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Review

Cutting Edge: A Comprehensive Guide to Colorectal Cancer Surgery in Inflammatory Bowel Diseases

by
Ionut Eduard Iordache
1,2,
Lucian-Flavius Herlo
3,*,
Razvan Popescu
1,2,
Daniel Ovidiu Costea
1,2,
Luana Alexandrescu
2,4,
Adrian Paul Suceveanu
4,
Sorin Deacu
5,
Gabriela Isabela Baltatescu
6,
Alina Doina Nicoara
2,7,
Nicoleta Leopa
1,2,
Andreea Nelson Twakor
7,
Andrei Octavian Iordache
2 and
Liliana Steriu
1,2
1
Department of General Surgery, “Sf. Apostol Andrei” Emergency County Hospital, 145 Tomis Blvd., 900591 Constanta, Romania
2
Faculty of Medicine and Pharmacy Constanta, Ovidius University, 900527 Constanta, Romania
3
Doctoral School, “Victor Babes” University of Medicine and Pharmacy Timisoara, Eftimie Murgu Square 2, 300041 Timisoara, Romania
4
Gastroenterology Department, “Sf. Apostol Andrei” Emergency County Hospital, 145 Tomis Blvd., 900591 Constanta, Romania
5
Department of Forensic Medicine, County Clinical Emergency Hospital of Constanta, 900591 Constanta, Romania
6
Clinical Service of Pathology, “Sf. Apostol Andrei” Emergency County Hospital, 145 Tomis Blvd., 900591 Constanta, Romania
7
Internal Medicine Department, “Sf. Apostol Andrei” Emergency County Hospital, 145 Tomis Blvd., 900591 Constanta, Romania
*
Author to whom correspondence should be addressed.
J. Mind Med. Sci. 2025, 12(1), 6; https://doi.org/10.3390/jmms12010006
Submission received: 19 January 2025 / Revised: 26 February 2025 / Accepted: 26 February 2025 / Published: 11 March 2025

Abstract

:
Over the past two decades, surgical techniques in colorectal cancer (CRC) have improved patient outcomes through precision and reduced invasiveness. Open colectomy, laparoscopic surgery, robotic-assisted procedures, and advanced rectal cancer treatments such as total mesorectal excision (TME) and transanal TME are discussed in this article. Traditional open colectomy offers reliable resection but takes longer to recover. Laparoscopic surgery transformed CRC care by improving oncological outcomes, postoperative pain, and recovery. Automated surgery improves laparoscopy’s dexterity, precision, and 3D visualisation, making it ideal for rectal cancer pelvic dissections. TME is the gold standard treatment for rectal cancer, minimising local recurrence, while TaTME improves access for low-lying tumours, preserving the sphincter. In metastatic CRC, palliative procedures help manage blockage, perforation, and bleeding. Clinical examples and landmark trials show each technique’s efficacy in personalised care. Advanced surgical techniques and multidisciplinary approaches have improved CRC survival and quality of life. Advances in CRC treatment require creativity and customised surgery.

1. Introduction

Patients with inflammatory bowel disease (IBD)—including ulcerative colitis (UC) and Crohn’s disease (CD)—face an increased risk of developing CRC [1]. While advances in medical therapies and surveillance techniques have reduced CRC rates in recent years, it remains a leading cause of mortality and colectomy among IBD patients [2]. The driving force behind CRC in IBD is chronic inflammation, which leads to precancerous dysplastic lesions. These lesions can appear in multiple parts of the colon simultaneously, a process referred to as field cancerisation [3]. Unlike sporadic CRC, colitis-associated cancers (CACs) present unique molecular characteristics, but much remains unknown about how these differences influence cancer development and behaviour [4]. Emerging evidence suggests that the gut microbiome, in coordination with the host immune system, plays a critical role in the progression of CAC. Certain treatments for IBD not only control inflammation but may also have cancer-preventive properties, which has created new hope for improved outcomes [2]. Anal HPV infection can cause squamous intraepithelial lesions (SILs), which are precursors of anal squamous cell carcinoma (SCC) [5].
This review offers a comprehensive, updated understanding of CAC’s epidemiology, development mechanisms, risk factors, and management strategies. With improved surveillance, chemoprevention, and a deeper appreciation of genetic and environmental factors, managing CAC risk will become more precise and effective in the years to come.

Epidemiology

Individuals with long-standing UC and extensive Crohn’s colitis (beyond proctitis) have a 2–3 times higher risk of developing CRC compared to the general population [6]. Fortunately, studies indicate a decreasing trend in CRC incidence, likely due to advancements in medical treatments and more effective colonoscopic screening programs [7,8]. Figure 1 below shows that CRC remains a significant concern, often leading to colectomy and mortality among IBD patients.
Older data suggested that the cumulative CRC risk in UC was about 2%, 8%, and 18% after 10, 20, and 30 years of disease duration, respectively [10]. Recent research, however, paints a more optimistic picture: cumulative risks are now reported to be closer to 1%, 3%, and 7% for the same time periods [11]. This decline highlights the success of improved therapies and surveillance strategies.
Figure 2 highlights the most common cancer types by country in absolute incidence numbers for both sexes in 2022, excluding non-melanoma skin cancer (NMSC).
Countries shaded in yellow represent regions where colorectal cancer is the most frequently diagnosed cancer. Notably, colorectal cancer dominates in areas such as Russia, Eastern Europe, and parts of Asia, reflecting dietary patterns, lifestyle factors, and healthcare access challenges that influence cancer incidence. The importance of this map lies in its ability to visually identify regional disparities in cancer prevalence, helping policymakers and healthcare professionals prioritise prevention, screening, and treatment strategies.
Interestingly, another similar trend is seen in Asian–Pacific regions, where IBD incidence has surged more recently.
The pie chart in Figure 3 illustrates the absolute number of CRC cases in both sexes across continents in 2022, based on data from the International Agency for Research on Cancer [9].
With a global total of 1,926,425 cases, the chart highlights that Asia accounts for the largest burden at 50.2% (966,399 cases), followed by Europe at 27.9% (538,262 cases) and North America at 9.5% (183,973 cases). Smaller proportions are observed in Latin America and the Caribbean (7.5%), Africa (3.7%), and Oceania (1.2%). The high burden in Asia and Europe reflects factors such as ageing populations, dietary patterns, and screening practices, while the lower incidence in Africa and Oceania may be influenced by underreporting and differences in risk factors.
Another meta-analysis of over 31,000 UC patients across Asia found CRC prevalence to be 0.85%, with cumulative risks of 0.02% at 10 years, 4.8% at 20 years, and 13.9% at 30 years.
Whether ethnicity or geography influences CRC risk remains unclear. Differences in diet, surveillance practices, healthcare access, and genetics may explain regional variations.

2. Pathogenesis of Colitis-Associated CRC

Colitis-associated CRC is a prime example of inflammation-induced carcinogenesis [12]. Chronic inflammation causes oxidative stress and DNA damage, which can activate cancer-promoting genes while inactivating tumour-suppressing genes. Over time, this environment leads to mutations and epigenetic changes, driving the dysplasia-to-carcinoma sequence [13].
Unlike sporadic CRC, which develops through isolated adenomatous or serrated polyps, CAC develops in broader regions of inflamed mucosa—a phenomenon called field cancerisation [14]. Mutated epithelial cell clones spread across the colon, even before visible dysplasia appears [1]. These alterations explain why patients with IBD are prone to synchronous (multiple, simultaneous) and metachronous (new, sequential) tumours [15].

2.1. Molecular Mechanisms

Right-sided colorectal cancer, typically arising in the proximal colon, is characterised by mutations in KRAS, RAS, PIK3CA, PTEN, MSI (Microsatellite Instability), and BRAF [16]. In contrast, left-sided colorectal cancer, found in the distal colon, shows mutations in KRAS, RAS, PIK3CA, PTEN, TP53, and APC, reflecting differences in tumour biology and behaviour [17]. Rectal cancer, located in the rectum, frequently harbours mutations in KRAS, HER2, TP53, and APC, further distinguishing it from colon cancers [18,19].
Figure 4 shows that both sporadic CRC and CAC share similar genetic pathways—chromosomal instability, microsatellite instability (MSI), and CpG island methylator phenotype (CIMP) [20].
Figure 5 shows that in a healthy colon, CRC develops through the classic adenoma-carcinoma sequence, initiated by mutations in the APC gene, followed by alterations in KRAS and deletions in tumour-suppressor genes like P53 and DCC [21].
This progression leads to sporadic CRC through adenomatous and precancerous polyps. In IBD, chronic inflammation triggers epithelial abnormalities, low-grade dysplasia, and high-grade dysplasia [22]. Mutations in P53 often occur early, followed by alterations in CRC-specific genes and KRAS, driving the progression to IBD-associated CRC [23]. Thus, Figure 5 emphasises the key molecular differences between sporadic and inflammation-driven CRC, highlighting the importance of genetic mutations and chronic inflammation in cancer development.
The timing and frequency of mutations differ between the two. In sporadic CRC, APC mutations occur early, while P53 alterations happen later. In CAC, P53 mutations are among the earliest events, occurring even before dysplasia develops, whereas APC mutations occur less frequently and later in the sequence [24].
Recent studies also highlight the role of the microbiome [25]. Specific bacterial strains like Fusobacterium nucleatum, Escherichia coli (carrying polyketide synthetase genes), and Bacteroides fragilis have been implicated in CRC progression [26]. These bacteria can trigger inflammation, cause DNA damage, and promote tumour growth in experimental models, particularly under inflammatory conditions [27].

2.2. Types of Dysplasia

Long-term ulcerative and Crohn’s colitis increase colorectal cancer risk. Dysplasia, a precancerous CRC lesion in patients with long-term inflammatory bowel disease, can be indefinite, low-grade, or high-grade.
In IBD, dysplasia is the strongest predictor of CRC. Conventional dysplasia resembles sporadic adenomas but is often found in a more flat form across the inflamed colon [28]. Table 1 includes histologically details. Thus, dysplastic cells in IBD tend to span the full height of the crypts, unlike in sporadic adenomas, where changes start at the top (top-down dysplasia) [1]. Non-conventional dysplasia types, such as goblet cell-deficient or hypermucinous dysplasia, are increasingly recognised [28]. Though not fully incorporated into surveillance guidelines, they may carry a higher risk of progression to advanced neoplasia. Additionally, serrated epithelial changes, which mimic sporadic serrated lesions, can sometimes occur in IBD, further complicating diagnosis and risk stratification [29].

3. Clinical Outcomes

Effectively managing CAC requires a proactive approach that balances risk assessment, surveillance, and intervention strategies. The primary goal is to identify high-risk patients early and implement measures to reduce their risk of progression to advanced colorectal neoplasia (aCRN) [22]. This includes endoscopic surveillance, identifying clinical risk factors, and, where appropriate, employing chemoprevention.
Table 2 presents a risk stratification flowchart for CRC surveillance based on baseline colonoscopy findings [31].
The flowchart categorises patients into low risk, intermediate risk, and high risk, each with specific follow-up intervals. Low-risk patients (1–2 small adenomas) may not require surveillance for five years or can cease follow-up if no adenomas are found. Intermediate-risk patients (3–4 small adenomas or at least one ≥1 cm) are advised to undergo surveillance every three years, with follow-up decisions based on negative exams or new adenoma findings. High-risk patients (≥5 small adenomas or ≥3 with at least one ≥1 cm) require annual surveillance to monitor potential progression [31].

3.1. Patient-Related Factors

Certain patient characteristics influence the risk of CAC. Age plays a dual role: while older age itself increases the risk of CRC, younger age at inflammatory bowel disease diagnosis—particularly before 30 years—suggests a longer disease duration, which significantly increases cumulative risk [22]. Sex is another determinant, with males having a 1.5 times greater risk of developing advanced neoplasia compared to females. Additionally, a family history of CRC is critical; having a first-degree relative diagnosed with CRC, especially before the age of 50, markedly increases CAC risk [32].

3.2. Disease-Related Factors

The nature and severity of IBD significantly contribute to CAC risk. The duration of disease is a key predictor, as the risk of CAC begins to rise after 8–10 years of IBD diagnosis, which is why surveillance is recommended to start at this time [1]. The extent of the disease also matters: patients with extensive colitis involving more than 50% of the colon have a considerably higher risk than those with limited disease [33].
A particularly high-risk subgroup includes patients with primary sclerosing cholangitis (PSC). PSC increases the risk of CAC by 3–5 times, even in patients with minimal or quiescent IBD activity [34]. PSC-associated dysplasia tends to occur earlier and is frequently localised to the right colon. Finally, the severity of inflammation is one of the strongest predictors of CAC. Persistent, severe histological inflammation, often measured as a cumulative inflammatory burden (CIB), accelerates dysplastic changes and progression to CAC [35].

3.3. Pathology-Related Factors

Pathology findings provide important risk stratification for CAC. A history of dysplasia, whether low-grade or high-grade, significantly elevates the risk of CRC. Patients with indefinite dysplasia (IND)—a borderline finding indicating possible dysplastic changes—are also at higher risk [36]. When IND is confirmed by expert pathologists, it is associated with an increased likelihood of progression to advanced colorectal neoplasia (aCRN) compared to patients with no dysplasia [37].

3.4. Surveillance Strategies for CAC

The foundation of CAC prevention lies in a structured colonoscopic surveillance program, which remains the most effective tool for detecting dysplasia and early CRC. Surveillance strategies are guided by disease duration, severity, and patient-specific risk factors. Patients without PSC should initiate colonoscopic screening 8–10 years after IBD symptom onset [38]. In contrast, PSC patients face significantly elevated risk and should begin annual surveillance at the time of the diagnosis [1]. Surveillance intervals following the initial screening are determined by risk stratification: high-risk patients (e.g., prior dysplasia, PSC, or severe inflammation) require annual colonoscopies; intermediate-risk patients are monitored every 2–3 years; and low-risk patients (e.g., quiescent disease) can be screened every 5 years [39].
The quality of colonoscopic exams is critical for identifying dysplasia. High-definition white-light endoscopy (HD-WLE) is the current standard, but chromoendoscopy—using dye-based or virtual techniques—enhances the detection of subtle, flat lesions [40]. Studies demonstrate that chromoendoscopy improves the visualisation of dysplasia that might be missed by HD-WLE [41,42]. In cases of visible lesions, endoscopic techniques like endoscopic mucosal resection (EMR) or submucosal dissection allow for resection, helping patients avoid colectomy unless other high-risk features are present [43]. For invisible dysplasia detected via random biopsies, a repeat colonoscopy with chromoendoscopy is essential to locate visible lesions. In cases of high-grade dysplasia (HGD), endoscopically unresectable dysplasia, or dysplasia in PSC patients, surgical referral for colectomy is recommended due to the heightened risk of progression to CRC [44].

3.5. Chemoprevention for CAC

Chemoprevention aims to reduce the risk of CAC by controlling inflammation and targeting carcinogenic pathways. Although no randomised trials definitively confirm its efficacy, several therapies show promise [45].
Table 3 includes the main drug classes. 5-Aminosalicylates (5-ASAs), such as mesalamine, are widely used in ulcerative colitis and have demonstrated chemopreventive effects in observational studies, with patients on 5-ASAs showing a 49% lower risk of advanced neoplasia [46]. Higher doses and prolonged use may offer greater benefits, particularly in the early stages of the disease [18]. Thiopurines (e.g., azathioprine and 6-mercaptopurine) have mixed evidence regarding CAC prevention; while some studies suggest reduced dysplasia risk, concerns about non-CRC malignancies and safety issues limit their routine use for chemoprevention [47]. Finally, biologic therapies, such as anti-TNF agents and anti-integrins, have shown promise in reducing inflammation and potentially providing indirect chemopreventive effects, though robust evidence confirming their role in CAC prevention remains limited [48].
Among the Anti-TNF Alpha agents, Infliximab and Adalimumab show positive outcomes for induction, maintenance, and mucosal healing, while Certolizumab and Golimumab demonstrate effectiveness in induction and maintenance but lack available studies on mucosal healing. None of the Anti-TNF Alpha agents have available studies for combination therapies with thiopurine or methotrexate, nor for treating acute severe colitis. For Anti-Integrin therapies, Natalizumab does not have available studies in any category, whereas Vedolizumab has shown positive outcomes in induction and maintenance but lacks studies on mucosal healing or combination therapy options. Among the Other Biologic agents, Ustekinumab has been shown to be effective for induction but does not have available studies regarding its use for maintenance, mucosal healing, or combination therapy with thiopurine and methotrexate.

4. Surgical Approaches in CRC: Techniques and Applications

Surgery remains the cornerstone of treatment for CRC, particularly in localised and resectable diseases. Advances in surgical techniques and perioperative care have substantially improved outcomes, reducing morbidity and mortality while preserving organ function [49]. This section discusses key surgical approaches, including open, minimally invasive, and advanced techniques such as robotic-assisted surgery, with examples from clinical practice and literature.

4.1. Open Colectomy

Historically, open colectomy has been the gold standard surgical approach for colorectal cancer resection [50]. This involves creating a large midline abdominal incision to access and remove the diseased section of the colon, along with regional lymphadenectomy. Figure 6 presents the step-by-step process of surgical removal of a colon segment with bowel reattachment in patients with CRC.
The first panel highlights the presence of CRC in the colon, indicating the affected area requiring surgical intervention. In the second panel, the cancerous segment of the colon, along with nearby tissues, is surgically removed to ensure complete excision of malignant cells. Finally, the third panel illustrates the reattachment of the remaining healthy ends of the colon, restoring bowel continuity and function. This procedure, known as colon resection with anastomosis, is a standard treatment for localised CRC, aiming to eliminate the tumour while maintaining normal gastrointestinal function [50].

4.2. Laparoscopic Surgery

Laparoscopic colectomy has become the preferred approach for many colorectal cancers due to its benefits, including reduced postoperative pain, shorter hospital stays, and faster recovery [51]. This minimally invasive procedure involves making small incisions through which trocars are introduced, allowing a camera to provide clear visualisation of the operative field [52]. The key steps of the procedure include insufflation of the abdominal cavity with carbon dioxide (CO2) to create a sufficient working space, followed by the identification and isolation of key vascular structures using high-definition imaging [53]. The colon segment is then dissected and mobilised with specialised laparoscopic instruments. Finally, the colon is exteriorised through a small incision for extracorporeal resection and bowel anastomosis, restoring continuity [54]. This technique offers both oncologic safety and improved patient outcomes compared to open surgery.
Figure 7 shows a minimally invasive laparoscopic surgery for colorectal procedures, utilising small incisions and specialised instruments.
In a population-based study, Yamanashi et al. [55] analyzed short-term outcomes between robotic-assisted and laparoscopic surgeries for rectal cancer. The median postoperative hospital stay for the cohort was 10 days for robotic-assisted laparoscopic surgery (RALS) and 11 days for conventional laparoscopic surgery (CLS). The postoperative hospital stay was considerably shorter in the RALS group than the CLS group in the overall and matched cohorts [55].
Another retrospective propensity score-matched comparison evaluated laparoscopic, robotic, and transanal TME approaches concerning intraoperative, postoperative, quality, and survival outcomes [56]. Laparoscopy was associated with higher conversion rates to open surgery and increased postoperative complications. Transanal TME had a higher rate of Grade C anastomotic leakage (4.1%) compared to robotic (0.7%) and laparoscopic approaches (0%) [56].

4.3. Robotic-Assisted Surgery

Robotic-assisted colorectal surgery combines the benefits of laparoscopy with enhanced dexterity, precision, and visualisation offered by advanced robotic platforms like the da Vinci Surgical System [57]. This technique has become particularly valuable in rectal cancer cases, where pelvic dissection can be technically challenging. During the procedure, the surgeon operates from a console, manipulating robotic arms with wristed instruments that mimic human hand movements, enabling superior control [52].
High-definition 3D imaging further enhances the visualisation of critical structures, ensuring precise dissection and nerve preservation, which is essential for rectal cancer surgery [51]. However, the widespread adoption of robotic-assisted surgery remains limited due to high costs and restricted access in certain regions.
In a network meta-analysis conducted by Seow et al. [58], the authors evaluated operative and oncological outcomes. Robotic TME (RoTME) was associated with a reduced conversion to open surgery compared to laparoscopic TME (LapTME) (Relative Risk [RR] = 0.23; 95% Credible Interval [CrI] 0.034–0.70). Additionally, RoTME resulted in a shorter hospital stay than open TME (OpTME) (mean difference of 3.3 days; 95% CrI 0.12–6.0). No significant differences were observed in 5-year overall survival or disease-free survival among the techniques [58].

4.4. Total Mesorectal Excision: Rectal Cancer Standard

TME is the gold standard for operable rectal cancer, involving the precise dissection of the rectum and surrounding mesorectal fascia to ensure bloc removal of the tumour, lymphatics, and mesorectal fat [52]. The procedure is performed under direct or magnified visualization, allowing for the preservation of pelvic autonomic nerves to minimize urinary and sexual dysfunction [59].
The surgical approach (Figure 8) depends on the tumour location: for mid-to-upper rectal cancers, low anterior resection (LAR) is performed to preserve the sphincter, while for lower rectal cancers, where sphincter preservation is not feasible, abdominoperineal resection (APR) is required, resulting in a permanent colostomy [60].
The surgical resection of the affected rectal segment is performed through an abdominoperineal resection or low anterior resection, depending on tumour location and sphincter involvement. This procedure removes the cancerous tissue while considering oncological safety and functional outcomes, often necessitating a permanent colostomy if sphincter preservation is not feasible.
TME has been pivotal in reducing local recurrence rates and significantly improving survival outcomes for patients with rectal cancer, marking a major advancement in oncologic surgery [61].
Advances in surgical techniques allow for sphincter preservation in select patients with low rectal cancers [44].
A systematic review and meta-analysis conducted by Geitenbeek et al. [62] compared functional outcomes and quality of life following open, laparoscopic, robot-assisted, and TaTME procedures. No significant differences were found in urinary, sexual, and faecal functioning or quality of life among the different techniques [62].

4.5. Palliative Surgery for Advanced Disease

For advanced or metastatic CRC, surgery can provide symptomatic relief and improve quality of life. Examples include palliative colectomy for obstruction, perforation, or bleeding, and debulking surgery in combination with chemotherapy for selected patients with hepatic metastases [58].

4.6. Patent Analysis

Using the Lens database [63], from 2010 to 2024, 75,651 patents were filed related to colorectal cancer surgery, reflecting significant innovations in surgical techniques and technology. The patents cover advancements in minimally invasive procedures, robotic-assisted surgery, and enhanced post-operative recovery methods.
Patents (75,651) = colorectal AND (cancer AND surgery).
Filing Date = (1 January 2010–31 December 2024).
The graph in Figure 9 illustrates the trend in patent publications related to colorectal cancer surgery from 2010 to 2025, showing a steady increase in filings over the years.
The document count rises significantly from 2010 to 2020, with a peak around 2020–2022, reflecting a surge in innovation in minimally invasive, robotic-assisted, and precision surgical techniques. The document types included in the chart are Amended Application (a revised version of a previously submitted patent application, incorporating changes, corrections, or clarifications), Amended Patent (a patent that has been modified after its initial grant, typically due to legal challenges, additional claims, or corrections), Granted Patent (a patent that has successfully passed the examination process and has been officially issued by the patent office, giving the inventor exclusive rights), Limited Patent (A patent with restricted scope, either in terms of geographical coverage, duration, or the specific claims it protects), Search Report (a document issued by a patent office detailing existing technologies or publication relevant to a submitted patent application), Unknown (documents that do not fit into any predefined category or have incomplete classification), Design Right (a legal protection for the visual design of objects, covering aspects like shape, patterns, and overall appearance rather than functional innovations), and Patent Application (a formal request submitted to a patent office to seek legal protection for an invention, undergoing review before a grant is issued).
The primary patent types include granted patents, patent applications, and amended patents, with a notable proportion of search reports and design rights. The decline in 2025 suggests either a lag in reporting or a potential shift in research focus [63].
Using the Dimensions database [64], we were able to visually represent the trend in publications related to colorectal cancer surgery between 2010 and 2024 (shown in Figure 10).
Biomedical and Clinical Sciences led with a substantial 525,125 publications, followed by Biological Sciences (76,410) and Health Sciences (66,504). Chemical Sciences, Engineering, and Information and Computing Sciences contributed significantly but with lower counts. Fields such as Law and Legal Studies, Creative Arts and Writing, and Built Environment and Design had the fewest publications, indicating a lesser focus on colorectal cancer surgery in these disciplines.

5. Prospective Aspects

Technology, personalised treatment, and interdisciplinary care will shape colorectal cancer surgery, especially for IBD. Due to their precision, nerve preservation, and reduced postoperative complications, robotic-assisted surgery is expected to become increasingly popular [59]. Advances in artificial intelligence and machine learning in surgical planning and intraoperative guidance may improve real-time decision making and patient-specific surgery [61]. The integration of molecular profiling and biomarker-driven surgical decision-making will also change treatment. Jin et al. [65], in their latest research, show that better patient stratification using liquid biopsy and genetic screening could identify high-risk patients who would benefit from early preventive or aggressive surgery. Enhancing prehabilitation and post-surgery recovery will certainly improve patient outcomes. These methods improve preoperative conditioning, reduce surgical stress, and speed postoperative recovery, reducing hospital stays and problems [31]. Finally, globally standardising CRC surgical techniques and expanding surgical training programs would ensure equal access to high-quality surgical care, especially in resource-constrained settings.

6. Conclusions

Surgical intervention remains the cornerstone of treatment for CRC, playing a central role in both curative and palliative management. For early stage disease, surgical resection offers the highest chance of cure. Techniques such as open colectomy, laparoscopic surgery, and robotic-assisted procedures provide patients with options tailored to tumour location, disease stage, and patient-specific factors. Minimally invasive approaches, including laparoscopic and robotic surgeries, have revolutionised CRC treatment by improving precision, reducing postoperative pain, and enabling faster recovery while maintaining oncologic safety and efficacy. In rectal cancer, TME has emerged as the gold standard, ensuring precise removal of the tumour, lymphatics, and mesorectal tissue to reduce local recurrence and optimise survival outcomes. Procedures such as LAR allow for sphincter preservation in mid-to-upper rectal cancers, whereas APR remains necessary for lower rectal tumours where sphincter preservation is not feasible. For advanced or metastatic CRC, surgery retains significant value in improving quality of life through palliative interventions. Procedures such as palliative colectomy effectively relieve symptoms caused by obstruction, perforation, or bleeding, while debulking surgery combined with systemic chemotherapy offers survival benefits for select patients with hepatic metastases.
Future efforts should focus on refining surgical precision, expanding access to minimally invasive approaches, and optimising strategies to balance oncologic control with quality of life, ensuring the best possible outcomes for CRC patients.

Author Contributions

Conceptualisation I.E.I., R.P., N.L., D.O.C., A.D.N., A.O.I., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; methodology I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; software I.E.I., R.P., N.L., L.S., D.O.C., A.D.N., A.O.I., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; validation I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; formal analysis I.E.I., R.P., N.L., D.O.C., A.D.N., A.O.I., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; investigation I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; resources I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; data curation I.E.I., R.P., N.L., D.O.C., A.D.N., A.O.I., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; writing—original draft preparation I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; writing—review and editing I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; visualisation I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; supervision I.E.I., R.P., N.L., L.S., D.O.C., A.D.N., A.O.I., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; project administration I.E.I., R.P., N.L., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T.; funding acquisition I.E.I., R.P., N.L., D.O.C., A.D.N., A.O.I., L.S., L.-F.H., L.A., A.P.S., S.D., G.I.B. and A.N.T. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No new data were created or analyzed in this study.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Sato, Y.; Tsujinaka, S.; Miura, T.; Kitamura, Y.; Suzuki, H.; Shibata, C. Inflammatory Bowel Disease and Colorectal Cancer: Epidemiology, Etiology, Surveillance, and Management. Cancers 2023, 15, 4154. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  2. Shah, S.C.; Itzkowitz, S.H. Colorectal Cancer in Inflammatory Bowel Disease: Mechanisms and Management. Gastroenterology 2022, 162, 715–730.e3. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  3. Frigerio, S.; Lartey, D.A.; D’Haens, G.R.; Grootjans, J. The Role of the Immune System in IBD-Associated Colorectal Cancer: From Pro to Anti-Tumorigenic Mechanisms. Int. J. Mol. Sci. 2021, 22, 12739. [Google Scholar] [CrossRef] [PubMed]
  4. Glyn, T.; Williams, S.; Whitehead, M.; Eglinton, T.; West, N.; Purcell, R.V. Digital spatial profiling identifies molecular changes involved in development of colitis-associated colorectal cancer. Front. Oncol. 2024, 14, 1247106. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  5. Sambo, M.; Bailoni, A.; Mariani, F.; Granai, M.; Calomino, N.; Mancini, V.; D’Antiga, A.; Montagnani, F.; Tumbarello, M.; Lazzi, S.; et al. Prevalence, Incidence and Predictors of Anal HPV Infection and HPV-Related Squamous Intraepithelial Lesions in a Cohort of People Living with HIV. Diagnostics 2025, 15, 198. [Google Scholar] [CrossRef] [PubMed]
  6. Lakatos, P.L.; Lakatos, L. Risk for colorectal cancer in ulcerative colitis: Changes, causes and management strategies. World J. Gastroenterol. 2008, 14, 3937–3947. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  7. Shaukat, A.; Levin, T.R. Current and future colorectal cancer screening strategies. Nat. Rev. Gastroenterol. Hepatol. 2022, 19, 521–531. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  8. Zauber, A.G. The impact of screening on colorectal cancer mortality and incidence: Has it really made a difference? Dig. Dis. Sci. 2015, 60, 681–691. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  9. Homepage—IARC. Available online: https://www.iarc.who.int/ (accessed on 11 December 2024).
  10. Marabotto, E.; Kayali, S.; Buccilli, S.; Levo, F.; Bodini, G.; Giannini, E.G.; Savarino, V.; Savarino, E.V. Colorectal Cancer in Inflammatory Bowel Diseases: Epidemiology and Prevention: A Review. Cancers 2022, 14, 4254. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  11. Linet, M.S.; Slovis, T.L.; Miller, D.L.; Kleinerman, R.; Lee, C.; Rajaraman, P.; Berrington de Gonzalez, A. Cancer risks associated with external radiation from diagnostic imaging procedures. CA Cancer J. Clin. 2012, 62, 75–100, Erratum in CA Cancer J. Clin. 2012, 62, 277. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  12. Grivennikov, S.I. Inflammation and colorectal cancer: Colitis-associated neoplasia. Semin. Immunopathol. 2013, 35, 229–244. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  13. Burgos-Molina, A.M.; Téllez Santana, T.; Redondo, M.; Bravo Romero, M.J. The Crucial Role of Inflammation and the Immune System in Colorectal Cancer Carcinogenesis: A Comprehensive Perspective. Int. J. Mol. Sci. 2024, 25, 6188. [Google Scholar] [CrossRef] [PubMed]
  14. Zhou, R.W.; Harpaz, N.; Itzkowitz, S.H.; Parsons, R.E. Molecular mechanisms in colitis-associated colorectal cancer. Oncogenesis 2023, 12, 48. [Google Scholar] [CrossRef] [PubMed]
  15. Mattar, M.C.; Lough, D.; Pishvaian, M.J.; Charabaty, A. Current management of inflammatory bowel disease and colorectal cancer. Gastrointest. Cancer Res. 2011, 4, 53–61. [Google Scholar] [PubMed] [PubMed Central]
  16. Birgisson, H.; Edlund, K.; Wallin, U.; Påhlman, L.; Kultima, H.G.; Mayrhofer, M.; Micke, P.; Isaksson, A.; Botling, J.; Glimelius, B.; et al. Microsatellite instability and mutations in BRAF and KRAS are significant predictors of disseminated disease in colon cancer. BMC Cancer 2015, 15, 125. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  17. Ciepiela, I.; Szczepaniak, M.; Ciepiela, P.; Hińcza-Nowak, K.; Kopczyński, J.; Macek, P.; Kubicka, K.; Chrapek, M.; Tyka, M.; Góźdź, S.; et al. Tumor location matters, next generation sequencing mutation profiling of left-sided, rectal, and right-sided colorectal tumors in 552 patients. Sci. Rep. 2024, 14, 4619. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  18. Tang, Y.; Fan, Y. Combined KRAS and TP53 mutation in patients with colorectal cancer enhance chemoresistance to promote postoperative recurrence and metastasis. BMC Cancer 2024, 24, 1155. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  19. Scientific Image and Illustration Software|BioRender. Available online: https://www.biorender.com/ (accessed on 11 December 2024).
  20. Armaghany, T.; Wilson, J.D.; Chu, Q.; Mills, G. Genetic alterations in colorectal cancer. Gastrointest. Cancer Res. 2012, 5, 19–27. [Google Scholar] [PubMed] [PubMed Central]
  21. Nguyen, L.H.; Goel, A.; Chung, D.C. Pathways of Colorectal Carcinogenesis. Gastroenterology 2020, 158, 291–302. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  22. Baker, K.T.; Salk, J.J.; Brentnall, T.A.; Risques, R.A. Precancer in ulcerative colitis: The role of the field effect and its clinical implications. Carcinogenesis 2018, 39, 11–20. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  23. Du, L.; Kim, J.J.; Shen, J.; Chen, B.; Dai, N. KRAS and TP53 mutations in inflammatory bowel disease-associated colorectal cancer: A meta-analysis. Oncotarget 2017, 8, 22175–22186. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  24. Hsu, C.W.; Sowers, M.L.; Hsu, W.; Eyzaguirre, E.; Qiu, S.; Chao, C.; Mouton, C.P.; Fofanov, Y.; Singh, P.; Sowers, L.C. How does inflammation drive mutagenesis in colorectal cancer? Trends Cancer Res. 2017, 12, 111–132. [Google Scholar] [PubMed] [PubMed Central]
  25. Brusnic, O.; Onisor, D.; Boicean, A.; Hasegan, A.; Ichim, C.; Guzun, A.; Chicea, R.; Todor, S.B.; Vintila, B.I.; Anderco, P.; et al. Fecal Microbiota Transplantation: Insights into Colon Carcinogenesis and Immune Regulation. J. Clin. Med. 2024, 13, 6578. [Google Scholar] [CrossRef] [PubMed]
  26. Clay, S.L.; Fonseca-Pereira, D.; Garrett, W.S. Colorectal cancer: The facts in the case of the microbiota. J. Clin. Investig. 2022, 132, e155101. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  27. Kay, J.; Thadhani, E.; Samson, L.; Engelward, B. Inflammation-induced DNA damage, mutations and cancer. DNA Repair 2019, 83, 102673. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  28. Choi, W.T. Non-conventional dysplastic subtypes in inflammatory bowel disease: A review of their diagnostic characteristics and potential clinical implications. J. Pathol. Transl. Med. 2021, 55, 83–93. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  29. Parian, A.M.; Lazarev, M.G. Serrated Colorectal Lesions in Patients with Inflammatory Bowel Disease. Gastroenterol. Hepatol. 2018, 14, 19–25. [Google Scholar] [PubMed] [PubMed Central]
  30. Cairns, S.R.; Scholefield, J.H.; Steele, R.J.; Dunlop, M.G.; Thomas, H.J.; Evans, G.D.; Eaden, J.A.; Rutter, M.D.; Atkin, W.P.; Saunders, B.P.; et al. Guidelines for colorectal cancer screening and surveillance in moderate and high risk groups (update from 2002). Gut 2010, 59, 666–689. [Google Scholar] [CrossRef] [PubMed]
  31. Fanizza, J.; Bencardino, S.; Allocca, M.; Furfaro, F.; Zilli, A.; Parigi, T.L.; Fiorino, G.; Peyrin-Biroulet, L.; Danese, S.; D’Amico, F. Inflammatory Bowel Disease and Colorectal Cancer. Cancers 2024, 16, 2943. [Google Scholar] [CrossRef]
  32. White, A.; Ironmonger, L.; Steele, R.J.C.; Ormiston-Smith, N.; Crawford, C.; Seims, A. A review of sex-related differences in colorectal cancer incidence, screening uptake, routes to diagnosis, cancer stage and survival in the UK. BMC Cancer 2018, 18, 906. [Google Scholar] [CrossRef]
  33. Abu-Freha, N.; Cohen, B.; Gordon, M.; Weissmann, S.; Kestenbaum, E.H.; Vosko, S.; Abu-Tailakh, M.; Ben-Shoshan, L.; Cohen, D.L.; Shirin, H. Colorectal cancer among inflammatory bowel disease patients: Risk factors and prevalence compared to the general population. Front. Med. 2023, 10, 1225616. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  34. Fung, B.M.; Lindor, K.D.; Tabibian, J.H. Cancer risk in primary sclerosing cholangitis: Epidemiology, prevention, and surveillance strategies. World J. Gastroenterol. 2019, 25, 659–671. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  35. Zhang, R.; Rabinovitch, P.S.; Mattis, A.N.; Lauwers, G.Y.; Choi, W.T. DNA content abnormality frequently develops in the right/proximal colon in patients with primary sclerosing cholangitis and inflammatory bowel disease and is highly predictive of subsequent detection of dysplasia. Histopathology 2023, 83, 116–125. [Google Scholar] [CrossRef] [PubMed]
  36. Henn, A.J.; Song, K.Y.; Gravely, A.A.; Mesa, H.; Sultan, S.; Shaheen, N.J.; Shaukat, A.; Hanson, B.J. Persistent indefinite for dysplasia in Barrett’s esophagus is a risk factor for dysplastic progression to low-grade dysplasia. Dis. Esophagus 2020, 33, doaa015. [Google Scholar] [CrossRef] [PubMed]
  37. Mahmoud, R.; Shah, S.C.; Torres, J.; Castaneda, D.; Glass, J.; Elman, J.; Kumar, A.; Axelrad, J.; Harpaz, N.; Ullman, T.; et al. Association Between Indefinite Dysplasia and Advanced Neoplasia in Patients with Inflammatory Bowel Diseases Undergoing Surveillance. Clin. Gastroenterol. Hepatol. 2020, 18, 1518–1527.e3. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  38. Clarke, W.T.; Feuerstein, J.D. Colorectal cancer surveillance in inflammatory bowel disease: Practice guidelines and recent developments. World J. Gastroenterol. 2019, 25, 4148–4157. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  39. Wijnands, A.M.; Mahmoud, R.; Lutgens, M.W.M.D.; Oldenburg, B. Surveillance and management of colorectal dysplasia and cancer in inflammatory bowel disease: Current practice and future perspectives. Eur. J. Intern. Med. 2021, 93, 35–41. [Google Scholar] [CrossRef] [PubMed]
  40. Buchner, A.M. The Role of Chromoendoscopy in Evaluating Colorectal Dysplasia. Gastroenterol. Hepatol. 2017, 13, 336–347. [Google Scholar] [PubMed] [PubMed Central]
  41. Shukla, R.; Salem, M.; Hou, J.K. Use and barriers to chromoendoscopy for dysplasia surveillance in inflammatory bowel disease. World J. Gastrointest. Endosc. 2017, 9, 359–367. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  42. Pal, P.; Singh, A.P.; Kanuri, N.D.; Banerjee, R. Electronic chromo-endoscopy: Technical details and a clinical perspective. Transl. Gastroenterol. Hepatol. 2022, 7, 6. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  43. Yilmaz, S.; Gorgun, E. Endoscopic Mucosal Resection and Endoscopic Submucosal Dissection. Clin. Colon. Rectal Surg. 2023, 37, 277–288. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  44. Reznicek, E.; Arfeen, M.; Shen, B.; Ghouri, Y.A. Colorectal Dysplasia and Cancer Surveillance in Ulcerative Colitis. Diseases 2021, 9, 86. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  45. Reddy, K.; Gharde, P.; Tayade, H.; Patil, M.; Reddy, L.S.; Surya, D. Advancements in Robotic Surgery: A Comprehensive Overview of Current Utilizations and Upcoming Frontiers. Cureus 2023, 15, e50415. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  46. Ford, A.C.; Achkar, J.P.; Khan, K.J.; Kane, S.V.; Talley, N.J.; Marshall, J.K.; Moayyedi, P. Efficacy of 5-aminosalicylates in ulcerative colitis: Systematic review and meta-analysis. Am. J. Gastroenterol. 2011, 106, 601–616. [Google Scholar] [CrossRef] [PubMed]
  47. Singh, A.; Mahajan, R.; Kedia, S.; Dutta, A.K.; Anand, A.; Bernstein, C.N.; Desai, D.; Pai, C.G.; Makharia, G.; Tevethia, H.V.; et al. Use of thiopurines in inflammatory bowel disease: An update. Intest Res. 2022, 20, 11–30. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  48. Velikova, T.; Sekulovski, M.; Peshevska-Sekulovska, M. Immunogenicity and Loss of Effectiveness of Biologic Therapy for Inflammatory Bowel Disease Patients Due to Anti-Drug Antibody Development. Antibodies 2024, 13, 16. [Google Scholar] [CrossRef]
  49. Lee, B.; Han, H.S. Tackling Surgical Morbidity and Mortality through Modifiable Risk Factors in Cancer Patients. Nutrients 2022, 14, 3107. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  50. Marano, L.; Verre, L.; Carbone, L.; Poto, G.E.; Fusario, D.; Venezia, D.F.; Calomino, N.; Kaźmierczak-Siedlecka, K.; Polom, K.; Marrelli, D.; et al. Current Trends in Volume and Surgical Outcomes in Gastric Cancer. J. Clin. Med. 2023, 12, 2708. [Google Scholar] [CrossRef]
  51. Fadlallah, H.; El Masri, J.; Fakhereddine, H.; Youssef, J.; Chemaly, C.; Doughan, S.; Abou-Kheir, W. Colorectal cancer: Recent advances in management and treatment. World J. Clin. Oncol. 2024, 15, 1136–1156. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  52. Colon Cancer Laparoscopic or Open Resection Study Group. Laparoscopic surgery versus open surgery for colon cancer: Short-term outcomes of a randomised trial. Lancet Oncol. 2005, 6, 477–484. [Google Scholar] [CrossRef]
  53. Ahmad, G.; Baker, J.; Finnerty, J.; Phillips, K.; Watson, A. Laparoscopic entry techniques. Cochrane Database Syst. Rev. 2019, 1, CD006583. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  54. van Weteringen, W.; Sterke, F.; Vlot, J.; Wijnen, R.M.H.; Dankelman, J. Automated control for investigation of the insufflation-ventilation interaction in experimental laparoscopy. PLoS ONE 2023, 18, e0285108. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  55. Yamanashi, T.; Miura, H.; Tanaka, T.; Watanabe, A.; Goto, T.; Yokoi, K.; Kojo, K.; Niihara, M.; Hosoda, K.; Kaizu, T.; et al. Comparison of short-term outcomes of robotic-assisted and conventional laparoscopic surgery for rectal cancer: A propensity score-matched analysis. Asian J. Endosc. Surg. 2022, 15, 753–764. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  56. Keller, D.S. Right tool for the right job in the right way: Robotic, transanal, or laparoscopic approach for rectal cancer. BJS Open 2024, 8, zrae069. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  57. Probst, P. A Review of the Role of Robotics in Surgery: To DaVinci and Beyond! Mo. Med. 2023, 120, 389–396. [Google Scholar] [PubMed] [PubMed Central]
  58. Seow, W.; Dudi-Venkata, N.N.; Bedrikovetski, S.; Kroon, H.M.; Sammour, T. Outcomes of open vs laparoscopic vs robotic vs transanal total mesorectal excision (TME) for rectal cancer: A network meta-analysis. Tech. Coloproctol. 2023, 27, 345–360. [Google Scholar] [CrossRef]
  59. Zhou, M.W.; Huang, X.Y.; Chen, Z.Y.; Li, Z.Y.; Zhou, Y.M.; Yang, Y.; Wang, Z.H.; Xiang, J.B.; Gu, X.D. Intraoperative monitoring of pelvic autonomic nerves during laparoscopic low anterior resection of rectal cancer. Cancer Manag. Res. 2018, 11, 411–417. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  60. Bordeianou, L.; Maguire, L.H.; Alavi, K.; Sudan, R.; Wise, P.E.; Kaiser, A.M. Sphincter-sparing surgery in patients with low-lying rectal cancer: Techniques, oncologic outcomes, and functional results. J. Gastrointest. Surg. 2014, 18, 1358–1372. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  61. Maurer, C.A.; Renzulli, P.; Kull, C.; Käser, S.A.; Mazzucchelli, L.; Ulrich, A.; Büchler, M.W. The impact of the introduction of total mesorectal excision on local recurrence rate and survival in rectal cancer: Long-term results. Ann. Surg. Oncol. 2011, 18, 1899–1906. [Google Scholar] [CrossRef] [PubMed]
  62. Geitenbeek, R.T.J.; Burghgraef, T.A.; Moes, C.A.; Hompes, R.; Ranchor, A.V.; Consten, E.C.J. Functional outcomes and quality of life following open versus laparoscopic versus robot-assisted versus transanal total mesorectal excision in rectal cancer patients: A systematic review and meta-analysis. Surg. Endosc. 2024, 38, 4431–4444. [Google Scholar] [CrossRef]
  63. Lens. Available online: https://www.lens.org/lens/labs (accessed on 12 January 2025).
  64. Support. Dimensions. Available online: https://dimensions.freshdesk.com/support/home (accessed on 11 December 2024).
  65. Jin, D.; Khan, N.U.; Gu, W.; Lei, H.; Goel, A.; Chen, T. Informatics strategies for early detection and risk mitigation in pancreatic cancer patients. Neoplasia 2025, 60, 101129. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
Figure 1. Cancer site ranking—incidence and mortality. Retrieved with the permission of International Agency for Research on Cancer [9].
Figure 1. Cancer site ranking—incidence and mortality. Retrieved with the permission of International Agency for Research on Cancer [9].
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Figure 2. Global map of the most common cancer sites by country, 2022 (excluding non-melanoma skin cancer). Retrieved with the permission of International Agency for Research on Cancer [9].
Figure 2. Global map of the most common cancer sites by country, 2022 (excluding non-melanoma skin cancer). Retrieved with the permission of International Agency for Research on Cancer [9].
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Figure 3. Global colorectal cancer incidence by continent in 2022. Retrieved with the permission of International Agency for Research on Cancer [9].
Figure 3. Global colorectal cancer incidence by continent in 2022. Retrieved with the permission of International Agency for Research on Cancer [9].
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Figure 4. Molecular differences in right-sided, left-sided, and rectal cancer. Created with Biorender [19].
Figure 4. Molecular differences in right-sided, left-sided, and rectal cancer. Created with Biorender [19].
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Figure 5. Molecular pathways to colorectal cancer: sporadic vs. IBD-associated progression. Created with Biorender [19].
Figure 5. Molecular pathways to colorectal cancer: sporadic vs. IBD-associated progression. Created with Biorender [19].
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Figure 6. Surgical resection of the colon with bowel reattachment in CRC.
Figure 6. Surgical resection of the colon with bowel reattachment in CRC.
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Figure 7. Laparoscopic surgery for CRC. Created with Biorender [19].
Figure 7. Laparoscopic surgery for CRC. Created with Biorender [19].
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Figure 8. Surgical resection of the affected rectal segment. Created with Biorender [19].
Figure 8. Surgical resection of the affected rectal segment. Created with Biorender [19].
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Figure 9. Patent publications related to colorectal cancer surgery from 2010 to 2025.
Figure 9. Patent publications related to colorectal cancer surgery from 2010 to 2025.
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Figure 10. Number of publications in various research categories related to colorectal cancer surgery.
Figure 10. Number of publications in various research categories related to colorectal cancer surgery.
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Table 1. Adaptation of Paris Classification. Source: SCENIC consensus statement—International guidelines for surveillance of colorectal endoscopic neoplasia in inflammatory bowel disease patients [30].
Table 1. Adaptation of Paris Classification. Source: SCENIC consensus statement—International guidelines for surveillance of colorectal endoscopic neoplasia in inflammatory bowel disease patients [30].
CategoryDescription
Polypoid (0-I)Lesion protruding from the mucosa into the lumen ≥ 2.5 mm
Pedunculated (0-Ip)Lesion attached to the mucosa by a stalk
Sessile (0-Is)Lesion without a stalk; the entire base is contiguous with the mucosa
Non-polypoid (0-II)Lesion with little (<2.5 mm) or no protrusion above the mucosa
Superficial elevated (0-IIa)Lesion with protrusion < 2.5 mm above the lumen (or less than the height of a closed biopsy forceps cup)
Flat (0-IIb)Lesion without protrusion above the mucosa
Depressed (0-IIc)Lesion with at least a portion depressed below the mucosal surface
Table 2. CRC surveillance risk stratification flowchart.
Table 2. CRC surveillance risk stratification flowchart.
Risk CategoryCriteriaFollow-Up IntervalFindings at Follow-Up
Low Risk (A)1–2 adenomas, both < 1 cmNo surveillance or 5 years
-
No adenomas → Cease follow-up
-
Low-risk adenomas → A *
-
Intermediate-risk adenomas → B *
-
High-risk adenomas → C *
Intermediate Risk (B)3–4 small adenomas OR at least one ≥1 cm3 years
-
1 negative exam → B
-
2 consecutive negative exams → Cease follow-up
-
Low or intermediate-risk adenomas → B
-
High-risk adenomas → C
High Risk (C)≥5 small adenomas OR ≥3 with at least one ≥ 1 cm1 year
-
Negative, low, or intermediate-risk adenomas → B
-
High-risk adenomas → C
* A = no surveillance or 5 years; B = 3 years; C = 1 year.
Table 3. Biologic therapies in IBD.
Table 3. Biologic therapies in IBD.
Drug ClassDrugEffectivenessCombination Therapy Availability
Anti-TNF AlphaInfliximabInduction (+), Maintenance (+), Mucosal Healing (+)Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
AdalimumabInduction (+), Maintenance (+), Mucosal Healing (+)Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
CertolizumabInduction (+), Maintenance (+)Mucosal Healing (NA), Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
GolimumabInduction (+), Maintenance (+)Mucosal Healing (NA), Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
Anti-IntegrinNatalizumabNo available studies (NA)NA for all categories
VedolizumabInduction (+), Maintenance (+)Mucosal Healing (NA), Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
Other BiologicUstekinumabInduction (+)Maintenance (NA), Mucosal Healing (NA), Thiopurine (NA), Methotrexate (NA), Acute Severe Colitis (NA)
(+)—Positive study outcome.
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Iordache, I.E.; Herlo, L.-F.; Popescu, R.; Costea, D.O.; Alexandrescu, L.; Suceveanu, A.P.; Deacu, S.; Baltatescu, G.I.; Nicoara, A.D.; Leopa, N.; et al. Cutting Edge: A Comprehensive Guide to Colorectal Cancer Surgery in Inflammatory Bowel Diseases. J. Mind Med. Sci. 2025, 12, 6. https://doi.org/10.3390/jmms12010006

AMA Style

Iordache IE, Herlo L-F, Popescu R, Costea DO, Alexandrescu L, Suceveanu AP, Deacu S, Baltatescu GI, Nicoara AD, Leopa N, et al. Cutting Edge: A Comprehensive Guide to Colorectal Cancer Surgery in Inflammatory Bowel Diseases. Journal of Mind and Medical Sciences. 2025; 12(1):6. https://doi.org/10.3390/jmms12010006

Chicago/Turabian Style

Iordache, Ionut Eduard, Lucian-Flavius Herlo, Razvan Popescu, Daniel Ovidiu Costea, Luana Alexandrescu, Adrian Paul Suceveanu, Sorin Deacu, Gabriela Isabela Baltatescu, Alina Doina Nicoara, Nicoleta Leopa, and et al. 2025. "Cutting Edge: A Comprehensive Guide to Colorectal Cancer Surgery in Inflammatory Bowel Diseases" Journal of Mind and Medical Sciences 12, no. 1: 6. https://doi.org/10.3390/jmms12010006

APA Style

Iordache, I. E., Herlo, L.-F., Popescu, R., Costea, D. O., Alexandrescu, L., Suceveanu, A. P., Deacu, S., Baltatescu, G. I., Nicoara, A. D., Leopa, N., Nelson Twakor, A., Iordache, A. O., & Steriu, L. (2025). Cutting Edge: A Comprehensive Guide to Colorectal Cancer Surgery in Inflammatory Bowel Diseases. Journal of Mind and Medical Sciences, 12(1), 6. https://doi.org/10.3390/jmms12010006

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