Revised: March 21, 2026
Accepted: May 22, 2026
Published online: July 28, 2026
Processing time: 144 Days and 23.7 Hours
Pancreatic cystic neoplasms are being identified with increasing frequency, largely because high-resolution cross-sectional imaging is now routinely per
Core Tip: Magnetic resonance imaging combined with magnetic resonance cholangiopancreatography plays a pivotal role in the evaluation of cystic pancreatic neoplasms. Familiarity with both typical and atypical imaging features of intraductal papillary mucinous neoplasms, serous cystic neoplasms, mucinous cystic neoplasms, and solid pseudopapillary tumors improves lesion characterization, supports accurate differential diagnosis, and guides appropriate risk stratification and clinical management, particularly in incidentally detected lesions.
- Citation: Boraschi P, Cervelli R, Donati F. Common cystic pancreatic neoplasms: A comprehensive magnetic resonance imaging-based review of typical and atypical imaging features. World J Radiol 2026; 18(7): 120526
- URL: https://www.wjgnet.com/1949-8470/full/v18/i7/120526.htm
- DOI: https://dx.doi.org/10.4329/wjr.120526
Incidental detection of pancreatic cystic lesions has become increasingly common over the last two decades. The widespread use of high-resolution cross-sectional imaging, particularly computed tomography (CT) and magnetic resonance imaging (MRI), together with continuous technical improvements in multiparametric imaging, has substantially increased the number of pancreatic cysts identified in asymptomatic patients.
This phenomenon is especially evident in the elderly population. Several MRI-based studies have reported a re
From a clinical perspective, the main challenge is no longer simply detecting these lesions, but accurately characterizing them and stratifying their malignant potential. Correct classification is essential because management strategies differ substantially among the various cystic entities. Non-mucinous lesions such as serous cystic neoplasms (SCNs) are generally benign and usually do not require surgical treatment in asymptomatic patients. By contrast, mucin-producing neoplasms, including intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs), carry a variable risk of malignant transformation and may require closer surveillance or surgical resection.
MRI has progressively become the imaging modality of choice for the evaluation of pancreatic cystic neoplasms because of its excellent soft-tissue contrast, multiplanar capability, and detailed assessment of the pancreatic ductal system[3]. In particular, MRCP allows non-invasive evaluation of ductal anatomy and facilitates the identification of communication between cystic lesions and the pancreatic ducts, a finding that is crucial for differential diagnosis. Recognition of ductal communication is clinically relevant because it strongly supports the diagnosis of branch-duct (BD) IPMN and directly influences patient management.
This review summarizes the main MRI findings of the most common cystic pancreatic neoplasms, including SCNs, MCNs, IPMNs, and solid pseudopapillary neoplasms (SPNs). Both typical and atypical imaging appearances are discussed, with particular attention to imaging findings that may complicate differential diagnosis and influence clinical management.
A dedicated pancreatic MRI protocol is essential for accurate lesion detection and characterization. A comprehensive examination should combine high-resolution morphological sequences with functional imaging techniques in order to obtain both anatomical and biological information.
The protocol generally includes T1-weighted three dimensional sequences, axial and coronal T2-weighted images, diffusion-weighted imaging with multiple b values, thin-slab and thick-slab MRCP sequences, three dimensional MRCP reconstructions, and dynamic contrast-enhanced T1-weighted imaging.
T2-weighted and MRCP sequences are particularly valuable for evaluating cyst morphology, internal septations, wall thickness, and communication with the pancreatic ductal system. In particular, heavily T2-weighted MRCP images provide non-invasive visualization of pancreatic ducts and allow accurate assessment of main pancreatic duct dilatation, side-branch ectasia, and duct–cyst communication, findings that are essential for differential diagnosis among pancreatic cystic lesions.
Recognition of ductal communication is clinically relevant because it strongly favors the diagnosis of BD-IPMN, whereas absence of communication supports alternative diagnoses such as serous or MCNs.
Diffusion-weighted imaging also plays an increasingly important role in pancreatic MRI. The use of multiple b values improves lesion conspicuity and allows calculation of apparent diffusion coefficient (ADC) maps[4]. Restricted diffusion, appearing as high signal intensity on high b value images associated with low ADC values, may reflect increased cellu
In cystic lesions, diffusion weighted imaging (DWI) may additionally help distinguish simple fluid-containing cysts from lesions containing proteinaceous material, hemorrhage, or solid internal components. Although several studies have proposed ADC ranges to differentiate mucinous from serous lesions or benign from malignant IPMNs, no universally accepted cutoff value has yet been established because of substantial overlap among reported measurements[4].
Furthermore, DWI is especially useful in patients who cannot receive intravenous contrast agents, providing additional lesion characterization without gadolinium administration.
Dynamic contrast-enhanced imaging remains fundamental for evaluating vascularity and enhancement patterns. These sequences are particularly important for detecting mural nodules, enhancing septa, and solid components, all of which represent imaging features associated with increased malignant potential. Multiphasic acquisitions improve visualization of subtle enhancing components and allow better delineation of lesion margins and vascular relationships.
Overall, integration of high-resolution morphological imaging with functional techniques such as DWI significantly improves diagnostic confidence and contributes to more accurate lesion characterization and risk stratification.
IPMNs are mucin-producing epithelial tumors arising from the main pancreatic duct or its side branches. Histologically, they differ from MCNs because they lack ovarian-type stroma, while they are distinguished from pancreatic intraepithelial neoplasia by their macroscopic visibility, usually measuring at least 0.5-1 cm[5,6].
IPMNs include a broad spectrum of cytoarchitectural and immunophenotypic subtypes associated with different biological behavior and malignant potential. Gastric-type IPMNs more commonly involve the branch ducts and are generally associated with a lower risk of malignancy, whereas intestinal, pancreatobiliary, and oncocytic subtypes more frequently demonstrate high-grade dysplasia or invasive carcinoma.
The clinical significance of these lesions largely depends on the degree of dysplasia. Low-grade lesions usually show a more indolent biological behavior, whereas high-grade dysplasia, corresponding to carcinoma in situ, is associated with a substantially increased risk of invasive malignancy.
Another important aspect in IPMN management is the possibility of concomitant invasive mucinous adenocarcinoma. Approximately 4.1% of patients may develop synchronous or metachronous invasive carcinoma arising in a different pancreatic location independently from the primary IPMN[7,8]. This finding highlights the concept of a “field defect” involving the pancreatic ductal epithelium and explains why long-term surveillance remains clinically relevant even in apparently stable lesions.
Although the imaging findings associated with malignant transformation and the currently available surveillance strategies have been extensively investigated[9,10], several practical aspects of imaging interpretation and patient management remain incompletely standardized. Moreover, the lack of universally accepted imaging criteria still limits the development of fully standardized clinical pathways and may reduce reproducibility across large multicenter studies.
IPMNs are more frequently located in the pancreatic head and uncinate process, although any segment of the gland may be involved. On MRI, these lesions are characterized by their cystic nature and by their close relationship with the pancreatic ductal system.
The anatomic distribution on MRI/MRCP defines the clinical subtype as: (1) BD-IPMN; (2) Main-duct (MD) IPMN; and (3) Mixed-type IPMN.
BD-IPMNs typically appear as multilocular pleomorphic cystic lesions with the classic “cluster of grapes” morphology. Demonstration of communication between the cystic lesion and the main pancreatic duct on MRCP strongly supports the diagnosis (Figure 1)[10,11].
MD-IPMNs are characterized by dilatation of the main pancreatic duct greater than 5 mm in the absence of alternative obstructive causes such as stones or strictures. A main pancreatic duct diameter ≥ 10 mm is considered a highly specific high-risk feature associated with increased malignant potential[10-13].
Mixed-type IPMNs demonstrate findings of both main duct involvement and BD cystic lesions.
Beyond simple morphological evaluation, MRI provides important information regarding malignant risk. In particular, enhancing mural nodules represent one of the strongest imaging predictors of malignancy. Nodules measuring ≥ 5 mm are considered high-risk stigmata, whereas smaller nodules or non-enhancing mucin plugs are classified as worrisome features[10,14].
Moreover, lesion diameter ≥ 30 mm is also considered a worrisome feature and may justify closer surveillance or endoscopic ultrasound (EUS) evaluation[10]. Several recent studies have also explored MRI predictors of malignancy and differences among currently available guideline systems[14-16].
Diffusion-weighted imaging may further improve risk stratification. High signal intensity on high b value images associated with low ADC values within mural nodules or thickened cyst walls may suggest high-grade dysplasia or invasive carcinoma rather than low-grade disease[4,11,15].
Finally, abrupt caliber changes of the main pancreatic duct associated with distal pancreatic atrophy should always raise suspicion for an occult invasive component[14].
The imaging evaluation of IPMNs may become considerably more challenging in the presence of atypical morphology, unusual localization, congenital ductal variants, or associated inflammatory diseases that alter the classic imaging appearance[17,18].
MD-IPMNs may demonstrate either diffuse or segmental involvement of the pancreatic ductal system[18]. Although both the International Association of Pancreatology and the European Study Group recognize these patterns, a uni
Diffuse MD-IPMN is characterized by continuous moderate or marked dilatation of the entire main pancreatic duct and may closely resemble chronic pancreatitis because of associated parenchymal atrophy and ductal irregularity. By contrast, segmental MD-IPMN demonstrates focal ductal dilatation involving only a limited portion of the ductal system. In these cases, the lesion may mimic focal ductal strictures or other cystic neoplasms, particularly when associated with side-branch ectasia (Figures 2 and 3).
BD-IPMNs represent the most frequently encountered subtype, but atypical presentations may create important differential diagnostic challenges with other mucinous cystic lesions[20]. In young women, for example, a solitary unilocular cystic lesion with smooth margins may be difficult to distinguish from a mucinous cystic neoplasm. In these situations, demonstration of ductal communication on MRI/MRCP or endoscopic evaluation becomes the key diagnostic feature favoring BD-IPMN, since MCNs do not communicate with the pancreatic ductal system (Figure 4)[18,20,21].
The anatomical presentation of IPMN may also be influenced by congenital ductal anomalies or ectopic pancreatic tissue. Congenital variants such as pancreas divisum or annular pancreas alter the normal ductal anatomy and may lead to selective involvement of accessory ducts, including Santorini’s duct. When imaging findings strongly suggest a main duct origin, these lesions should generally be managed similarly to MD-IPMNs because of the associated malignant risk[22].
Rarely, IPMNs may also arise within ectopic pancreatic tissue located in the gastrointestinal tract, particularly in the stomach or duodenum. In these cases, the lesions may mimic duplication cysts or mesenchymal tumors. Although large series are lacking, several case reports support the occurrence of IPMNs within gastrointestinal heterotopia[22].
Associated pancreatic or extra-pancreatic diseases may further complicate image interpretation by distorting the ductal anatomy. Mechanical compression from adjacent masses may occasionally deform a BD-IPMN, producing a pseudo-microcystic appearance that mimics a Serous cystic neoplasm and complicates preoperative characterization (Figure 5). In these situations, careful evaluation of ductal communication, mural nodules, and ductal morphology remains essential for differential diagnosis[23].
Inflammatory diseases may create an even more challenging scenario. Several studies have described an association between IPMN and immunoglobulin G 4 (IgG4)-related autoimmune pancreatitis type 1, highlighting the complex relationship between epithelial neoplasia and IgG4-mediated fibroinflammatory disease[24-27].
From an imaging perspective, autoimmune pancreatitis may produce diffuse or segmental pancreatic enlargement, delayed enhancement, and long-segment strictures of the main pancreatic duct, findings that may obscure or mimic abnormalities related to MD-IPMN[26]. Moreover, inflammatory ductal narrowing caused by autoimmune pancreatitis type 1 may coexist with upstream ductal dilatation secondary to IPMN, creating an appearance that may resemble diffuse MD-IPMN or even invasive carcinoma[26,27].
In addition, lymphoplasmacytic infiltration and periductal fibrosis associated with IgG4-related disease may alter the morphology of BD-IPMNs, occasionally producing irregular cyst walls or pseudo-nodular components that may be misinterpreted as worrisome or high-risk features[27].
Because of these overlapping findings, differentiation between inflammatory ductal abnormalities and true neoplastic progression may be difficult. Elevated serum IgG4 levels, extrapancreatic manifestations of IgG4-related disease, and response to steroid therapy may help support the diagnosis of autoimmune pancreatitis-related changes, although these findings should not exclude appropriate oncologic surveillance in patients with concomitant IPMN[27].
SCNs are benign epithelial pancreatic tumors with extremely low malignant potential and account for approximately 20%-30% of pancreatic cystic neoplasms. They are most commonly detected incidentally and predominantly affect older women. Histologically, SCNs arise from glycogen-rich cuboidal epithelial cells and are composed of multiple cystic spaces filled with serous fluid. One of the most important diagnostic features is the absence of communication with the pancreatic ductal system, which represents a key element in the differential diagnosis of pancreatic cystic lesions[28-30].
The classic imaging appearance of SCNs is a microcystic lesion composed of numerous small cysts, typically measuring less than 2 cm and separated by thin fibrous septa; when these fall below the spatial resolution of MRI, the lesion may appear compact, producing a characteristic “honeycomb” pattern[28,29]. On MRI, SCNs are markedly hyperintense on T2-weighted images and hypointense on T1-weighted images due to their serous fluid content, often with thin septa that may converge toward a central fibrous scar showing delayed post-contrast enhancement.
Although calcifications within the central scar are better detected on CT, delayed post-contrast MRI sequences may assist in its depiction[28,30].
On diffusion-weighted imaging, SCNs generally do not demonstrate true diffusion restriction. Mild hyperintensity on high b value images is usually attributable to T2 shine-through, with preserved or elevated ADC values, consistent with their benign cystic nature (Figure 6)[31].
MRCP reliably demonstrates absence of communication with the pancreatic ductal system, while contrast-enhanced sequences typically show septal enhancement without true enhancing mural nodules, a feature that helps distinguish SCNs from MCNs[29,30].
SCNs may present with a wide spectrum of atypical imaging appearances, which represent a frequent source of di
The oligocystic, or macrocystic, variant – described in a minority of cases – is characterized by a limited number of larger cysts exceeding 2 cm in diameter. This pattern may closely mimic MCNs or BD-IPMNs, particularly when internal septations are present. Helpful differentiating features include a lobulated contour, frequent location in the pancreatic head, thin non-enhancing walls, and persistent absence of ductal communication on MRCP[29].
One of the most challenging variants is the unilocular SCN, which may be indistinguishable from MCNs on imaging alone, particularly when located in the pancreatic tail (Figure 7)[31,32]. When cross-sectional imaging does not allow a confident diagnosis, symptomatic patients may undergo further evaluation with EUS-guided cyst fluid sampling or be considered for surgical management[32,33].
Additional atypical forms include giant SCNs, usually larger than 10 cm (Figure 8), which may cause ductal com
Furthermore, a solid or pseudo-solid variant of SCN has been described, in which extremely small cysts and dense fibrous stroma produce a predominantly solid appearance with early and homogeneous enhancement related to rich capillary vascularisation (Figure 9). This variant may closely mimic pancreatic neuroendocrine tumors or hypervascular metastases and represents one of the most important diagnostic pitfalls[34].
Rare but clinically relevant atypical manifestations include intra-tumoral haemorrhage (Figure 10), which may result in intrinsic T1 hyperintensity, T2 signal heterogeneity, and partial obscuration of the microcystic architecture. This feature appears to be reported more frequently in SCNs than in MCNs and may mimic solid pancreatic tumors or hemorrhagic cystic lesions. In these settings, MRI, particularly heavily T2-weighted sequences, remains crucial to disclose the underlying cystic nature of the lesion, even when CT suggests a solid mass[28,30,31]. Finally, others less common but clinically relevant variants include disseminated and multifocal forms of serous cystic neoplasm.
The disseminated variant (Figure 11) is characterized by extensive replacement of the pancreatic parenchyma by innumerable microcysts, resulting in marked enlargement of the gland while generally preserving the caliber of the main pancreatic duct[35]. Despite the diffuse pancreatic involvement, the imaging appearance usually maintains the typical benign microcystic pattern, including very high T2 signal intensity, thin enhancing septa, absence of mural nodules, and lack of ductal communication on MRCP[35].
Another atypical presentation is the multifocal form, in which multiple discrete serous cystic lesions are distributed throughout the pancreas. In this setting, the possibility of an underlying hereditary syndrome, particularly von Hippel-Lindau (VHL) disease, should always be considered[36,37]. Patients with VHL frequently present with multiple simple pancreatic cysts and serous cystadenomas (Figure 12), and these lesions may coexist with pancreatic neuroendocrine tumors. Careful evaluation of enhancement characteristics therefore becomes essential in order to avoid misclassification[36,37].
Recognition of this association is clinically important because pancreatic lesions may represent one of the earliest manifestations of the syndrome and may occasionally lead to the initial diagnosis of VHL disease.
MCNs are mucin-producing epithelial pancreatic tumors that predominantly affect middle-aged women[38]. Although many of these lesions show relatively indolent behavior, malignant transformation has been reported in approximately 6%-27% of cases[39,40]. Because of this intrinsic malignant potential, surgical resection is generally recommended whenever clinically appropriate.
The characteristic histopathological feature of MCNs is the presence of mucin-secreting epithelium supported by ovarian-type stroma, a finding considered virtually pathognomonic and not observed in other pancreatic cystic neoplasms[41].
MCNs occur most commonly in the pancreatic tail and only rarely involve the pancreatic head[42]. Morphologically, they typically present as large (> 2 cm), well-circumscribed, unilocular macrocystic lesions that lack communication with the pancreatic ductal system and are surrounded by a well-defined fibrous capsule. On contrast-enhanced CT and MRI, the cyst wall is characteristically thickened and demonstrates homogeneous enhancement on delayed-phase multiphasic imaging (Figure 13)[41].
On MRI, MCNs usually show homogeneous high signal intensity on T2-weighted images and variable signal intensity on T1-weighted images depending on mucin concentration or hemorrhagic content, features that may aid in lesion characterization.
The presence of mural nodules or solid enhancing components warrants careful evaluation because of their association with an increased risk of malignant progression.
In some cases, differentiation between true mural nodules and mucin plugs may be challenging, as mucin plugs appear as relatively small intraluminal nodular lesions that do not enhance yet may closely mimic mural nodules on cross-sectional imaging[30,39,42]. Owing to its superior spatial resolution, EUS enables reliable discrimination between mucin plugs and true mural nodules, with reported sensitivity and specificity ranging from 89%-96% and 64%-88%, respectively[38,39,41,42].
Finally, although peripheral “eggshell” calcification is an infrequent finding, occurring in approximately 15% of cases, it is considered highly specific for MCN and strongly predictive of malignant transformation[38,39,41].
Although MCNs classically appear as unilocular macrocystic lesions with smooth margins and a thick enhancing wall, atypical imaging appearances are not uncommon and may significantly complicate differential diagnosis.
Some MCNs may demonstrate internal septations or a more complex “cyst-within-cyst” architecture, partially losing the typical unilocular appearance. In addition, peripheral eggshell-like calcifications surrounding the internal cystic compartments may further complicate image interpretation[43,44].
Lesion size may also vary considerably from the classic description. While MCNs are traditionally described as medium-sized or large-sized lesions, often exceeding 5 cm, increasingly widespread use of high-resolution imaging has led to more frequent incidental detection of small MCNs measuring less than 3 cm (Figure 14). These smaller lesions are usually asymptomatic and, according to currently available series, are more frequently associated with low-grade dysplasia and lower malignant potential compared with larger tumors[43].
Some atypical MCNs may overlap with the imaging appearance of cystic parasitic lesions, particularly pancreatic hydatid cysts. Hydatid disease may present with daughter cysts or multiloculated morphology (Figure 15), closely resembling MCNs. This differential diagnosis is especially relevant in patients from endemic regions and highlights the importance of integrating epidemiological information and systemic findings into radiological interpretation[44].
Another less common but clinically important presentation is the association between MCNs and episodes of acute pancreatitis. Although MCNs are often asymptomatic or associated with nonspecific abdominal discomfort, some lesions may initially be misinterpreted as pancreatic pseudocysts in patients with recent or concomitant pancreatitis. In these situations, unilocular morphology, absence of obvious septations or mural nodules, and surrounding inflammatory changes may delay the correct diagnosis and potentially lead to inappropriate management[32,38].
Finally, several MRI findings have been associated with increased malignant risk in MCNs. These include heterogeneous T2 signal intensity related to mucin layering, hemorrhagic or proteinaceous debris, cyst wall thickness ≥ 5 mm, mural nodules ≥ 9 mm, and enhancing septa[39,40,45]. Although these findings should raise suspicion for invasive disease, they may also overlap with imaging features of pancreatic ductal adenocarcinoma, occasionally making differential diagnosis challenging.
SPN is a rare epithelial pancreatic tumor accounting for approximately 1%-2% of all pancreatic neoplasms. It shows a marked female predominance and most commonly affects adolescents and young adults, particularly during the second and third decades of life. SPNs may arise in any pancreatic segment, although the body and tail are slightly more fre
SPN is generally considered a low-grade malignant neoplasm. Nevertheless, local invasion, recurrence, and metastatic spread – most commonly involving the liver or peritoneum – have all been described. Clinically, many lesions are discovered incidentally, whereas larger tumors may cause nonspecific abdominal pain because of mass effect on adjacent structures.
From a pathological perspective, SPNs are typically well-demarcated encapsulated lesions composed of variable proportions of solid tissue, cystic degeneration, necrosis, and intratumoral hemorrhage. Microscopically, the tumor is characterized by poorly cohesive epithelial cells arranged in solid and pseudopapillary structures, explaining its characteristic heterogeneous imaging appearance[46,47].
On MRI, SPNs usually appear as well-circumscribed encapsulated lesions with mixed solid and cystic internal architecture. T1-weighted images frequently demonstrate heterogeneous signal intensity with areas of intrinsic hyperintensity related to haemorrhagic content, whereas T2-weighted sequences often show heterogeneous signal because of the variable contribution of viable tumor tissue, cystic degeneration, necrosis, and haemorrhage[46,47].
A peripheral capsule, commonly hypointense on T2-weighted images, is frequently visible and may enhance after contrast administration. Dynamic contrast-enhanced imaging typically demonstrates progressive and heterogeneous enhancement of the solid components, which often become more conspicuous during delayed phases[46].
On diffusion-weighted imaging, the solid portions of SPNs commonly show high signal intensity associated with intermediate ADC values, reflecting moderate cellularity. However, these findings are not specific and should always be interpreted together with lesion morphology and enhancement characteristics (Figure 16). Communication with the pancreatic ductal system is usually absent, and dilatation of the main pancreatic duct is uncommon unless significant mass effect is present[46,47].
The MRI appearance of SPNs may vary considerably, particularly according to lesion size.
Smaller tumors may appear predominantly solid and relatively homogeneous, closely resembling pancreatic neuroendocrine tumors (Figure 17). By contrast, larger lesions – often exceeding 5 cm – more commonly demonstrate extensive cystic degeneration, necrosis, and intratumoral hemorrhage (Figure 18). In these cases, the lesion may mimic MCNs or complicated pseudocysts, especially when the solid component is subtle or poorly visible. Intralesional calcifications, more easily appreciated on CT than MRI, may further contribute to diagnostic variability[47].
A rare but increasingly recognized complication of SPN is spontaneous tumor rupture, which may result in intraperitoneal hemorrhage and, less commonly, gastrointestinal bleeding with presentation as an acute abdomen. This complication has been described in both adult and pediatric populations and usually occurs in large tumors with prominent hemorrhagic components in the absence of trauma. Proposed mechanisms include marked intratumoral vascularity, stromal fragility, and pre-existing intralesional hemorrhage[48-50].
Although uncommon, awareness of spontaneous rupture is clinically important, particularly when MRI demonstrates rapidly enlarging SPNs with extensive hemorrhagic components, because prompt recognition may significantly influence patient management (Figure 19)[48-50].
MRI provides comprehensive evaluation of cyst morphology, ductal anatomy, enhancement characteristics, and diffusion features. Careful assessment of these findings is essential not only for lesion characterization but also for estimating malignant potential and guiding the choice between imaging surveillance, endoscopic evaluation, or surgical treatment[51].
Certain MRI findings may strongly orient the diagnosis toward a specific cystic neoplasm. In particular, demonstration of ductal communication on MRCP strongly supports the diagnosis of intraductal papillary mucinous neoplasm, whereas a microcystic lesion containing a central scar is highly suggestive of serous cystic neoplasm. Conversely, a thick-walled cystic lesion located in the pancreatic body or tail without ductal communication favors mucinous cystic neoplasm. Mixed solid-cystic lesions containing hemorrhagic components, especially in young women, are characteristic of SPN. These principal imaging associations are summarized in Table 1.
| Key imaging feature | Most suggestive diagnosis | Recommended clinical action |
| Ductal communication on magnetic resonance cholangiopancreatography | IPMN | Surveillance or EUS-FNA depending on risk features |
| Microcystic lesion with central scar | Serous cystic neoplasm | Surveillance (typically benign, no intervention unless symptomatic) |
| Thick-walled cyst in body/tail, no ductal communication | MCN | Surgical referral (especially in fit patients due to malignant potential) |
| Mixed solid-cystic lesion with hemorrhage in young female | Solid pseudopapillary tumor | Surgical referral (generally recommended due to malignant potential) |
| Enhancing mural nodule | IPMN or malignant MCN | EUS-FNA and strong consideration for surgical referral |
| Main pancreatic duct dilatation > 10 mm | Main duct IPMN | Surgical referral (high-risk stigmata) |
From a prognostic perspective, several MRI findings are associated with increased malignant risk. Enhancing mural nodules, enhancing solid components, and marked dilatation of the main pancreatic duct – particularly when exceeding 10 mm – are considered high-risk imaging features, especially in MD-IPMNs. Restricted diffusion on DWI, reflecting increased cellularity, may suggest high-grade dysplasia or invasive carcinoma. Likewise, irregular or thickened cyst walls should raise concern for malignant transformation.
Interpretation of these findings should always take into account the overall imaging appearance together with the clinical context, since overlap among different cystic lesions may occasionally occur. The main MRI features associated with increased malignant risk and their clinical implications are summarized in Table 2.
| Imaging finding | Clinical implication |
| Enhancing mural nodules | Increased risk of malignancy |
| Main pancreatic duct dilatation | High-risk intraductal papillary mucinous neoplasm |
| Solid enhancing components | Suggestive of invasive disease |
| Restricted diffusion | Possible high-grade dysplasia or malignancy |
| Irregular cyst walls | Suspicion of malignant transformation |
Overall, a structured MRI-based approach integrating both morphological and functional information plays a central role in accurate diagnosis, risk stratification, and multidisciplinary management planning.
The growing availability of radiological, clinical, pathological, and molecular data has stimulated increasing interest in the application of artificial intelligence (AI) to pancreatic imaging[52]. In recent years, several machine learning and deep learning models have been developed with the aim of improving the diagnosis and risk stratification of pancreatic cystic lesions.
One of the most relevant fields of application concerns the identification of malignant transformation in premalignant lesions, particularly IPMNs. Current management strategies are still largely based on imaging findings and guideline-defined “worrisome features” or “high-risk stigmata”, although these criteria may show limited specificity in some clinical settings[53]. In this context, AI-based approaches may help integrate multiple variables simultaneously, potentially improving risk prediction.
MRI represents a particularly suitable modality for AI applications because it provides both morphological and functional information. Features such as cyst wall thickness, mural nodules, enhancement characteristics, and diffusion-related parameters can be quantitatively analyzed through radiomics and deep learning algorithms. Several studies have reported promising results using convolutional neural networks and radiomics-based models to distinguish low-grade from high-grade dysplasia in IPMNs[54-56].
AI has also been investigated for the differential diagnosis of pancreatic cystic lesions. Radiomics-based models applied to CT and MRI datasets have shown encouraging performance in differentiating IPMNs, MCNs, SCNs, and SPNs[57-60]. In some studies, the diagnostic accuracy achieved by these models was comparable to that of experienced ra
Nevertheless, despite these promising results, the clinical implementation of AI in pancreatic cystic lesions remains limited. Many currently available studies are retrospective, based on relatively small datasets, and often lack external validation. Furthermore, variability in imaging protocols, segmentation methods, and feature extraction techniques still represents an important limitation for reproducibility and generalizability.
At present, AI should therefore be considered a complementary tool rather than a replacement for radiological in
Cystic pancreatic neoplasms are increasingly encountered in routine imaging practice, largely because of the widespread use of high-resolution cross-sectional imaging techniques. MRI remains the preferred modality for lesion characterization thanks to its excellent soft-tissue contrast and its ability to evaluate communication with the pancreatic ductal system, which represents a key element in the differential diagnosis of pancreatic cystic lesions.
Recognition of the typical MRI appearance of the most common cystic pancreatic neoplasms is essential for accurate diagnosis. However, awareness of atypical presentations is equally important, since unusual morphology, hemorrhagic content, atypical enhancement patterns, or unexpected ductal involvement may lead to diagnostic uncertainty and potentially inappropriate management.
A comprehensive MRI evaluation integrating morphological findings, MRCP features, contrast-enhanced sequences, and diffusion-weighted imaging can substantially improve lesion characterization and risk stratification. Correlation with clinical history, laboratory findings, and, when necessary, EUS remains fundamental in complex or indeterminate cases.
AI techniques may provide additional support in the future, particularly for lesion classification and prediction of malignant transformation. Although current results are promising, these approaches still require further validation before widespread clinical application.
Overall, accurate recognition of both typical and atypical MRI findings of pancreatic cystic neoplasms plays a fun
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