Histology and histopathology, Vol.41, Nº1, (2026)

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    Expression of mucins MUC1 and MUC4 in curative resected gallbladder adenocarcinoma
    (Editum, 2026) Michiyo Higashi; Ikumi Kitazono; Seiya Yokoyama; Takashi Tasaki; Hirotsugu Noguchi; Mari Kirishima; Miki Murakami; Akihide Tanimoto; Masako Noumi; Biología Celular e Histología
    Background and Aims. Gallbladder adenocarcinoma (GBAC) is associated with high mortality because of the difficulty in its early detection and treatment. Therefore, identifying prognostic factors is crucial for managing patients with GBAC. We aimed to elucidate the relationship between immunohisto-chemical profiles of mucin expression, clinico-pathological behavior, and prognosis for curatively resected gallbladder adenocarcinoma (GBAC) and to prove that mucin expression is a prognostic factor for GBAC. Methods. We examined the expression of mucins (MUC1, MUC2, and MUC4) using immunohisto-chemical analyses and compared the prevalence of each mucin with clinicopathological features in patients with early-stage (stage 0 to IIB) GBAC. Results. MUC1 expression was significantly expressed in patients with GBAC with lymphatic invasion, vascular invasion, perineural invasion, and recurrence. MUC2 was significantly expressed in patients with GBAC with perineural invasion and recurrence but not with prognosis. Patients with MUC1-high expression exhibited worse prognoses than those with MUC1-low expression. In contrast, patients with positive MUC4 expression had significantly better prognoses than those without MUC4 expression. Conclusion. The expression of MUC1 and MUC4 in GBAC is an independent prognostic factor for survival and a useful marker for predicting the outcomes of patients with GBAC.
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    High histamine expression by early-stage squamous cell carcinoma of the tongue is associated with a poor prognosis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Hirotsugu Noguchi; Hiroaki Sato; Shohei Shimajiri; Toshiyuki Nakayama; Satoshi Kimura; Biología Celular e Histología
    Background. Although not widely known, several types of cancers express histamine. Squamous cell carcinoma (SCC) of the tongue is one such cancer, and histamine expression is associated with the tumor microenvironment. Our aim was to examine whether histamine expression is a useful prognostic factor for tongue SCC. Methods. Histamine cannot be accurately measured directly because it is rapidly degraded after secretion. Therefore, L-histidine decarboxylase (HDC), an enzyme that synthesizes histamine in a single step, was used to estimate histamine secretion. In a retrospective study, tongue SCC samples from patients were immunohisto-chemically stained for HDC; the staining intensity was semi-quantified and evaluated relative to indices used in histopathological diagnosis. Results. High expression of HDC was associated with the worst tumor invasion and tumor budding. Overall survival curves revealed that patients with tongue SCC showing high HDC expression had a poor prognosis. Conclusion. The expression of histamine may be a prognostic indicator for tongue SCC.
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    Bioartificial human corneas generated by tissue engineering. A historical and technical review
    (2026) Pascual-Vicente Crespo; José-Manuel García; Maria-Carmen Sánchez-Quevedo; Antonio Campos; Miguel Alaminos; Biología Celular e Histología
    Different types of bioartificial corneas have been generated by tissue engineering through combining cells, biomaterials, and bioactive molecules. Orthotypical corneal cells can be obtained from corneal biopsies, and include epithelial, stromal, and endothelial cells, whereas heterotypical cells are obtained from alternative cell sources with corneal differentiation potential, such as mesenchymal stem cells. In turn, two main types of biomaterials have been applied to corneal tissue engineering: those generated by the de-cellularization of natural tissues and biomaterials generated de novo using synthetic or natural biomaterials, especially collagen, fibrin, and agarose. Cells and biomaterials are combined with bioactive factors, inducing cell proliferation and differentiation. A review of previous studies revealed that most bioartificial corneas were not able to fulfill the complex requirements required for clinical translation, which include a thorough preclinical characterization, generation of the tissue as an advanced therapy medicinal product, a clinical research phase, and a final authorization by the European Medicines Agency or another competent regulatory agency. Most authorized products correspond to partial corneal substitutes consisting of one cell type associated or not with a scaffold, and only one product consisting of a human bioartificial cornea containing a fibrin-agarose scaffold and two corneal cell lineages (epithelial and stromal cells) called NANOULCOR was evaluated in patients in the context of an advanced therapy medicinal product. These findings confirm the existence of a bottleneck between basic and clinical research and suggest the need to implement novel clinical studies to develop new therapies that can improve the results of current corneal therapies.
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    KIF22 promotes the proliferation and immune escape of endometrial cancer cells by activating the STAT3/PDL1 pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Chaohe Zhang; Chaoqun Wang; Biología Celular e Histología
    Objective. Endometrial cancer (EC) is a common gynecologic malignancy with high morbidity and mortality. Kinesin Family member 22 (KIF22) is regarded as a critical oncogene, but its functions in EC progression remained elusive. Hence, this research elucidated the role of KIF22 in EC development and studied the possible mechanism. Methods. KIF22 expression in EC and the relationship with the overall survival of EC cases were determined by GEPIA and online K-M plotter. After transfection with sh-KIF22, cell viability and invasion were evaluated utilizing CCK-8 and Transwell assays. The content of IFN-γ, IL-2, and TNF-α was assessed utilizing an ELISA assay. The protein levels of p-STAT3, STAT3, and PD-L1 were examined using western blot. A xenograft tumor was constructed to assess tumor growth. Results. KIF22 was elevated in EC, with high KIF22 levels presenting poor overall survival. Additionally, silenced KIF22 restrained EC cell viability, invasion ability, and STAT3/PD-L1 pathway, enhanced the viability of CD8+ T cells, and elevated the levels of IFN-γ, IL-2, and TNF-α. Moreover, the rescue assay revealed that STAT3 overexpression counteracted the inhibitory effect of silenced KIF22 on EC cell proliferation, invasion and immune escape. Furthermore, silenced KIF22 repressed EC tumor growth and p-STAT3 and PD-L1 levels, and elevated the IFN-γ level in vivo. Conclusion. The findings demonstrated that KIF22 was elevated in EC and correlated with a poor prognosis. Silenced KIF22 repressed cell proliferation, invasion, and immune escape via suppressing the STAT3/PD-L1 pathway in EC.
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    Trophoblast-derived proteins and their effects on the pathogenesis of preeclampsia
    (Editum, 2026) Yanan Wang; Xueling Chen; Haifeng Zhang; Yunshan Xue; Haibin Chen; Ju Yang; Biología Celular e Histología
    Trophoblast cells are crucial structural units of the placenta, responsible for maintaining its integrity and function. These cells synthesize and secrete specific proteins that play essential roles in placental vascularization, maternal and fetal immune tolerance, and other critical processes. An abnormal level of trophoblast-derived secreted proteins has been closely linked to pregnancy-related diseases. Preeclampsia, a severe complication of pregnancy characterized by de-novo development of hypertension and proteinuria after 20 weeks of gestation, poses significant health risks to both the mother and fetus. This article reviews several key trophoblast-derived proteins that are widely recognized for their roles in preeclampsia. The specific mechanisms of action and interconnections among these proteins in preeclampsia are discussed, along with novel insights into the underlying pathological mechanisms of this disease.
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    Pachymic acid ameliorates polycystic ovary syndrome via inactivating Akt/ERK signaling
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Chunhua Zhang; Fang Fang; Yuanyuan Yi; Dongmei Ji; Biología Celular e Histología
    Objective. Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder that adversely affects women’s health and quality of life. Pachymic acid (PA), a bioactive ingredient from Poria cocos (Schw.) Wolf, has demonstrated protective effects against PCOS in a murine model. This study aims to investigate the underlying mechanism by which PA exerts protective effects against PCOS. Methods. Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS in vitro. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for in vitro cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells. Results. PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001). Conclusion. PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.
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    The evolution of mast cells across all vertebrate classes: The mystery continues
    (Editum, 2026) Stefano Bacci; Biología Celular e Histología
    The paper examines what the mast cell, a cell that arose in urochordates and reached humans with the same morphological profile, is used for. Activated mast cells contribute to the regulation of the local immune response and major inflammation and healing processes with the help of a broad range of mediators. Located primarily at the interface between the host and the external environment, mast cells are widely distributed. The local microenvironment directly affects mast cell development, phenotype, and function, which in turn affects the cells' capacity to identify and react to different stimuli by releasing a variety of physiologically active mediators. By interacting with a range of other cells involved in physiological and immunological responses, mast cells can react to changes in their surroundings and serve as first responders in dangerous situations. Consequently, the mast cell’s crucial function in innate and adaptive immunity, including immuno-logical tolerance, has come to light more frequently. On the other hand, mast cell malfunction has identified these cells as the primary culprits in a number of autoimmune illnesses, cancer, and chronic allergic/inflammatory conditions.
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    Therapeutic potential of porphyran in mitigating ischemia-reperfusion injury in gerbil hippocampus
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Tae-Kyeong Lee; Joon Ha Park; Dae Won Kim; Choong-Hyun Lee; Moo-Ho Won; Il Jun Kang; Ji Hyeon Ahn; Biología Celular e Histología
    Cerebral ischemia-reperfusion (IR) injury is a critical pathological event that leads to extensive neuronal loss, neuroinflammation, and blood-brain barrier (BBB) dysfunction. Porphyran, a sulfated polysaccharide derived from Porphyra spp., has demonstrated anti-inflammatory and neuroprotective effects in various neurological conditions. This study aimed to evaluate the post-ischemic therapeutic potential of porphyran in a gerbil model of transient forebrain ischemia. Our findings reveal that porphyran administration (50 mg/kg orally once daily for five days) following IR significantly mitigated IR-induced cognitive decline, as evidenced by the Y-maze test, but porphyran treatment did not significantly prevent neuronal death in the CA1 subregion of the hippocampus, as revealed by Cresyl Violet (CV) and Fluoro-Jade B (FJB) staining. However, porphyran treatment after IR injury effectively attenuated the IR-induced decrease in acetylcholine (ACh) levels, suggesting potential preservation of cognitive function in surviving neurons. Furthermore, porphyran significantly mitigated microglial activation and reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), indicating its anti-inflammatory properties. Additionally, porphyran administration reduced BBB disruption, as evidenced by decreased extravasation of immuno-globulin G (IgG), suggesting a role in maintaining vascular integrity. In summary, although porphyrin administration after IR does not protect pyramidal neurons directly, it may improve cognitive function by mitigating ACh depletion, suppressing microglial activation, and reducing inflammatory cytokine levels
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    ENO3 regulates ferroptosis by interaction with PKM2 to promote the progression of metabolic dysfunction-associated steatotic liver disease
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Qian Hao; Xue Li; Jing Liu; Minghao Li; Baoding Li; Shengjuan Hu; Yanling Li; Xiaofei Li; Yuanyuan Tang; Fuliang Pan; Yanxia Liu; Min Niu; Zhenzi Cao; Biología Celular e Histología
    Background. Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder characterized by excessive lipid accumulation in the liver. The glycolytic enzyme enolase 3 (ENO3) is reported to be most significantly elevated in the analysis of MASLD-related sequencing results based on the GEO database. However, the specific mechanism by which ENO3 regulates MASLD is not fully understood. Objective. To investigate the role and possible molecular mechanism of ENO3 in MASLD. Methods. The expression of ENO3 and PKM2 in the liver tissues of control and MASLD rats was detected by immunohistochemistry and western blot. In vitro studies involved treating THLE-2 cells with free fatty acids (FFA) and Ferrostatin-1 (Fer-1), as well as manipulating ENO3 expression via small interfering RNA (siRNA) and overexpression plasmids, and manipulating PKM2 expression via siRNA. Fat accumulation was assessed using Oil Red O staining and measurements of intracellular total cholesterol (TC) and triglycerides (TG). Ferroptosis markers, including SLC7A11, GPX4, Fe2+, and malondialdehyde (MDA), were evaluated. Protein-protein interactions between ENO3 and PKM2 were examined using co-immunoprecipitation (Co-IP) and immunofluorescence. Results. MASLD liver tissues exhibited significantly higher levels of ENO3 and PKM2. Silencing ENO3 in FFA-treated THLE-2 cells reduced fat accumulation, downregulated PKM2 expression, and decreased ferroptosis markers. Conversely, ENO3 overexpression promoted fat accumulation and ferroptosis, which were mitigated by Fer-1 or si-PKM2. Co-IP and immuno-fluorescence confirmed the physical interaction and co-localization of ENO3 and PKM2 in THLE-2 cells. Conclusions. ENO3 interacted with PKM2 to regulate ferroptosis and further promoted the progression of MASLD.
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    Lysophosphatidylcholine negatively reverses the effects of human umbilical cord-derived mesenchymal stem cells on high glucose-induced cell dysfunction
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Yong Chai; Han Liu; Yao Zhao; ChunYi Liu; Rui Luo; Qiang Gan; Xian Liu; Biología Celular e Histología
    Background. Increasing attention has been attracted to the application of human umbilical cord-derived mesenchymal stem cells (HUCMSCs) in the cell therapy of various diabetic complications, including diabetic retinopathy (DR). Lysophosphatidylcholine (LPC) has been reported to induce cell apoptosis and an inflammatory response. The present study aimed to investigate the mechanism of HUCMSCs in high glucose (HG)-treated retinal microvascular endothelial cells (RMECs) and the effect of LPC on this mechanism. Methods. To mimic DR in vitro, RMECs were treated with HG. Flow cytometry analysis was used to identify HUCMSCs and the expression of their surface markers. The apoptosis of RMECs was also accessed using flow cytometry analysis. A CCK-8 assay was performed to measure the viability of RMECs. ELISA was used to detect the concentration of inflammatory cytokines (TNF-α, IL-6, and IL-1β) in RMECs. The protein expression of tight junction proteins in RMECs was examined using western blot analysis. Results. HUCMSCs were identified to present positive markers (CD105, CD73, and CD90) and loss of negative markers (CD45, CD34, and HLA-DR). In RMECs, HG significantly induced a decrease in cell viability and an increase in cell apoptosis and tight junction proteins. Moreover, HG treatment promoted the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) and facilitated oxidative stress. However, these dysregulated cellular behaviors were alleviated by the treatment of the culture medium of HUCMSCs. Furthermore, LPC treatment reversed the effect of HUCMSCs on HG-induced RMEC injury and impaired the blood-retinal barrier. Moreover, the effect of HUCMSCs on the inflammatory response and oxidative stress of RMEC was also neutralized by LPC treatment. Conclusion. LPC reverses the effects of HUCMSCs on HG-induced RMEC dysfunction, impaired blood-retinal barrier, inflammation, and oxidative stress
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    HMMR inhibition by 4-methylumbelliferone is effective in preclinical hepatocellular carcinoma models
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Ge Sang Wang Dui2; Suo Lang Bai Ma; Ci Yang; Wen Xu; Jianguo Xu; Ying Zhu; Biología Celular e Histología
    The poor prognosis of hepatocellular carcinoma (HCC), especially in advanced stages, underscores the need for new therapeutic strategies. In this study, we show that hyaluronan-mediated motility receptor (HMMR) is highly expressed in HCC tumors compared with normal liver tissues. Knockdown of HMMR using siRNA significantly reduced cell proliferation and migration in both parental and doxorubicin-resistant HCC cell lines without inducing apoptosis. Similarly, treatment with 4-Methyl-umbelliferone (4-MU), a pharmacological HMMR inhibitor, led to dose-dependent decreases in proliferation and migration in vitro. In vivo, 4-MU treatment significantly inhibited tumor growth in a HepG2 xenograft model, resulting in a 44% reduction in tumor volume by day 20 and an 80% decrease in HMMR expression in tumor tissues. These results demonstrate that HMMR promotes growth and migration in HCC, and targeting HMMR effectively inhibits both parental and drug-resistant HCC cells. Additionally, our findings suggest that 4-MU, an approved drug for biliary tract disorders, holds promise as a repurposed therapeutic candidate for HCC treatment.
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    AHSA1 promotes the progression of lung cancer by enhancing the expression of HSP90α
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Zifeng Jiang; Kun Gao; Min Wang; Biología Celular e Histología
    Background. Lung cancer (LC) is a leading cause of malignancy-related morbidity and mortality worldwide. The activator of 90 kDa heat shock protein ATPase homolog 1 (AHSA1), one of the chaperones of heat shock protein 90 kDa (heat shock protein 90, HSP90), is involved in the maturation, stabilization, degradation, and function of oncogenic proteins. The aim of this study was to investigate the specific mechanism and role of AHSA1 in LC development. Methods. Expression of AHSA1 in LC was analyzed using The Cancer Genome Atlas (TCGA) database. AHSA1 expression in LC cells and tissues was assessed by qRT-PCR and western blotting. In addition, Kaplan-Meier plotter analysis and univariate and multivariate Cox analyses were used to evaluate the relationship between AHSA1 and clinicopathological variables and prognosis. The effects of AHSA1 on LC cell proliferation and migration were observed using cell counting kit-8, flow cytometry, wound healing, and Transwell assays. Target genes were predicted by bioinformatics and subsequently validated using a qRT-PCR assay. Results. AHSA1 exhibited significant upregulation in LC tissues and cell lines, with its elevated expression correlating with adverse prognostic outcomes in LC patients. Functional assays revealed that downregulation of AHSA1 markedly impedes the proliferation, migration, and invasion of LC cells. Conversely, overexpression of AHSA1 enhanced these malignant behaviors. Furthermore, bioinformatics analysis suggested a potential interaction between AHSA1 and HSP90α, which was also found to be highly expressed in LC cells, exhibiting a notable increase in expression levels following AHSA1 upregulation. Conclusions. AHSA1 is implicated in promoting the progression of LC by enhancing the malignant phenotype of cancer cells through the upregulation of HSP90α expression, which may underlie the association of AHSA1 expression with adverse clinicopathologic features in LC patients. These findings indicate that AHSA1 serves as a potential prognostic biomarker and represents a viable therapeutic target for LC
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    Osteofibrous dysplasia (OFD) and adamantinoma: A comprehensive review and updates
    (2026) Bharat Rekhi; Radhika Jayan; Biología Celular e Histología
    Osteofibrous dysplasia (OFD) and adamantinoma constitute rare bone tumors. Currently, the World Health Organization (WHO) classification of soft tissue and bone tumors stratifies adamantinoma into three main subtypes, namely OFD-like adamantinoma, classic adamantinoma, including its various growth patterns, and an extremely uncommon subtype, dedifferentiated adamantinoma. Given the wide clinicopathological spectrum of adamantinoma, several tumors constitute the differential diagnoses. An exact diagnosis in these scenarios has significant treatment-related implications, such as synovial sarcoma vs. spindle cell-type adamantinoma, and metastatic sarcomatoid carcinoma vs. adamantinoma, to name but a few. There have been studies attempting to explore the proximity/relationship between OFD, OFD-like adamantinoma, and classic adamantinoma. This review focuses on the clinical, radiological, and pathological features of OFD, as well as the histopathological spectrum of adamantinoma, including its updates and various subtypes and tumors that constitute its differential diagnosis.
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    Antagonism of GPR4 with NE 52-QQ57 alleviates gestational diabetes mellitus-induced placental insults mediated by inhibiting NF-κB
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Zongxu Qiao; Jinhui Feng; Yaning Wang; Xiaohui Zhao; Fang Li1; Biología Celular e Histología
    Gestational diabetes mellitus (GDM) refers to a diabetic condition observed in pregnant women, significantly affecting both the health of the mother and the growth of the offspring. G protein-coupled receptor 4 (GPR4) is a receptor widely distributed across various tissues, but its role in GDM remains unclear. Our research aims to investigate the role of GPR4 in GDM and explore the potential therapeutic effects of its antagonist, NE 52-QQ57, in treating this condition. First, we found that GPR4 was expressed in placental tissues. Mice were divided into three groups: wild-type, db/+ pair-fed, and db/+ pair-fed + NE 52-QQ57. GPR4 expression was significantly higher in the db/+ pair-fed mice compared with wild-type mice. Markedly increased blood glucose and serum insulin levels were observed in GDM mice on gestational days (GD), accompanied by disrupted lipid profiles, all of which were significantly alleviated by NE 52-QQ57. Moreover, undesirable fetal outcomes, including increased fetal mortality, decreased fetal weight, reduced crown-rump length, and decreased placental weight, were observed in GDM mice, however, all were notably improved by NE 52-QQ57. Increased oxidative stress (OS) and the release of inflammatory cytokines were observed in GDM mice, but these were significantly reversed by NE 52-QQ57. Additionally, activated nuclear factor κ-B (NF-κB) signaling in placental tissues of GDM mice was significantly suppressed by NE 52-QQ57. Collectively, antagonism of GPR4 protected against GDM-induced placental damage in mice, confirming the critical role of GPR4 in the development of GDM.
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    Tuoli Xiaodu powder ameliorated 5-fluorouracil-induced intestinal injury by reducing intestinal inflammation, oxidative stress, and intestinal flora imbalance
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Ling Jiang; Wanrou Jiang; Wanyi Zhang; Wenjuan Zheng; Hongjie Huang; Yu Xia; Xiuyun He; Chaofu Zhu; Yongjun Wu; Biología Celular e Histología
    Chemotherapy-induced diarrhea (CID) is a common adverse event in cancer patients treated with 5-fluorouracil (5-FU). This study aimed to investigate the potential protective effects of Tuoli Xiaodu (TLXD) powder on CID and to explore its possible mechanisms. Mice with CID induced by 5-FU were randomly divided into seven groups: Blank group, CID group, positive drug (loperamide) group, and TLXD powder low, medium, and high groups. The degree of diarrhea, tumor growth, intestinal barrier damage, intestinal inflammation, oxidative stress, and gut microbiota diversity were assessed. The study showed that TLXD powder significantly inhibited diarrhea and tumor growth in 5-FU-induced CID mice. H&E staining and western blot showed that TLXD powder improved the intestinal mucosa and intestinal permeability of 5-FU-induced CID mice. Furthermore, TLXD powder elicited a reduction in the expression of inflammatory factors within the intestinal tract of mice with CID while simultaneously augmenting the expression of anti-inflammatory factors and maintaining a balanced Th17/Treg ratio. TLXD powder decreased intestinal oxidative stress and intestinal epithelial cell ferroptosis and activated the Nrf2/HO-1 signaling axis in CID mice. The results of the gut flora analysis showed that TLXD powder improved the intestinal flora structure of CID mice. TLXD powder significantly reduced the proportion of Proteobacteria, Actinobacteria, Deferribacteres, and TM7 at the phylum level and Desulfovibrio, Mucispirillum, Adlercreutzia, and Odoribacter at the genus level. These findings provide a new therapeutic approach for the management of CID in cancer patients treated with 5-FU