YS,
    7. Kim WS,
    8. Choi CM
    : Peroxiredoxin 4 as an independent prognostic marker for survival in patients with early-stage lung squamous cell carcinoma. Int J Clin Exp Pathol 8(6): 6627-6635, 2015.
    OpenUrlPubMed
  44. ↵
    1. Chang KP,
    2. Yu JS,
    3. Chien KY,
    4. Lee CW,
    5. Liang Y,
    6. Liao CT,
    7. Yen TC,
    8. Lee LY,
    9. Huang LL,
    10. Liu SC,
    11. Chang YS,
    12. Chi LM
    : Identification of PRDX4 and P4HA2 as metastasis-associated proteins in oral cavity squamous cell carcinoma by comparative tissue proteomics of microdissected specimens using iTRAQ technology. J Proteome Res 10(11): 4935-4947, 2011. DOI: 10.1021/pr200311p
    OpenUrlCrossRefPubMed
  45. ↵
    1. Pedro NF,
    2. Biselli JM,
    3. Maniglia JV,
    4. Santi-Neto D,
    5. Pavarino ÉC,
    6. Goloni-Bertollo EM,
    7. Biselli-Chicote PM
    : Candidate biomarkers for oral squamous cell carcinoma: differential expression of oxidative stress-related genes. Asian Pac J Cancer Prev 19(5): 1343-1349, 2018. DOI: 10.22034/APJCP.2018.19.5.1343
    OpenUrlCrossRefPubMed
  46. ↵
    1. Li H,
    2. Wang Z,
    3. Chen X,
    4. Li S,
    5. Zhang F
    : Resveratrol downregulated PRDX4 expression to inhibit the progression of renal cell carcinoma via Wnt/β-catenin pathway. Food Sci Nutr 13(6): e70352, 2025. DOI: 10.1002/fsn3.70352
    OpenUrlCrossRef
  47. ↵
    1. Chen B,
    2. Lan J,
    3. Xiao Y,
    4. Liu P,
    5. Guo D,
    6. Gu Y,
    7. Song Y,
    8. Zhong Q,
    9. Ma D,
    10. Lei P,
    11. Liu Q
    : Long noncoding RNA TP53TG1 suppresses the growth and metastasis of hepatocellular carcinoma by regulating the PRDX4/β-catenin pathway. Cancer Lett 513: 75-89, 2021. DOI: 10.1016/j.canlet.2021.04.022
    OpenUrlCrossRefPubMed
  48. ↵
    1. Hugh TJ,
    2. Dillon SA,
    3. O’Dowd G,
    4. Getty B,
    5. Pignatelli M,
    6. Poston GJ,
    7. Kinsella AR
    : beta-Catenin expression in primary and metastatic colorectal carcinoma. Int J Cancer 82(4): 504-511, 1999. DOI: 10.1002/(sici)1097-0215(19990812)82:4<504::aid-ijc6>3.0.co;2-6
    OpenUrlCrossRefPubMed
  49. ↵
    1. Bahmad HF,
    2. Wegner C,
    3. Nuraj J,
    4. Avellan R,
    5. Gonzalez J,
    6. Mendez T,
    7. Jabbour D,
    8. Gomez-Fernandez C
    : Perineural invasion in breast cancer: a comprehensive review. Cancers (Basel) 17(12): 1900, 2025. DOI: 10.3390/cancers17121900
    OpenUrlCrossRefPubMed
  50. ↵
    1. Bhal S,
    2. Das B,
    3. Sinha S,
    4. Das C,
    5. Acharya SS,
    6. Maji J,
    7. Kundu CN
    : Resveratrol nanoparticles induce apoptosis in oral cancer stem cells by disrupting the interaction between β-catenin and GLI-1 through p53-independent activation of p21. Med Oncol 41(7): 167, 2024. DOI: 10.1007/s12032-024-02405-6
    OpenUrlCrossRefPubMed
    1. Esteban-Román NF,
    2. Taddei E,
    3. Castro-Velázquez E,
    4. Villafuentes-Vidal L,
    5. Velez-Herrera A,
    6. Rubio-Osornio M,
    7. Rubio C
    : Redox-regulated pathways in glioblastoma stem-like cells: mechanistic insights and therapeutic implications. Brain Sci 15(8): 884, 2025. DOI: 10.3390/brainsci15080884
    OpenUrlCrossRefPubMed
  52. ↵
    1. Nagano O,
    2. Okazaki S,
    3. Saya H
    : Redox regulation in stem-like cancer cells by CD44 variant isoforms. Oncogene 32(44): 5191-5198, 2013. DOI: 10.1038/onc.2012.638
    OpenUrlCrossRefPubMed
  53. ↵
    1. Ishikawa K,
    2. Suzuki H,
    3. Kaneko MK,
    4. Kato Y
    : Establishment of a novel anti-CD44 variant 10 monoclonal antibody C(44)Mab-18 for immunohistochemical analysis against oral squamous cell carcinomas. Curr Issues Mol Biol 45(7): 5248-5262, 2023. DOI: 10.3390/cimb45070333
    OpenUrlCrossRefPubMed
  54. ↵
    1. Guo L,
    2. Ke H,
    3. Zhang H,
    4. Zou L,
    5. Yang Q,
    6. Lu X,
    7. Zhao L,
    8. Jiao B
    : TDP43 promotes stemness of breast cancer stem cells through CD44 variant splicing isoforms. Cell Death Dis 13(5): 428, 2022. DOI: 10.1038/s41419-022-04867-w
    OpenUrlCrossRefPubMed
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PRDX4 Potentially Serves as an Independent Marker for Early Recurrence of Oral Squamous Cell Carcinoma
TAIJIRO HASHIMOTO, TAKERU OYAMA, YANGXIAN ZHANG, YUKINOBU ITO, JIA HAN, YAO LIU, MITSUAKI YOSHIDA, AKIHIRO SHIOYA, MASASHI OKURO, MORIMASA KITAMURA, SOHSUKE YAMADA
Anticancer Research May 2026, 46 (5) 2583-2597; DOI: 10.21873/anticanres.18139
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