Published online Dec 28, 2026. doi: 10.3748/wjg.121570
Revised: April 18, 2026
Accepted: June 26, 2026
Published online: December 28, 2026
Processing time: 221 Days and 6 Hours
The early detection of pancreatic adenocarcinoma remains a major clinical cha
To evaluate cadherin-17 (CDH17) as a potential diagnostic and prognostic bio
CDH17 expression was assessed in pancreatic tissue samples using immunohistochemistry quantified by the M-score method. This included 25 paired tumor and normal adjacent tissues, along with 22 healthy controls. Plasma levels of soluble CDH17 were measured in 242 samples (28 patients pre/post-treatment, 156 heal
In tissue samples, CDH17 expression was significantly higher in cancer tissues compared to both normal adjacent tissues (P = 0.0005) and healthy controls (P = 0.000001). Analysis of 242 plasma samples showed that soluble CDH17 could distinguish early-stage cancer patients from healthy controls with 86% sensitivity and 86% specificity (area under the curve = 0.920). By contrast, CA19-9 demonstrated diagnostic value only in late-stage disease (area under the curve = 0.813). Prognostically, elevated CA19-9 was significantly asso
CDH17 is consistently upregulated in pancreatic adenocarcinoma and it shows potential as a complementary bio
Core Tip: In this pilot study, cadherin-17 (CDH17) was markedly upregulated in pancreatic adenocarcinoma tissue, and its soluble form in plasma distinguished early-stage patients from healthy controls with 86% sensitivity and specificity. These findings point to the biomarker panel consisting of CDH17 and carbohydrate antigen 19-9 offers a possible strategy to address the pressing need for both earlier detection and monitoring disease burden in this malignancy.
- Citation: Cho WC, Yu WS, Hon TC, Cheung ETY, Wang XQ, Wong DA, Wong CSC, Cheuk W, Luk JM. Cadherin-17: A potential biomarker for early detection in pancreatic adenocarcinoma. World J Gastroenterol 2026; 32(48): 121570
- URL: https://www.wjgnet.com/1007-9327/full/v32/i48/121570.htm
- DOI: https://dx.doi.org/10.3748/wjg.121570
Pancreatic cancer is among the most aggressive and lethal malignancies, with a five-year survival rate of only 13%, primarily due to late diagnosis, rapid progression, and resistance to conventional therapies[1,2]. The clinical management of pancreatic cancer is further complicated by a highly complex tumor microenvironment, pronounced genetic heterogeneity, and the lack of reliable biomarkers for early detection[3]. Early symptoms are often vague or absent, leading to delayed detection and advanced disease at presentation[4]. While novel diagnostic tools have emerged, including liquid biopsies and artificial intelligence-based technologies, issues with sensitivity, specificity, and clinical integration persist[5,6]. Recent research has focused on molecular pathways, immune evasion, and tumor-stroma interactions to identify therapeutic targets[7]. Nevertheless, treating advanced disease remains difficult, and biological complexity continues to drive resistance and recurrence[8,9]. Thus, the development of robust biomarkers for early detection and disease moni
Cadherin 17 (CDH17) is a differentiation marker in intestinal cells that interacts with and activates α2β1 integrin, enhancing cell adhesion and proliferation during cancer metastasis[11]. It has been shown to promote the progression of digestive system tumors[12]. CDH17 is associated with heightened invasiveness and metastatic potential in certain gastrointestinal (GI) cancers, contributing to disease advancement[13,14]. Critically, CDH17 is consistently overexpressed across a spectrum of GI cancers, including colorectal[15,16], gastric[17,18], and pancreatic[19] malignancies. Given its elevated expression in these cancers, soluble form of CDH17 may serve as a diagnostic biomarker and prognostic indi
Recent reports consistently showed CDH17 overexpression in tumor tissues of GI cancers[20,21]. Methodologically, the field has largely relied on tissue-based immunohistochemistry (IHC) with semiquantitative scoring, only a few studies have explored circulating CDH17. Emerging evidence from tissue microarray (TMA) studies has confirmed CDH17 expression across multiple GI malignancies[22]. TMA-based studies, while valuable for high-throughput screening, are inherently limited by the small, geographically fixed tissue cores examined, which may not capture intratumoural heterogeneity or reflect expression patterns in whole tissue sections. Moreover, direct comparisons between CDH17 and established clinical biomarkers, carbohydrate antigen 19-9 (CA19-9), have yet to be undertaken. As a result, the incre
Tissue samples were obtained from 25 patients with pathologically confirmed pancreatic adenocarcinoma at Queen Elizabeth Hospital (Hong Kong, China). Both tumor and normal adjacent tissues were collected during surgery and subsequently processed into formalin-fixed, paraffin-embedded (FFPE) blocks. Corresponding clinicopathological data, such as patient demographics and tumor characteristics (including tumor-node-metastasis stage and recurrence status), were retrieved for subsequent statistical analysis. Inclusion criteria for cancer patients were: (1) Pathologically confirmed pancreatic adenocarcinoma; (2) Available FFPE tissue blocks or plasma samples; and (3) Complete clinicopathological data. Exclusion criteria were: (1) Prior neoadjuvant therapy; (2) Concurrent second malignancy; and (3) Insufficient sample quality. All diagnoses were verified by a board-certified pathologist. The study protocol was approved by the Institutional Review Board. In addition, FFPE TMAs comprising 22 normal pancreatic tissue samples were obtained from Biomax (Rockville, United States) and used as controls.
The study also analyzed a total of 242 plasma samples, including 28 paired samples collected from pancreatic adeno
Automated IHC staining for CDH17 was performed on both tumor tissues and TMAs using an autostainer (Thermo Fisher Scientific, Waltham, United States) following the manufacturer’s protocol. Antigen retrieval was conducted using an automated system with retrieval buffer preheated to 60 °C, followed by retrieval at 98 °C for 20 minutes and cooling to 80 °C. The tissue slides were rinsed under running tap water for 5 minutes and then placed in an automatic stainer for staining. Detection used a ready-to-use mouse horseradish peroxidase-conjugated secondary antibody (BioLegend, Seattle, United States), with signal development using 3,3'-diaminobenzidine reagents (GeneTech SH, Shanghai, China). All reagents were diluted in phosphate-buffered saline (PBS), and Tris-buffered solution containing 0.05% Tween-20 was used as wash buffer between steps. After staining, slides were rinsed and counterstained with hematoxylin.
Images of stained tissues were captured at 20X magnification using an Olympus microscope (BX63) and an Applied Spectral Imaging System (Applied Spectral Imaging, Carlsbad, United States). Five representative areas were analyzed per section, focusing on areas with well-preserved tissue morphology while avoiding areas of necrosis or artifacts. Over 10000 cells were counted per sample. CDH17 immunostaining was quantified using the M-score method. The M-score is a quantitative measure of membrane staining that integrates staining intensity (i: 0 = none, 1 = weak, 2 = moderate, 3 = strong) and the percentage of stained cells at each intensity level (Pi: 0%-100%), calculated ranging from 0 to 50. For each tissue section, the M-score was calculated by the sum of ‘I’ multiplied by the corresponding ‘Pi’ divided by 6 as shown in the following formula: M-score = [(0 × P0) + (1 × P1) + (2 × P2) + (3 × P3)]/(0 + 1 + 2 + 3). Immunohistochemical quantification and analysis were performed in a blinded manner to clinical data. The cut-off for CDH17 positivity was set at an M-score ≥ 1. This threshold was determined from visual inspection of the staining patterns and M-score distribution in healthy pancreatic tissues. Healthy controls consistently showed weak, non-specific background staining without definite membranous CDH17 expression, with all M scores < 1 and a maximum value of 0.9. We therefore considered 0.9 as the upper bound of background signal and selected an M score ≥ 1 to distinguish specific positive CDH17 expression from background noise. To assess the performance of digital image analysis, whole slide images from stained cancer cases were independently reviewed by a board-certified pathologist. For each intensity level (i), the pathologist estimated the percentage of positively stained cells, and these figures were then used to derive the M-score.
EDTA plasma samples were assayed using a human CDH17 ELISA kit (catalog # TIB-EK01, Tiberias Technology (HK) Limited, Hong Kong, China). The immunoassay used a mixture of three in-house anti-CDH17 monoclonal antibodies (Tib-01, Tib-02, Tib-03, 3 μg/mL) and commercially available pooled healthy human EDTA plasma (catalog # PR100-K2-100-U1, TCS Biosciences, Buckingham, United Kingdom) as the matrix. It has been determined that a 1:10 dilution of plasma in wash buffer (0.1% bovine serum albumin, 0.05% Tween-20 in 1X PBS) was optimal for the detection of CDH17 in human EDTA plasma. Unless otherwise stated, all dilutions and incubation times were performed at room tempera
EDTA plasma samples were assayed using a commercially available human CA19-9 ELISA kit (catalog # E-EL-H0637, Elabscience, Houston, TX, United States) according to the manufacturer’s instructions. The signal was measured using a microtiter plate reader (model # SpectraMax i3X, Molecular Device) with a 450 nm filter.
All statistical analyses were conducted using IBM SPSS Statistics 26 (New York, NY, United States), GraphPad Prism 10 (Boston, MA, United States), and R software (Vienna, Austria). The distribution of sample data was first assessed for normality, complemented by visual inspection of Q-Q plots and histograms. These assessments revealed that the majority of continuous variables, including CDH17 M-scores and plasma CDH17 and CA19-9 levels, deviated significantly from a normal distribution (P < 0.05), with evidence of positive skewness and unequal variances across groups. Accordingly, non-parametric methods were selected for all group comparisons to avoid the assumptions of normality required by parametric tests. Group comparisons between independent groups were therefore performed using the Mann-Whitney U test, while comparisons between paired samples used the Wilcoxon signed-rank test. Disease-free survival (DFS) and overall survival (OS) outcomes were analyzed using Kaplan-Meier survival curves, and differences between groups were evaluated with the log-rank (Mantel-Cox) test. The diagnostic performance of plasma CDH17 and CA19-9 was assessed using receiver operating characteristic (ROC) curve analysis, with the optimal cut-off values determined by the Youden Index. Multiple logistic regression models were constructed to evaluate the combined diagnostic performance of CDH17 and CA19-9. The predicted probability from the model was used to generate a combined ROC curve. Subgroup analyses for prognosis were considered exploratory, exact sample sizes and 95% confidence intervals (CIs) for median survival were reported where applicable. A P value of less than 0.05 was considered statistically significant.
A total of 72 pancreatic tissue samples were evaluated for CDH17 antigen expression by IHC. These included 25 paired tumor and normal adjacent tissue specimens, along with 22 normal pancreatic tissue samples obtained from TMAs. The demographic characteristics of these subjects are summarized in Table 1. The cancer group consisted of 25 patients with a balanced gender distribution: 12 males (48%) and 13 females (52%). Their median age was 65 years, ranging from 35 to 75. In terms of smoking status, the majority were non-smokers (68%), while 8% were current smokers and 12% were ex-smokers, data were unavailable for the remaining 12%. Histologically, all tumors were adenocarcinomas, with adenocarcinoma not otherwise specified being the most common subtype (56%), followed by ductal adenocarcinoma (40%). Most tumors were moderately differentiated (76%), with 20% classified as poorly differentiated. The majority (76%) were diagnosed at stage II, only 8% of patients were diagnosed at stage IV. Clinically, most patients subsequently presented with advanced disease. Lymph node involvement was observed in nearly all cases (96%), while distant metastasis was reported in over half (52%) of the cohort. The healthy control group included 22 individuals, with a median age of 35 years (range: 1-50), and comprised 59% males and 41% females. Smoking history was not available for this group.
| Variables | Pancreatic cancer patients (n = 25) | Healthy controls (n = 22) |
| Gender | ||
| Male | 12 (48) | 13 (59) |
| Female | 13 (52) | 9 (41) |
| Age, median (range) | 65 (35-75) | 35 (1-50) |
| Smoking history | ||
| Non-smoker | 17 (68) | |
| Ex-smoker | 3 (12) | |
| Smoker | 2 (8) | |
| Unknown | 3 (12) | 22 (100) |
| Histology | ||
| Adenocarcinoma | 14 (56) | |
| Ductal adenocarcinoma | 10 (40) | |
| Mucinous adenocarcinoma | 1 (4) | |
| Differentiation | ||
| Well | 0 (0) | |
| Moderately | 19 (76) | |
| Poorly | 5 (20) | |
| Unknown | 1 (4) | |
| Tumor site | ||
| Head | 19 (76) | |
| Body | 2 (8) | |
| Tail | 4 (16) | |
| Stage at diagnosis | ||
| I | 1 (4) | |
| II | 19 (76) | |
| III | 3 (12) | |
| IV | 2 (8) | |
| Lymph node invasion | ||
| Yes | 24 (96) | |
| No | 1 (4) | |
| Metastasis | ||
| Yes | 13 (52) | |
| No | 12 (48) | |
Plasma samples were collected from 28 pancreatic adenocarcinoma patients and 156 healthy controls. The cancer group was slightly female predominance (61%), with a median age of 63 (ranging from 33 to 76), closely matching the control group, which was 60% female and had a median age of 62 (spanning 45 to 83). Most participants in both groups were non-smokers, accounting for 71% of patients and 83% of controls. Clinically, the cohort presented with predominantly advanced disease: The majority were at stage IV (68%), and 68% had confirmed metastases, with lymph node involve
| Variables | Pancreatic cancer patients (n = 28) | Healthy controls (n = 156) |
| Gender | ||
| Male | 11 (39) | 61 (40) |
| Female | 17 (61) | 95 (60) |
| Age, median (range) | 63 (33-76) | 62 (45-83) |
| Smoking history | ||
| Non-smoker | 20 (71) | 129 (83) |
| Ex-smoker | 5 (18) | |
| Smoker | 3 (11) | 27 (17) |
| Stage at diagnosis | ||
| I | 2 (7) | |
| II | 5 (18) | |
| III | 2 (7) | |
| IV | 19 (68) | |
| Lymph node invasion | ||
| Yes | 26 (93) | |
| No | 2 (7) | |
| Metastasis | ||
| Yes | 19 (68) | |
| No | 9 (32) |
Analysis of pancreatic tissue samples showed that CDH17 expression was absent in all healthy controls (median M-score = 0.4), whereas variable staining was observed in normal adjacent tissues (median M-score = 3.1). In pancreatic cancer tissues, CDH17 levels were markedly elevated (median M-score = 8.9), significantly higher than those in both normal adjacent tissues (P = 0.0005) and healthy controls (P = 0.000001) (Figure 1A). To assess potential age-related confounding, a Spearman’s rank correlation analysis was performed to evaluate the association between age and tissue CDH17 expression in healthy controls and pancreatic cancer patients separately. No significant correlation was observed in either group (healthy controls: Spearman r = -0.068, 95%CI: -0.486 to 0.375; cancer patients: Spearman r = -0.089, 95%CI: -0.478 to 0.328), suggesting that the observed group difference in CDH17 expression is unlikely to be driven by age. These findings indicate substantial upregulation of CDH17 in pancreatic adenocarcinoma, suggesting its potential as a diagnostic mar
We further examined the relationship between CDH17 expression (as measured by the IHC M-score) and clinicopathological features in pancreatic adenocarcinoma. No significant associations were found with any of the factors assessed, including sex, age, tumor site, differentiation, stage, relapse, or prognosis (Figure 1B-H).
A diagnostic test was used to classify healthy control, normal adjacent, and pancreatic tumor tissues based on CDH17 M-scores. Using an M-score cutoff of ≥ 1, all healthy control tissues (22/22) tested negative for CDH17 staining, while 88% (22/25) of normal adjacent tissues and 92% (23/25) of pancreatic tumor tissues tested positive (Figure 2A and B). ROC analysis of pancreatic tissue samples showed that the CDH17 M-score yielded area under the curve (AUC) values of 0.944 (95%CI: 0.871-1.000, P < 0.0001) for detecting normal adjacent tissue and 0.981 (95%CI: 0.949-1.000, P < 0.0001) for detecting pancreatic tumor tissue (Figure 2C and D).
We evaluated DFS and OS using Kaplan-Meier curves with the log-rank test, stratifying pancreatic tumor tissues by median-high vs median-low CDH17 M-scores. No significant differences in survival were observed between the two groups for either DFS or OS (Figure 2E and F).
Pre-treatment plasma CDH17 levels were significantly elevated in pancreatic cancer patients compared to healthy controls (Table 3). This elevation was observed in both early-stage (I/II) (1.49 ng/mL vs 7.14 ng/mL, P < 0.0001) and late-stage (III/IV) patients (1.49 ng/mL vs 2.03 ng/mL, P < 0.0001) (Figure 3A). In contrast, CA19-9 levels were higher than controls only in late-stage patients (167 U/mL vs 43 U/mL, P = 0.0228), whereas early-stage patients did not differ from controls (Figure 3B). Post-treatment levels of CDH17 showed a non-significant decrease in early-stage
| Healthy | Pre-treatment | Post-treatment | ||||
| Controls | Stage I/II | Stage III/IV | Stage I/II | Stage III/IV | ||
| CDH17 | No. of samples | 156 | 7 | 21 | 7 | 21 |
| Median (ng/mL) | 1.5 | 7.1 | 2.0 | 4.0 | 2.4 | |
| Range (ng/mL) | 0.1-2.9 | 1.6-11.2 | 0.6-11.0 | 0.8-10.2 | 0.6-32.4 | |
| Mean (ng/mL) | 1.5 | 6.4 | 3.5 | 4.7 | 5.7 | |
| CA19-9 | No. of samples | 30 | 7 | 20 | 7 | 20 |
| Median (U/mL) | 43 | 81 | 167 | 21 | 183 | |
| Range (U/mL) | 33-66 | 0-1858 | 0-195081 | 0-5540 | 0-61185 | |
| Mean (U/mL) | 45 | 471 | 15581 | 846 | 3438 | |
ROC analysis of pre-treatment samples revealed that CDH17 had AUC values of 0.920 (95%CI: 0.807-1.00, P = 0.0002), 0.757 (CI: 0.626-0.887, P = 0.0001), and 0.747 (CI: 0.613-0.881, P = 0.0001) for detecting early-stage, late-stage, and all-stage cancer, respectively (Figure 3C). At a specificity of 86%, the corresponding sensitivities were 86%, 52%, and 61%. ROC analysis revealed that CA19-9 demonstrated lower AUC values of 0.539 (95%CI: 0.251-0.828) and 0.720 (CI: 0.558-0.881, P = 0.0038) for early-stage and all stages cancer, respectively, but a higher AUC of 0.813 (CI: 0.621-1.00, P = 0.0005) for late-stage detection (Figure 3D), with sensitivities of 55%, 81%, and 72% for detecting early-stage, late-stage, and all-stage cancer, respectively. These data suggest that CDH17 has higher sensitivity for early-stage disease and could be more useful for ‘ruling in’ early pancreatic cancer, whereas CA19-9 demonstrates higher sensitivity in later stages, aligning with its established role in advanced disease monitoring. With a sensitivity of 86% for early-stage cancer, CDH17 demon
Given that the prognosis is influenced by multiple factors, we focused OS analysis on late-stage patients who had received at least one cycle of chemotherapy. Kaplan-Meier analysis in this cohort suggested that high pre-treatment CDH17 was not significantly associated with OS compared to low CDH17 (median 12.5 months vs 8 months, log-rank P = 0.1403) (Figure 4A). Conversely, high CA19-9 was significantly associated with shorter OS compared to low CA19-9 (median 7.5 months vs 13 months, log-rank P = 0.002) (Figure 4B). When combined, patients with a high-CDH17/Low-CA19-9 profile (n = 5) appeared to have the most favorable prognosis (median OS = 16 months, 95%CI: 8-21.2), whereas a low-CDH17/high-CA19-9 profile (n = 10) was linked to the poorest outcomes (median OS = 7 months, 95%CI: 4.3-11.4) (Figure 4C). These findings, while fascinating, are derived from small sample size (total n = 26 for survival analysis). They should be considered hypothesis-generating rather than conclusive, and require validation in larger prospective cohorts.
Pancreatic cancer poses unique diagnostic challenges from other GI cancers. Its deep anatomical location complicates reliable imaging diagnosis. Initial computed tomography scans fail to detect approximately 9.4% of cases[23]. Coupled with the asymptomatic and non-specific nature of early disease, these factors contribute to frequent late diagnosis and high mortality. This context underscores the urgent need for improved diagnostic biomarkers for early detection.
To our knowledge, this is the first study to evaluate both tissue and circulating CDH17 in pancreatic adenocarcinoma patients and to directly compare the diagnostic performance of circulating CDH17 with CA19-9. Our tissue-based ana
The absence of correlation with differentiation, stage, and relapse was somewhat unexpected, given CDH17’s canonical function as a cell adhesion molecule[25]. This dissociation suggests that while CDH17 may contribute to early tumorigenesis, the progression cascade in pancreatic adenocarcinoma is likely driven by a complex interplay of other molecular pathways. The relatively homogeneous composition of our cohort (predominantly stage II disease) may also have limited our ability to detect statistical signals for these specific variables. Despite the strong diagnostic performance of tissue CDH17, we found no correlation with DFS or OS in our cohort, suggesting that while tissue CDH17 is a robust diagnostic marker, its expression level alone may not serve as a direct prognostic indicator.
Both tissue CDH17 expression and soluble CDH17 levels were highest in early-stage patients and decreased in advanced disease. The analysis of soluble CDH17 in patient plasma observed that CDH17 levels are significantly elevated in pancreatic adenocarcinoma patients (even at early stages) compared to healthy controls. In contrast, CA19-9 failed to distinguish early-stage patients from controls. The lack of sensitive and specific biomarkers for early detection remains a primary reason for the abysmal prognosis of pancreatic cancer, as most patients present with surgically unresectable disease[26]. The ability of CDH17 to identify early-stage disease with 86% sensitivity at 86% specificity (AUC = 0.920) positions it as a potential biomarker, but validation in larger, more diverse cohorts will be essential.
Our ROC analysis further illuminates the complementary roles of these two biomarkers. While CDH17 excelled in early-stage detection, CA19-9 performed as expected in advanced disease, with a higher AUC for late-stage cancer. This aligns with CA19-9’s established utility in monitoring advanced disease and detecting recurrence, rather than diagnosis[27]. These different performance profiles suggest a potential dual-biomarker strategy: CDH17 for early detection and CA19-9 for monitoring disease burden and treatment response. The biological basis for this difference remains unclear but may relate to mechanisms of marker shedding. CA19-9 is a sialyl-Lewis antigen whose expression can be influenced by inflammation and biliary obstruction (conditions more common in advanced disease). The release of CDH17, by con
The biological mechanisms driving these patterns merits further investigation. CDH17 is a GI-specific adhesion mole
The unexpected inverse relationship between CDH17 levels and disease stage (a pattern that runs counter to what we typically expect from a cancer biomarker) deserves careful consideration. While our favored explanation involves the loss of CDH17 expression during epithelial-mesenchymal transition, other factors could be at play. For instance, it’s possible that the immunoassay we used is sensitive to specific CDH17 isoforms or protein complexes that change in abundance as the disease evolves. We also can’t rule out the influence of our relatively small sample size, which might have skewed the distribution. This observation is in line with our tissue data, which showed a trend toward higher CDH17 expression in early-stage tumors than in late-stage tumors, further supporting the idea that CDH17 dysregulation occurs early in pancreatic carcinogenesis. This observation is compelling enough to merit a closer look in larger, well-characterized cohorts where detailed molecular subtyping could help validate and contextualize the findings.
Nevertheless, our results position CDH17 and CA19-9 as complementary markers that capture distinct aspects of tumor biology. CA19-9 is closely tied to tumor volume and systemic inflammation[33], making it a reliable indicator of disease burden and progression in advanced stages. In contrast, CDH17 may serve as an early warning signal, reflecting active tumorigenesis within a more differentiated cellular context. The observed survival patterns (particularly the association between a high-CDH17/Low-CA19-9 profile and more favorable outcomes) lend further support to this concept.
The CDH17 + CA19-9 dual panel represents a novel, functionally complementary strategy that may enhance current clinical practice in pancreatic adenocarcinoma. CDH17 emerges as a promising biomarker for early detection, capable of identifying molecular changes associated with early epithelial tumorigenesis before structural imaging abnormalities become evident. In contrast, CA19-9 retains its established value for monitoring disease burden and assessing treatment response once pancreatic adenocarcinoma is diagnosed. Importantly, these biomarkers do not need to be combined into a single composite score, they should be interpreted and assessed individually to preserve their distinct clinical roles. While CDH17 is particularly sensitive at detecting early-stage pancreatic adenocarcinoma, CA19-9 is more sensitive in late-stage disease, together capturing a broader spectrum of patients over time. This complementary behavior suggests that the dual panel could flag both early neoplastic changes and more advanced, biologically aggressive disease within the same diagnosis setting. By leveraging the strengths of each marker, CDH17 identifies high-risk individuals and early-stage disease, while CA19-9 supports longitudinal follow-up and therapeutic decision-making.
Several limitations warrant acknowledgment. Firstly, sample size (particularly for survival analyses and early-stage subgroups) is modest. While the tissue findings achieved high statistical significance, the subgroup analyses in our prog
Despite these limitations, our data highlights CDH17 as a candidate worthy of further investigation. The current work was conducted as an initial exploratory study. The findings are promising but necessitate independent validation in larger cohorts before any clinical application can be considered. Future research should validate its diagnostic perfor
This pilot study evaluated CDH17 as a potential biomarker in pancreatic adenocarcinoma. Our findings demonstrate significant upregulation of CDH17 in pancreatic cancer tissues relative to both normal adjacent tissue and healthy pan
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