Search Results (323)

Introduction: Uterine leiomyosarcoma (uLMS) is a rare, highly aggressive malignancy arising from the smooth muscle tissue of the uterine wall. It typically presents with abnormal vaginal bleeding, pelvic pain, or a pelvic mass. In rare instances, symptoms may result from local invasion or metastasis. We report a case of uLMS initially diagnosed following colonic perforation due to direct tumor invasion, accompanied by a comprehensive narrative review of the literature on the incidental identification of uterine sarcomas during emergency general surgery to further emphasize the diagnostic challenges, treatment approaches, and need for individualized care in these complex cases. Case Presentation: A 45-year-old woman presented to the Emergency Department with acute abdominal pain of several hours’ duration, in the absence of other associated symptoms. An emergency exploratory laparotomy was performed, revealing feculent peritonitis secondary to sigmoid colon rupture, resulting from local invasion by a large uterine mass. A total abdominal hysterectomy with bilateral salpingo-oophorectomy was undertaken, followed by en bloc resection of the sigmoid colon, appendectomy and construction of a terminal colostomy. Her postoperative course was uneventful, and she was discharged on postoperative day eight. Histopathological examination of the specimen revealed a high-grade uterine leiomyosarcoma. Following evaluation by a multidisciplinary oncology board, the patient received adjuvant chemotherapy. Methods and Results: A narrative review of the literature was performed to identify cases of uterine sarcomas incidentally diagnosed during emergency surgery performed by general surgeons. Including the present case, six cases were identified. Most patients presented with acute abdomen mimicking gastrointestinal pathology, with diagnosis established intraoperatively or postoperatively. Definitive surgical management was achieved during the initial emergency procedure in all cases. Conclusion: Although exceptionally rare, uterine sarcoma should be considered in the differential diagnosis of acute abdomen in female patients undergoing emergency surgery. Awareness of this atypical presentation, the appropriate diagnostic approach, real-time intraoperative adaptability, and individualized multidisciplinary management are essential for ensuring appropriate surgical management and optimizing patient care. Full article

Peritoneal metastasis (PM) is the most frequent and lethal pattern of dissemination in gastrointestinal malignancies. Despite advances in systemic chemotherapy, outcomes remain poor because the unique biology of PM, characterized by poor vascularization and the peritoneal–plasma barrier (PPB), limits drug penetration and contributes to treatment resistance. To address these challenges, several locoregional treatment strategies have been developed, including cytoreductive surgery plus hyperthermic intraperitoneal chemotherapy (CRS + HIPEC) and pressurized intraperitoneal aerosol chemotherapy (PIPAC). However, their widespread adoption is constrained by invasiveness, strict patient selection, and inconsistent survival benefits. Normothermic intraperitoneal and systemic treatment (NIPS) has emerged as a practical and less invasive alternative, particularly in East Asia. Through an implanted intraperitoneal port, NIPS enables repeated drug administration, providing sustained regional exposure while imposing minimal procedural burden. Importantly, it can be readily integrated with systemic chemotherapy, making it suitable for long-term multimodal treatment. Among available agents, paclitaxel (PTX) is particularly well suited for intraperitoneal administration because of its prolonged retention within the peritoneal cavity and limited systemic absorption. These pharmacokinetic properties allow high local drug concentrations with relatively low systemic toxicity. Consequently, PTX-based NIPS represents a biologically rational and clinically feasible treatment strategy for PM. This review summarizes the pharmacological rationale, clinical evidence, and emerging innovations in drug formulation and delivery that may further enhance the efficacy of PTX-based intraperitoneal chemotherapy for this challenging disease. Full article

Metastatic involvement of the male genitourinary tract by lung cancer is exceedingly rare. We report a 56-year-old man with metastatic lung adenocarcinoma (initial stage T3N2M1b) under pembrolizumab, who presented with severe pelvic pain. Pelvic magnetic resonance imaging and computed tomography demonstrated a large mass with an imaging epicentre favouring the left seminal vesicle, involving the prostate and fistulising to the distal rectum, without pelvic ascites or peritoneal disease. A total PSA of 0.81 ng/mL and a previous negative prostate biopsy made a primary prostatic malignancy less likely. Biopsy of the rectal component revealed a poorly differentiated carcinoma with an immunophenotype (CK7+, TTF-1+, p40−, CDX2−, NKX3.1−, PAX8−) consistent with metastatic adenocarcinoma of pulmonary origin. The patient underwent palliative pelvic radiotherapy, with improvement of pelvic pain; he subsequently developed pneumaturia and faecaluria and died eight months later from disease progression. Seminal vesicle metastasis from lung carcinoma has been reported previously; to our knowledge, however, this is the first report presenting with rectal fistulisation. This case highlights a diagnostically challenging presentation and the need to consider metastatic disease when evaluating atypical seminal vesicle masses in oncological patients. Full article

For decades, peritoneal metastases (PM) have been regarded as a terminal manifestation of advanced malignancies and managed primarily with palliative intent because of limited sensitivity to systemic therapies. Accumulating clinical, molecular, and immunological evidence now supports the view that PM is not merely an anatomic pattern of spread but a distinct metastatic niche with characteristic biological, microenvironmental, and therapeutic features. This review summarizes the major routes of PM development—transcoelomic, lymphatic, and hematologic dissemination—and emphasizes how these pathways converge through shared biological programs. Core mechanisms include epithelial–mesenchymal transition (EMT), adhesion signaling, extracellular matrix remodeling, and tumor–immune cell interactions. A central focus is the peritoneal tumor microenvironment: mesothelial-to-mesenchymal transition, cancer-associated fibroblast activity, adipocyte-derived metabolic support, macrophage polarization, and regulatory T-cell enrichment collectively shape an immunotolerant and treatment-resistant niche on the peritoneal surface. In addition, evidence from pre-metastatic niche biology suggests that primary tumor-derived exosomes and epitranscriptomic regulation can prime the peritoneal environment before overt implantation. These features provide a biological rationale for locoregional strategies such as cytoreductive surgery and hyperthermic intraperitoneal chemotherapy, as well as emerging intraperitoneal modalities and microenvironment-targeted approaches. Finally, organoid platforms, liquid biopsy-based minimal residual disease monitoring, and theranostic technologies may enable more personalized, biology-driven management of PM. Full article

Background/Objectives: Accurate preoperative assessment of peritoneal dissemination is essential in ovarian cancer because it influences surgical strategy and the achievement of complete gross resection. However, [¹⁸F]FDG-PET may be limited in detecting lesions with low glycolytic activity and in differentiating malignancy from inflammatory changes. This case series evaluated the clinical relevance of [¹⁸F]FAPI-74 PET/CT for preoperative assessment of peritoneal dissemination in ovarian cancer. Methods: Four patients underwent [¹⁸F]FAPI-74 PET/CT as part of preoperative evaluation, with comparison to [¹⁸F]FDG-PET/CT when available. Imaging findings were correlated with intraoperative observations and histopathological results, including immunohistochemical assessment of fibroblast activation protein and α-smooth muscle actin. Results: FAPI-PET detected peritoneal dissemination not identified by FDG-PET in several cases, including occult metastasis confirmed histologically and additional lesions after neoadjuvant chemotherapy. FAPI-avid lesions showed stromal activation on immunohistochemistry, supporting the biological basis of FAPI uptake. In one case, additional FAPI uptake may have been partly influenced by inflammatory changes associated with bloody ascites. Conclusions: FAPI-PET may provide complementary information by visualizing stromal components of ovarian cancer and may support preoperative mapping of peritoneal dissemination, although interpretation should consider inflammatory conditions. Full article

Background: Invasive lobular carcinoma (ILC) of the breast has a unique metastatic pattern due to E-cadherin deficiency, with a predilection for peritoneal, gastrointestinal, and pelvic organ involvement. Ovarian metastasis from ILC is rare but can mimic primary ovarian cancer clinically and radiologically, leading to misdiagnosis and unnecessary radical surgery. This study aimed to summarize the imaging features of ovarian metastasis from ILC and analyze the causes of misdiagnosis, while highlighting the value of preoperative biopsy. Methods: Clinical and imaging data of six patients with pathologically confirmed ovarian metastasis from ILC were retrospectively analyzed. All six patients were female (age range 33–65 years), had a history of breast cancer (ILC subtype), and were found to have ovarian masses either during follow-up or at initial diagnosis. Imaging findings of the ovaries, peritoneum, and ascites were analyzed and compared with initial clinical diagnoses and pathological results. Results: Among the six patients, five were initially clinically misdiagnosed as having primary ovarian cancer and underwent unnecessary total hysterectomy with bilateral salpingo-oophorectomy. One patient (case 6) was correctly diagnosed via percutaneous biopsy of the omentum and skin nodules, which confirmed metastatic ILC, thereby avoiding unnecessary gynecological surgery. Imaging findings: All six patients had bilateral ovarian masses, appearing as solid or cystic-solid lesions. Peritoneal changes were observed in four cases. Ascites was present in five cases. Laboratory findings showed marked variability in CA125 levels (normal in three cases, elevated in three cases). Immunohistochemistry confirmed breast origin in all cases (GATA3+, PAX8−, E-cadherin−). In case 6, after four cycles of chemotherapy (albumin-bound paclitaxel + carboplatin + bevacizumab), follow-up CT demonstrated significant reduction in ovarian masses and regression of peritoneal and omental lesions. Conclusions: Ovarian metastasis from ILC is easily misdiagnosed as primary ovarian cancer without histologic confirmation, leading to unnecessary radical surgery. However, as demonstrated in case 6, percutaneous biopsy of accessible metastatic sites (omentum, peritoneum, or skin nodules) can establish the correct diagnosis and guide systemic therapy, thereby avoiding unnecessary surgery. In case 6, the ILC ovarian metastasis showed a favorable response to chemotherapy, but this single-case finding requires cautious interpretation as ILC is generally considered less chemosensitive than invasive ductal carcinoma. In patients with a history of breast cancer or with suspected metastatic disease, ILC metastasis should be included in the differential diagnosis of ovarian masses. Full article

Gastric cancer peritoneal metastasis is not simply an extension of the primary tumor into the abdominal cavity. It represents a biologically distinct disease context shaped by interactions between disseminated tumor cells, peritoneal fluid, mesothelial surfaces, submesothelial stroma, extracellular matrix, immune populations, and malignant ascites. In this narrative review, we examine peritoneal metastasis as a transition between three related but physiologically different states: the primary gastric tumor, free-floating tumor cells or spheroids in the peritoneal fluid, and established mesothelial or submesothelial metastatic implants. We discuss how tumor cells acquire dissemination competence in the primary tumor, survive detachment and fluid-phase stress, adhere to remodeled mesothelium, recruit stromal and immune support, and adapt to ascites-mediated signaling. We also review how the peritoneal niche may contribute to biomarker discordance, immune exclusion, therapeutic resistance, and limitations of conventional response assessment. Where relevant, we distinguish evidence derived directly from gastric cancer peritoneal metastasis from preclinical data, extrapolation from other peritoneal malignancies, and hypothesis-generating interpretation. Finally, we summarize practical implications for tissue sampling, ascites and lavage analysis, biomarker interpretation, translational modeling, and peritoneal-directed therapeutic strategies. A clearer understanding of the biological divergence between the primary tumor, the fluid-phase compartment, and peritoneal implants may improve the study and clinical management of gastric cancer peritoneal metastasis. Full article

Mesothelin (MSLN) is a cell surface glycoprotein with limited expression in normal tissues but frequent overexpression in solid tumors, including gynecological malignancies. This review summarizes the state of the art on the biological role, diagnostic value, prognostic significance, and therapeutic potential of MSLN in ovarian, endometrial, and cervical cancers. Evidence from clinical and experimental studies indicates that MSLN contributes to tumor progression through interactions with CA125, promotion of cell adhesion and peritoneal metastasis, activation of oncogenic signaling pathways, modulation of immune responses, and development of chemoresistance. Elevated MSLN expression has been associated with advanced clinical stage of the disease, platinum resistance, and poorer survival outcomes, particularly in ovarian cancer patients, although prognostic findings remain inconsistent. Circulating soluble MSLN may serve as a minimally invasive biomarker and may improve diagnostic accuracy when combined with established markers. Therapeutic MSLN strategies—antibody-drug conjugates, CAR-T and NK cell therapies, monoclonal antibodies, immunotoxins, vaccines, and checkpoint blockade—provide promising pre-clinical and early clinical results, particularly in resistant or recurrent forms of the disease. Overall, MSLN constitutes a promising target for precision oncology in gynecological cancers, although further clinical studies are required to validate its diagnostic utility and optimize targeted therapeutic approaches. Full article

Background: Aspirin, initially recognized for its anti-inflammatory, antipyretic and analgesic properties, holds a prominent role in the treatment of cardiovascular disease. The utility of aspirin in cancer therapeutics has been explored and stratified into COX-dependent and -independent mechanisms. COX2 gene expression has been demonstrated to be significantly upregulated in colorectal cancer and various other gastrointestinal malignancies including pancreatic, esophageal, and gastric cancer. This study investigates the relationship of aspirin use and outcomes in patients with colorectal cancer. Methods: The Nationwide Inpatient Sample (NIS) database from 2017 to 2022 was analyzed for patients age > 18 who were hospitalized for colorectal cancer and its decompensations using ICD-10 diagnostic codes. These patients were further stratified based on the long-term use of aspirin. The principal outcome of this investigation are the odds of in-hospital mortality, with secondary outcomes including odds of pulmonary embolism, portal vein thrombosis, acute kidney injury, septic shock, requiring an ICU level of care and odds of hepatic, pulmonary, gastrointestinal and peritoneal or retroperitoneal metastatic disease. Multivariate logistic regression accounting for hospital and patient characteristics was implemented for analysis, with the Charlson Comorbidity Index used to adjust for coexisting comorbidity burden; a p-value (p) of <0.05 was considered statistically significant. Results: In our analysis of the NIS, 596,160 patients were identified with colorectal cancer and 11.7% (69,750) of this population were identified with long-term use of aspirin. Aspirin use was identified to have a significantly reduced odds of in-patient mortality (adjusted odds ratio) [aOR] 0.530, p value < 0.001 95% CI (confidence interval): 0.460–0.617. Patients with aspirin use also demonstrated significantly reduced odds of adverse outcomes and gastrointestinal, hepatic, pulmonary and retroperitoneal/peritoneal metastasis; (aOR 0.606, 95% CI: 0.564–0.653, p < 0.001), (aOR 0.628, 95% CI: 0.582–0.678, p < 0.001), (aOR 0.676, 95% CI: 0.605–0.755, p < 0.001) and (aOR 0.751, 95% CI: 0.685–0.825, p < 0.001) respectively. Conclusions: In recent years, there has been an alarming increase in incidence of colorectal cancer, particularly amongst younger individuals with increased associated mortality. This mortality increase, albeit alarming, is a driving force for treatment innovation with continual examination of our repertoire of medications for possible repurposed applications. COX2-mediated signaling serves as a key promotor of tumorigenic molecular signaling that directly contributes to tumor cell proliferation, angiogenesis and metastasis in colorectal cancer. Aspirin use and its inhibitory action on COX2 demonstrated a significantly reduced odds of in-hospital mortality. Aspirin use is also associated with significantly reduced odds of developing metastatic disease to the liver, gastrointestinal system, lungs and peritoneum in patients with colorectal cancer. These findings convey that aspirin use reduces the likelihood of in-hospital mortality, major comorbid conditions and of developing metastatic disease as compared to those who do not use aspirin. Full article

Background and Objectives: Malignant ascites reflects the tumor microenvironment and provides valuable insights into peritoneal metastasis. This study aimed to assess soluble immune system-related molecules in the ascites fluid of advanced gastrointestinal cancer patients with peritoneal carcinomatosis and to explore potential therapeutic opportunities. Methods: This multicenter prospective cohort study included 48 patients with gastrointestinal adenocarcinoma (17 colorectal, 16 gastric, and 15 pancreatic) with malignant ascites and 15 patients for comparison who required benign ascites drainage for advanced heart failure. Blood samples for routine parameters and ascites fluid for cytokine and soluble immune checkpoint analysis were collected. Parameters were compared between cancer patients and the comparison group, across cancer subgroups, and in correlation with survival. Results: The mean age of participants was 60.2 ± 14.9 years, with a female-to-male ratio of 11:20. The median survival of cancer patients was 84.0 days. Compared with heart failure-associated transudative ascites, malignant ascites demonstrated higher levels of TNF-α, IL-6, IL-10, IL-12p70, IL-18, IL-23, s4-1BB, and TGF-β1, while albumin levels were lower. Significant intergroup differences were observed in TNF-α, IL-6, IL-8, IL-10, IL-12p70, IL-23, 4-1BB, TGF-β1, and PD-L1 levels. In exploratory multivariable analysis, IL-10 and soluble 4-1BB emerged as potential predictors of shorter survival, although these findings require validation in larger cohorts. Survival was negatively correlated with PD-L1, TNF-α, IL-6, and IL-10 in colorectal cancer; 4-1BB, TGF-β1, IL-8, and IL-10 in gastric cancer; and TGF-β1, IL-6, and IL-10 in pancreatic cancer. Conclusions: These exploratory findings indicate that the immunosuppressive milieu in malignant ascites in gastrointestinal cancers may be mediated by cancer subtype-specific pathways, warranting further mechanistic and translational investigation. Full article

In ovarian cancer, reactive oxygen species (ROS) are both toxic byproducts and mediators of signaling and stress adaptation, such that the same “ROS change” can suppress or promote tumors in vivo. Here, we integratively summarize how ROS modulation reshapes tumor growth, metastasis, and treatment response in ovarian cancer, based on 22 original in vivo-containing studies that were selected from a five-database search of papers published from January 1990 to December 2025. On the antitumor axis, ROS amplification in xenograft models is accompanied by reduced tumor burden and increased markers of cell death, and can operate through diverse death programs beyond apoptosis, including pyroptosis and ferroptosis. ROS-based anticancer effects may vary depending on whether cytoprotective autophagy is co-induced. For example, in models treated with daphnetin, ROS-dependent cell death occurs together with induction of cytoprotective autophagy and the anticancer effect is strengthened when an autophagy inhibitor is added. In a therapeutic context, autophagy may thus function as an adaptive response in tumor cells to partially buffer ROS-induced stress. Conversely, on the pro-tumor axis, ROS can serve as an upstream signal driving inflammatory and metastatic processes. In a peritoneal metastasis model, GPX1 inhibition-induced ROS elevation was linked to increased metastatic burden. In the context of drug resistance, platinum resistance is proposed to be an adaptive state shaped not by the absolute level of ROS alone, but by integrated ROS-sensing and buffering circuits, the DNA damage response (DDR), and NF-κB networks. In vivo, AMPK–ROS axis activation through ACLY inhibition or resetting of drug responsiveness can be connected to tumor suppression and increased sensitivity. Furthermore, ROS modulation is not limited to tumor cell-intrinsic targets: it can also be linked to therapeutic response reprogramming at the tumor microenvironment (TME) level, such as via regulation of acidity/ROS conditions and coupling to macrophage polarization in immunocompetent syngeneic models. Taken together, these lines of in vivo evidence indicate that, in ovarian cancer, ROS should not be interpreted in a binary “increase/decrease” manner, but rather in terms of redox-buffering capacity, the engaged signaling axes (cell death, DDR, metastasis/inflammation), and interactions with TME factors. Full article

Background and Aim: Anti-epidermal growth factor receptor (EGFR) therapy is commonly associated with skin toxicity, which may reflect treatment response. This study evaluated the prognostic significance of anti-EGFR-related skin toxicity in patients with RAS wild-type metastatic colorectal cancer (mCRC) receiving palliative chemotherapy. Materials and Methods: We retrospectively analyzed 256 RAS wild-type mCRC patients treated with anti-EGFR monoclonal antibodies at Erciyes University, Kayseri, Turkey (June 2011–February 2024). Survival was estimated using the Kaplan-Meier method with log-rank comparisons. A landmark analysis at 2 months was performed to address guarantee-time bias. Univariate and multivariate Cox regression analyses were used to identify independent prognostic factors. Results: The median PFS was 17 months in patients with grade ≥ 2 skin toxicity versus 8 months in those with grade < 2 skin toxicity (p < 0.001). The median OS was 32 and 21 months, respectively (p < 0.001). In the landmark-adjusted multivariate analysis, grade ≥ 2 skin toxicity was an independent prognostic factor for both PFS (HR 0.52, 95% CI 0.39–0.70, p < 0.001) and OS (HR 0.50, 95% CI 0.37–0.68, p < 0.001). Additional independent factors for OS included albumin, LDH, peritoneal metastasis, age, tumor sidedness, and BMI. The objective response rates were 53.9% and 11.3% in the grade ≥ 2 and grade < 2 groups, respectively (p < 0.001). Conclusions: Grade ≥ 2 skin toxicity was significantly associated with longer PFS, OS, and a higher response rate, and was confirmed as an independent prognostic factor in multivariate analysis. These findings suggest that skin toxicity may serve as a non-invasive marker of treatment efficacy. Prospective studies with time-dependent methodologies are needed to validate these results. Full article

Background/Objectives: Peritoneal metastasis represents the most frequent and prognostically unfavorable metastatic pattern in gastric cancer, largely due to limited sensitivity of conventional imaging, delayed diagnosis, and insufficient response assessment. The aim of this review is to provide an overview of the current evidence on the diagnosis and treatment of gastric cancer with peritoneal metastases and to address current treatment limitations and options. Methods: This review was designed as a narrative review and is based on an extensive literature search in established databases. Results: Systemic chemotherapy remains the cornerstone of palliative treatment, improving the survival and quality of life compared with the best supportive care; however, outcomes in peritoneally metastatic disease remain poor. Advances in molecularly targeted and immune-based therapies have extended survival in selected patient populations, yet favorable molecular profiles are mainly unknown in peritoneal metastases. Staging laparoscopy and semi-quantitative assessment using the Peritoneal Cancer Index (PCI) are therefore essential for accurate diagnosis, prognostication, and treatment selection. Growing evidence from retrospective studies, multi-institutional cohorts, and selected randomized trials suggests that a multimodal approach—combining systemic therapy with intraperitoneal or bidirectional chemotherapy—may improve survival and quality of life. In carefully selected patients whose primary gastric tumor and peritoneal lesions respond to systemic treatment, complete cytoreductive surgery (CRS) followed by hyperthermic intraperitoneal chemotherapy (HIPEC) may further enhance outcomes and, in rare cases, achieve long-term survival. These potential benefits appear to be limited to highly selected patients with a low peritoneal tumor burden (PCI ≤ 6–7), positive cytology, good performance status, controlled extraperitoneal disease, and a high likelihood of achieving complete macroscopic cytoreduction (CC-0). Conclusions: Although the treatment intent in metastatic gastric cancer remains primarily palliative, carefully selected patients with limited peritoneal metastases may benefit from intensified multimodal treatment strategies when managed in specialized centers. Interdisciplinary evaluation, accurate staging, and individualized treatment planning are essential to optimize outcomes in this challenging disease setting. Full article

Background: Gastric cancer (GC) is characterized by aggressive invasion and early peritoneal dissemination, which are strongly driven by chronic inflammation and epithelial–mesenchymal transition (EMT). c-Jun N-terminal kinase (JNK), a stress-responsive serine/threonine kinase within the mitogen-activated protein kinase (MAPK) family, integrates inflammatory cues to promote EMT and metastasis. Huangjin Shuangshen granules (HJSS) is a multi-component traditional Chinese medicine (TCM) formula derived from Simiao Yong’an Decoction and clinically used as an adjuvant therapy for GC. However, whether HJSS restrains inflammation-driven metastasis through modulation of JNK-associated EMT signaling remains unclear. Methods: The anti-metastatic efficacy of HJSS was evaluated using integrated in vivo and in vitro models, combined with transcriptomics, network pharmacology and molecular validation. Results: HJSS markedly attenuated LPS-induced metastatic behavior and inflammatory activation. Multilevel analyses converged on MAPK8/JNK as a central regulatory node. HJSS reversed EMT progression and inhibited nuclear phosphorylation of JNK without affecting its upstream kinases. Thermal-shift assays and molecular docking supported potential target engagement of HJSS-derived constituents, including possible interactions with JNK-related signaling targets. Pharmacologic reactivation of JNK partially abrogated the inhibitory effects of HJSS, confirming JNK-dependent action. Conclusions: HJSS suppresses inflammation-driven GC metastasis primarily by attenuating JNK-associated EMT, potentially through modulation of JNK activation by its bioactive constituents. These findings provide mechanistic insight into HJSS as a low-toxicity anti-metastatic strategy and support further exploration of its active constituents. Full article

Patterns of colon cancer recurrence demonstrate a high degree of anatomical reproducibility, consistently aligning with mesofascial planes and compartmentalized vascular and lymphatic territories, as evidenced by pathological, surgical and imaging studies. These frameworks describe recognized routes of spread but do not provide an integrated anatomical explanation for understanding why tumor progression often aligns with mesofascial planes, embryological boundaries and cavity-specific niches, nor for why preservation of structural integrity during surgery is associated with improved oncological outcomes. This work proposes a spatial containment model of colon cancer progression, in which tumor dissemination reflects sequential breaches of anatomically defined barrier systems. The Colon Cancer Containment System is proposed as a three-tier framework in which tumor progression reflects sequential breaches of containment at the tissue (microcontainment), mesenteric (mesocontainment) and peritoneal or systemic (macrocontainment) levels. At each stage, anatomical structures function as barrier systems that constrain tumor spread and shape directionality of progression. Disruption of these barriers, whether tumor-driven or iatrogenic, is associated with relatively consistent patterns of local, regional, and distant recurrence. Within this approach, established prognostic features such as tumor–node–metastasis (TNM) stage, extramural vascular invasion, perineural invasion and margin status may also be interpreted as markers of containment integrity, in addition to their established roles as indicators of tumor aggressiveness. Surgical plane preservation is reframed as a biologically meaningful act of containment maintenance. By organizing validated observations within an anatomically patterned architecture, the containment framework provides a coherent model for interpreting reproducible recurrence patterns and clarifies the biological significance of surgical integrity. This perspective complements existing oncological paradigms, supports anatomically informed risk stratification and generates testable hypotheses for future clinical and translational research. Full article