Abstract
Background
Mucinous adenocarcinoma of the colon is defined by extracellular mucin occupying at least 50% of the tumour. Although it is often regarded as a distinct histological subtype, its clinicopathological profile remains variable across published series. We compared mucinous and classic adenocarcinoma in a colon-only surgical cohort.
Methods
We retrospectively reviewed patients who underwent oncological resection for colon adenocarcinoma between October 2021 and March 2026. Rectal tumours, neoadjuvant-treated cases and signet ring cell carcinoma were excluded. Clinicopathological variables were compared using Mann-Whitney U, Pearson chi-square or Fisher exact tests. Multivariable analyses were revised as parsimonious logistic regression models, with model size and event counts reported.
Results
The final cohort included 155 colon cancers: 29 mucinous and 126 classic adenocarcinomas. Mucinous tumours were more often right-sided (75.9% vs. 44.4%; p = 0.002) and more frequently poorly differentiated (24.1% vs. 4.8%; p = 0.003). Advanced pT stage was common in both groups (86.2% vs. 82.5%; p = 0.786). Nodal metastasis was numerically less frequent in mucinous adenocarcinoma (31.0% vs. 50.8%; p = 0.055), while lymphovascular invasion was significantly less common (10.3% vs. 32.5%; p = 0.017). Deficient mismatch repair was recorded in 13.8% of mucinous tumours and 8.7% of classic adenocarcinomas (p = 0.484). In parsimonious adjusted models, mucinous histology was not independently associated with advanced pT stage (adjusted OR 1.51, 95% CI 0.46–4.92; p = 0.496) or nodal metastasis (adjusted OR 0.48, 95% CI 0.19–1.19; p = 0.113).
Conclusions
In this colon-only cohort, mucinous adenocarcinoma was associated with right-sided location and poor differentiation, but not with independently higher local invasion or nodal spread. These findings support a cautious, clinicopathology-based interpretation of mucinous histology and should not be extrapolated to prognosis without molecular and survival data.
Keywords: Mucinous adenocarcinoma, Non-mucinous adenocarcinoma, Colon cancer, Clinicopathological features, Lymph node metastasis, Lymphovascular invasion
Introduction
Colorectal cancer remains a major global health problem. According to the most recent GLOBOCAN estimates, it is still among the most commonly diagnosed malignancies worldwide and one of the leading causes of cancer-related death. More recent burden analyses tell much the same story from another angle: even where age-standardised mortality has fallen, the absolute number of cases, deaths and disability-adjusted life years continues to rise, driven largely by population ageing and growth. Against that background, even less common histological subtypes deserve careful attention because they still represent a substantial group of patients in everyday colorectal practice [1, 2].
Within this broader disease spectrum, mucinous adenocarcinoma warrants separate consideration. It is defined by extracellular mucin occupying at least 50% of the tumour and accounts for roughly 10–15% of colorectal adenocarcinomas in contemporary series [3, 4]. The argument for treating mucinous adenocarcinoma as more than a purely descriptive microscopic variant has become stronger in recent years. Compared with classic adenocarcinoma, these tumours are more often proximal, more frequently poorly differentiated, and enriched for molecular features associated with mismatch repair deficiency, microsatellite instability and BRAF-related biology. Multi-omic and immunopathology studies have also suggested that the mucinous phenotype may be associated with a distinct tumour microenvironment and mucin-associated expression patterns, particularly involving MUC2 and MUC5AC [4–6].
What remains less clear is how these biological differences translate into routine clinicopathological findings. Recent retrospective cohorts have linked mucinous histology with larger tumours, more advanced T stage and, in some settings, a greater metastatic burden [3, 4, 7]. Yet the signal has not been uniform. A 2024 systematic review and meta-analysis including 56 studies and more than 800,000 patients found that mucinous adenocarcinoma differs from conventional adenocarcinoma across several clinicopathological variables and is associated with poorer overall survival, but not with a clear difference in disease-free survival; lymphatic and perineural invasion were not consistently different between groups [7]. Contemporary cohort data have therefore added nuance rather than settling the issue. Some series suggest that adverse outcomes are influenced by tumour site and stage, whereas others indicate that mucinous differentiation is strongly associated with proximal location, high grade, MMR deficiency and BRAF mutation without retaining independent prognostic value after multivariable adjustment [4, 6–8].
That uncertainty is precisely why a focused colon-only analysis still has value. When colon and rectal cancers are examined together, and when treatment-related factors such as neoadjuvant therapy are not separated, interpretation becomes more difficult. In the present study, we compared mucinous adenocarcinoma with classic adenocarcinoma in patients undergoing resection for colon cancer, concentrating on the clinicopathological variables most likely to inform routine postoperative assessment: tumour location, differentiation, pathological T and N stage, lymphovascular invasion and perineural invasion. We hypothesised that mucinous adenocarcinoma would be associated with more advanced local invasion and with a distinct pattern of nodal and invasion-related pathological findings.
Materials and methods
Study design and patient selection
This retrospective observational study compared the clinicopathological features of mucinous adenocarcinoma with those of classic adenocarcinoma in surgically treated colon cancer. Patients were identified from the study database covering the period from October 2021 to March 2026. Eligibility was limited to patients with histopathologically confirmed colorectal adenocarcinoma who underwent oncological resection and had complete pathological staging data available for review. Patients with neuroendocrine tumours, metastatic secondary involvement of the colon, recurrent tumours, concurrent malignancy or incomplete pathological data were not eligible.
For the present colon-only analysis, three further exclusions were applied a priori: tumours recorded as rectal, patients who had received neoadjuvant chemotherapy, and patients with signet ring cell carcinoma. After these exclusions, the final cohort comprised 155 patients: 126 with classic adenocarcinoma and 29 with mucinous adenocarcinoma.
Histological subtype was assigned from the final resection pathology report. Mucinous adenocarcinoma was defined as adenocarcinoma containing at least 50% extracellular mucin. Tumours recorded as adenocarcinoma and not meeting that threshold were classified as classic (non-mucinous) adenocarcinoma. The database did not record focal mucinous differentiation below the 50% threshold; therefore, tumours with a minor mucinous component could not be analysed separately.
Pathological assessment and variable definitions
Clinical records, operative notes and final pathology reports were reviewed retrospectively, and the relevant variables were entered into an electronic database for analysis. The demographic variables analysed were age and sex. The pathological and anatomical variables of interest were tumour location, histological subtype, differentiation grade, pT category, pN category, pM category, overall pathological stage, total lymph node count, number of metastatic lymph nodes, lymphovascular invasion, perineural invasion and mismatch repair status.
Tumour site was available in the database in two forms: a broad anatomical location field and a detailed subsite field. The broad location field classified tumours as right colon, left colon, right flexure or rectum. The detailed subsite field recorded the precise site as caecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, rectosigmoid colon or rectum. Cohort selection was based on the broad location field. Tumours classified overall as rectal were excluded, whereas cases recorded as rectosigmoid in the detailed subsite field were retained if the primary location field classified them as left colon. Tumours coded as right colon or right flexure were classified as right-sided; those coded as left colon were classified as left-sided.
Differentiation grade was recorded as well differentiated (grade 1), moderately differentiated (grade 2) or poorly differentiated (grade 3). Classic adenocarcinomas were graded according to gland formation. For mucinous adenocarcinoma, grading was based on the viable neoplastic epithelial component, including glandular formation and epithelial maturation, rather than on the volume of extracellular mucin [9, 10]. The final signed pathology report was used as the source of grading data. A formal blinded re-review by two independent pathologists was not part of the original retrospective design; consequently, interobserver agreement for grading could not be calculated. This point has been explicitly acknowledged as a limitation.
Tumour budding scores were present in the source pathology reports. However, because tumour budding is difficult to apply to mucinous adenocarcinoma unless an assessable well or moderately differentiated conventional adenocarcinoma component is present, and because the presence and extent of such a component were not consistently documented in the database, tumour budding was not retained as a formal comparative endpoint in the revised analysis [9].
Outcomes
The primary outcome was advanced local tumour invasion, defined a priori as pT3-T4. The main secondary outcomes were nodal metastasis (pN positivity), distant metastasis (pM1), overall pathological stage, lymphovascular invasion, perineural invasion, differentiation grade, mismatch repair status and lymph node yield.
For selected analyses, some variables were examined in dichotomised form to improve clinical interpretability. Differentiation was analysed both as a three-level categorical variable and as poor differentiation (grade 3) versus grades 1–2. Overall stage was considered in its original I-IV form and, where relevant, as stage I-II versus stage III-IV. All pathological variables were taken from the final resection specimen report rather than from preoperative biopsy material.
Statistical analysis
Because this was a retrospective study based on a fixed study period, no a priori sample size calculation was performed. Continuous variables were assessed for distributional normality using the Shapiro-Wilk test. As the continuous variables included in the analysis were not normally distributed in at least one comparison group, they were summarised as medians and interquartile ranges (IQRs) and compared using the Mann-Whitney U test.
Categorical variables were presented as numbers (n) and percentages (%). Between-group comparisons were performed using Pearson’s chi-square test or Fisher’s exact test, as appropriate according to expected cell counts. All tests were two-sided, and p values < 0.05 were considered statistically significant.
Univariable odds ratios (ORs) with 95% confidence intervals (CIs) were calculated from 2 × 2 contingency tables to quantify selected associations between mucinous histology and clinicopathological features. In response to concerns about overfitting, the multivariable analysis was revised to use more parsimonious logistic regression models. The first model examined advanced pT stage (pT3-T4) and included histological subtype and tumour laterality. The second model examined nodal metastasis (pN+) and included histological subtype, tumour laterality and advanced pT stage. For each model, we report the number of complete cases, the number of outcome events, the number of fitted parameters including the intercept, adjusted ORs, 95% CIs and exact p values.
The final analytic dataset was complete for all variables included in the reported analyses; no missing-data imputation was required. All analyses were carried out in Python 3.11 (Python Software Foundation, Wilmington, DE, USA). Data management was performed using pandas 2.2.3 and NumPy 2.3.5. Statistical testing was undertaken with SciPy 1.17.0 and statsmodels 0.14.6. Figures were prepared using Matplotlib 3.10.8.
Ethics approval and consent to participate
This retrospective observational study was approved by the Giresun University Faculty of Medicine Clinical Research Ethics Committee (Approval No: 11.06.2026/07; approval date: 11 June 2026). The study was conducted in accordance with the ethical principles of the Declaration of Helsinki, as revised in 2013. Because the study was based on retrospective review of existing clinical and pathological records and all data were analysed anonymously, the requirement for written informed consent to participate was waived by the Giresun University Faculty of Medicine Clinical Research Ethics Committee.
Results
The final cohort comprised 126 classic adenocarcinomas and 29 mucinous adenocarcinomas; mucinous adenocarcinoma accounted for 18.7% of eligible colon cancers. No missing values were present in the variables entered into the analysis.
Table 1 summarises the demographic profile and tumour distribution. Age was somewhat higher in the mucinous group, with a median of 76 years (IQR 64–84), compared with 70 years (IQR 64–77) in the classic group, although the difference was not statistically significant (p = 0.113). Sex distribution was similar between groups (male sex: 55.2% vs. 61.9%; p = 0.503). The clearest anatomical difference was tumour laterality. Mucinous adenocarcinomas were more often right-sided than classic adenocarcinomas (75.9% vs. 44.4%; p = 0.002). Detailed subsite distribution also differed significantly (p = 0.015), with mucinous tumours proportionally more frequent in the caecum, ascending colon and hepatic flexure, while classic adenocarcinomas were concentrated mainly in the sigmoid and rectosigmoid colon.
Table 1.
Clinicodemographic characteristics and tumour distribution
| Characteristic | Classic adenocarcinoma (n = 126) | Mucinous adenocarcinoma (n = 29) | p value |
|---|---|---|---|
| Patients, n | 126 | 29 | - |
| Age, years, median (IQR) | 70 (64–77) | 76 (64–84) | 0.113 |
| Male sex, n (%) | 78 (61.9%) | 16 (55.2%) | 0.503 |
| Tumour laterality, n (%) | 0.002 | ||
| Left-sided | 70 (55.6%) | 7 (24.1%) | |
| Right-sided | 56 (44.4%) | 22 (75.9%) | |
| Detailed colonic subsite, n (%) | 0.015 | ||
| Caecum | 21 (16.7%) | 8 (27.6%) | |
| Ascending colon | 18 (14.3%) | 6 (20.7%) | |
| Hepatic flexure | 10 (7.9%) | 6 (20.7%) | |
| Transverse colon | 8 (6.3%) | 3 (10.3%) | |
| Splenic flexure | 4 (3.2%) | 1 (3.4%) | |
| Descending colon | 6 (4.8%) | 3 (10.3%) | |
| Sigmoid colon | 44 (34.9%) | 1 (3.4%) | |
| Rectosigmoid colon | 15 (11.9%) | 1 (3.4%) |
Data are presented as n (%) unless otherwise indicated. Percentages are column percentages. Continuous variables are shown as median (IQR). Rectosigmoid cases were retained when the broad location field classified the tumour as left colon rather than rectum
Statistically significant p values are presented in bold (p< 0.05)
Pathological stage and lymph node findings are shown in Table 2. Local tumour depth was similar between the two histological groups. Advanced pT stage (T3-T4) was common in both mucinous and classic tumours (86.2% vs. 82.5%; p = 0.786), and the full pT distribution did not differ significantly (p = 0.670).
Table 2.
Pathological stage and lymph node findings
| Characteristic | Classic adenocarcinoma (n = 126) | Mucinous adenocarcinoma (n = 29) | p value |
|---|---|---|---|
| pT category, n (%) | 0.670 | ||
| T1 | 6 (4.8%) | 0 (0.0%) | |
| T2 | 16 (12.7%) | 4 (13.8%) | |
| T3 | 90 (71.4%) | 21 (72.4%) | |
| T4 | 14 (11.1%) | 4 (13.8%) | |
| Advanced pT stage (T3-T4), n (%) | 104 (82.5%) | 25 (86.2%) | 0.786 |
| pN category, n (%) | 0.157 | ||
| N0 | 62 (49.2%) | 20 (69.0%) | |
| N1 | 44 (34.9%) | 6 (20.7%) | |
| N2 | 20 (15.9%) | 3 (10.3%) | |
| Nodal metastasis (pN+), n (%) | 64 (50.8%) | 9 (31.0%) | 0.055 |
| Distant metastasis (pM1), n (%) | 9 (7.1%) | 5 (17.2%) | 0.141 |
| TNM stage, n (%) | 0.014 | ||
| Stage I | 18 (14.3%) | 2 (6.9%) | |
| Stage II | 41 (32.5%) | 16 (55.2%) | |
| Stage III | 58 (46.0%) | 6 (20.7%) | |
| Stage IV | 9 (7.1%) | 5 (17.2%) | |
| Stage III-IV disease, n (%) | 67 (53.2%) | 11 (37.9%) | 0.139 |
| Total lymph nodes examined, median (IQR) | 18 (13-25.8) | 20 (14–27) | 0.341 |
| Positive lymph nodes, median (IQR) | 0.5 (0–2) | 0 (0–1) | 0.088 |
Data are presented as n (%) unless otherwise indicated. Continuous variables are shown as median (IQR). pN+ denotes any pathological nodal category above N0
Statistically significant p values are presented in bold (p< 0.05)
Nodal disease showed a different numerical pattern. Nodal metastasis was less frequent in mucinous adenocarcinoma than in classic adenocarcinoma (31.0% vs. 50.8%), although this difference did not reach statistical significance (p = 0.055). Pathological M1 disease was numerically more frequent in mucinous tumours (17.2% vs. 7.1%; p = 0.141). Overall TNM stage distribution differed between groups (p = 0.014), with stage II disease more frequent in mucinous adenocarcinoma and stage III disease more frequent in classic adenocarcinoma. When stage was collapsed into stages I-II versus III-IV, the difference was not statistically significant (37.9% vs. 53.2%; p = 0.139). Median lymph node yield was similar in the two groups.
Histological and selected molecular features are presented in Table 3. Differentiation grade differed materially between groups (overall p = 0.003). Poor differentiation was more common in mucinous adenocarcinoma, affecting 24.1% of cases compared with 4.8% in the classic group (p = 0.003). By contrast, lymphovascular invasion was less frequent in mucinous tumours (10.3% vs. 32.5%; p = 0.017). Perineural invasion did not differ significantly (10.3% vs. 21.4%; p = 0.173).
Table 3.
Histological aggressiveness markers and MMR status
| Characteristic | Classic adenocarcinoma (n = 126) | Mucinous adenocarcinoma (n = 29) | p value |
|---|---|---|---|
| Differentiation grade, n (%) | 0.003 | ||
| Well differentiated (Grade 1) | 82 (65.1%) | 15 (51.7%) | |
| Moderately differentiated (Grade 2) | 38 (30.2%) | 7 (24.1%) | |
| Poorly differentiated (Grade 3) | 6 (4.8%) | 7 (24.1%) | |
| Poor differentiation (Grade 3), n (%) | 6 (4.8%) | 7 (24.1%) | 0.003 |
| Lymphovascular invasion, n (%) | 41 (32.5%) | 3 (10.3%) | 0.017 |
| Perineural invasion, n (%) | 27 (21.4%) | 3 (10.3%) | 0.173 |
| MMR status, n (%) | Exploratory | ||
| Proficient MMR | 109 (86.5%) | 21 (72.4%) | |
| Deficient MMR | 11 (8.7%) | 4 (13.8%) | |
| Indeterminate/discordant | 6 (4.8%) | 4 (13.8%) | |
| Deficient MMR, n (%) | 11 (8.7%) | 4 (13.8%) | 0.484 |
Data are presented as n (%). MMR, mismatch repair. The p value for deficient MMR refers to the binary comparison of dMMR versus all other recorded categories and was analysed using Fisher’s exact test. Tumour budding was not retained for formal comparison because its applicability in mucinous adenocarcinoma could not be confirmed consistently from the source reports
Statistically significant p values are presented in bold (p< 0.05)
Mismatch repair status was available as an exploratory descriptor, but broader molecular data were not available. Deficient MMR was recorded in 13.8% of mucinous tumours and 8.7% of classic adenocarcinomas (p = 0.484). Because tumour budding could not be applied consistently to mucinous tumours in the absence of documented conventional adenocarcinoma components, it was not retained in the formal comparative analysis.
Univariable effect estimates are summarised in Fig. 1. Mucinous histology was associated with right-sided location (OR 3.93, 95% CI 1.57–9.86) and poor differentiation (OR 6.36, 95% CI 1.95–20.74). It was inversely associated with lymphovascular invasion (OR 0.24, 95% CI 0.07–0.84). Confidence intervals for advanced pT stage, nodal metastasis, distant metastasis, stage III-IV disease and perineural invasion crossed unity.
Fig. 1.
Univariable odds ratios for selected clinicopathological features. Markers indicate point estimates and horizontal lines indicate 95% confidence intervals. Odds ratios greater than 1 indicate higher prevalence in mucinous adenocarcinoma
Two parsimonious multivariable logistic regression models were fitted (Table 4). The first model used advanced pT stage (T3-T4) as the dependent variable and included histological subtype and tumour laterality. In this model, mucinous histology was not independently associated with advanced pT stage (adjusted OR 1.51, 95% CI 0.46–4.92; p = 0.496).
Table 4.
Parsimonious multivariable binary logistic regression models
| Outcome / model detail | Covariate | Adjusted OR (95% CI) | p value |
|---|---|---|---|
| Model 1: Advanced pT stage (T3-T4) | |||
| Complete cases: 155; outcome events: 129; fitted parameters: 3 (including intercept) | |||
| Mucinous histology (vs. classic) | 1.51 (0.46–4.92) | 0.496 | |
| Right-sided location | 0.65 (0.27–1.56) | 0.335 | |
| Model 2: Nodal metastasis (pN+) | |||
| Complete cases: 155; outcome events: 73; fitted parameters: 4 (including intercept) | |||
| Mucinous histology (vs. classic) | 0.48 (0.19–1.19) | 0.113 | |
| Right-sided location | 0.58 (0.30–1.15) | 0.120 | |
| Advanced pT stage (T3-T4) | 3.66 (1.36–9.84) | 0.010 | |
Model 1: AIC = 145.04, likelihood-ratio p = 0.556. Model 2: AIC = 207.93, likelihood-ratio p = 0.002. OR Odds ratio, CI Confidence interval
The second model used nodal metastasis as the dependent variable and included histological subtype, tumour laterality and advanced pT stage. Mucinous histology again did not emerge as an independent predictor (adjusted OR 0.48, 95% CI 0.19–1.19; p = 0.113). Advanced pT stage was associated with nodal metastasis (adjusted OR 3.66, 95% CI 1.36–9.84; p = 0.010). Both models were fitted on all 155 complete cases.
Discussion
This colon-only study compared mucinous adenocarcinoma with classic adenocarcinoma after excluding rectal tumours, neoadjuvant-treated cases and signet ring cell carcinoma. Within this cleaner surgical cohort, mucinous tumours showed a distinct clinicopathological profile: they were predominantly right-sided and more often poorly differentiated. At the same time, mucinous histology was not independently associated with advanced local invasion or nodal metastasis after adjustment, and lymphovascular invasion was less frequent. These findings should be interpreted as clinicopathological associations within the present dataset rather than as direct evidence of prognosis or tumour biology.
Recent outcome studies have reported inconsistent findings regarding mucinous histology. Kim et al. found that the adverse prognostic effect of mucinous histology in stage II and III colon cancer was driven mainly by stage III disease, whereas Powers et al. did not find an overall survival disadvantage for mucinous stage III colon cancer after multivariable adjustment. Bong et al. reported no survival difference in stages I-II but worse outcomes in stage III mucinous cancers, while Zhang et al. found poorer prognosis for mucinous histology in a meta-analysis of patients treated with postoperative first-line adjuvant chemotherapy [11–14]. These studies show why mucinous histology should not be reduced to a single prognostic label. Its clinical meaning appears to depend on stage, treatment context and possibly underlying molecular background.
The strongest signal in our cohort was anatomical. Mucinous tumours were substantially more likely to arise in the right colon. This is consistent with previous reports linking mucinous morphology with proximal location and molecular features such as dMMR/MSI-H and BRAF-related biology [15–17]. In our dataset, MMR status was available only as a limited descriptor, and deficient MMR did not differ significantly between groups. We did not have complete MSI-H confirmation, BRAF, KRAS, NRAS, MLH1 methylation or broader molecular profiling. Therefore, any mechanistic interpretation remains beyond the reach of the present study.
Poor differentiation was also more frequent in mucinous adenocarcinoma. We have clarified in the revised Methods how grading was recorded and applied to mucinous tumours. Even so, this finding should be read with appropriate caution. Histological grading in colorectal cancer is subject to interobserver variation, and a formal blinded consensus re-review was not part of the original design. The observation is therefore important, but it should be treated as a feature of the final pathology reports rather than as a centrally reviewed biomarker.
The lower rate of lymphovascular invasion among mucinous tumours was unexpected but not implausible. Yuan et al. reported that mucinous adenocarcinomas mixed with other adverse pathological components, particularly signet ring cell or neuroendocrine differentiation, had higher rates of lymphovascular and perineural invasion than classic mucinous adenocarcinoma [18]. Our analysis deliberately excluded signet ring cell carcinoma, which may partly explain why the mucinous group did not show a uniformly adverse invasion profile. A small pilot study from Bangladesh also reported an inverse association between mucinous histology and lymphovascular invasion, although the sample was limited [19]. The safest interpretation is that invasion-related features in mucinous adenocarcinoma are heterogeneous and should be reported directly rather than inferred from histological subtype alone [20].
The multivariable analyses were revised in response to reviewer concern about overfitting. Instead of retaining the original broader models, we fitted parsimonious models focused on the main exposure and the most clinically relevant covariates. These models showed that mucinous histology was not independently associated with advanced pT stage or nodal metastasis. Advanced pT stage, rather than mucinous histology, was the clearest predictor of nodal disease. Given the modest number of mucinous cases, these models should be interpreted as exploratory and hypothesis-generating.
This study has several limitations. First, it was retrospective and single-centre in design, and the number of mucinous cases was modest. This limits statistical precision and increases the possibility of type II error, especially for nodal status and metastatic disease. Second, focal mucinous differentiation below the 50% threshold was not recorded in the database, so tumours with a minor mucinous component could not be evaluated as a potential intermediate phenotype. Third, although grading criteria were clarified, formal interobserver agreement could not be calculated. Fourth, tumour budding was removed from the formal comparative analysis because its applicability in mucinous adenocarcinoma could not be confirmed consistently from the source reports. Fifth, newer histological markers such as SARIFA were not assessed because slide-level re-review for that purpose was not part of the original dataset or ethics-approved analysis. Finally, the study did not include survival, recurrence, complete molecular profiling or treatment response data. As a result, the conclusions must remain limited to clinicopathological differences observed at resection.
Despite these limitations, the study adds a focused colon-only comparison to the literature. Mucinous adenocarcinoma showed clear right-sided predominance and a higher frequency of poor differentiation, but it was not independently associated with advanced local invasion or nodal metastasis. These findings support reporting mucinous adenocarcinoma as a distinct subtype while avoiding the assumption that it is uniformly more aggressive in every pathological domain. Larger colon-only studies incorporating central pathology review, molecular profiling, survival outcomes and newer invasion-front markers will be needed to define which mucinous tumours carry genuinely adverse behaviour.
Conclusion
In this carefully selected colon-only surgical cohort, mucinous adenocarcinoma was associated with right-sided location and poor differentiation. It was not independently associated with advanced local invasion or nodal metastasis after parsimonious adjustment. The findings support a nuanced clinicopathological interpretation of mucinous histology and underline the need for larger studies with molecular and survival data before drawing stronger prognostic conclusions.
Acknowledgements
None.
Clinical trial number
Not applicable.
Authors’ contributions
(1) Conceptualisation: Berkan ACAR, Ali MUHTAROĞLU, Elif YILMAZ. (2) Design: Ali MUHTAROĞLU, Berkan ACAR. (3) Supervision: Berkan ACAR. (4) Fundings: Yavuz ÇEKİÇ,Serdar ACAR, Tuğrul KESİCİOĞLU. (5) Materials: Berkan ACAR, Ali MUHTAROĞLU, Tuğrul KESİCİOĞLU. (6) Data collection and/or processing: Ali MUHTAROĞLU, Elif YILMAZ, Yavuz ÇEKİÇ. (7) Analysis and/or interpretation: Elif YILMAZ, Yavuz ÇEKİÇ. (8) Literature review: Elif YILMAZ, Serdar ACAR, Berkan ACAR. (9) Writing: Ali MUHTAROĞLU, Berkan ACAR. (10) Critical review: Berkan ACAR, Ali MUHTAROĞLU, Tuğrul KESİCİOĞLU, Serdar ACAR, Elif YILMAZ, Yavuz ÇEKİÇ. All authors read and approved the final version of the manuscript.
Funding
The authors declare that no funds, grants or other support were received during the preparation of this manuscript.
Data availability
The datasets generated and analysed during the current study are not publicly available due to participant confidentiality. An anonymised aggregate dataset may be made available from the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
This retrospective observational study was approved by the Giresun University Faculty of Medicine Clinical Research Ethics Committee (Approval No: 11.06.2026/07; approval date: 11 June 2026). The requirement for written informed consent to participate was waived by the Giresun University Faculty of Medicine Clinical Research Ethics Committee because the study used anonymised retrospective clinical and pathological records.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets generated and analysed during the current study are not publicly available due to participant confidentiality. An anonymised aggregate dataset may be made available from the corresponding author on reasonable request.