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. 2025 Jul 8;16:1280. doi: 10.1007/s12672-025-02482-7

Clinical characteristics of duodenal-type follicular lymphoma

Lu Wang 1,2, Wenyan Shen 3, Xiaoyuan Zhang 2, Ling Xue 3, Beili Hu 2,✉
PMCID: PMC12238708  PMID: 40627253

Abstract

Duodenal-Type Follicular Lymphoma (DFL) is a rare extranodular B-cell lymphoma, which mainly involves the duodenum. It typically affects middle-aged individuals and occurs equally in both genders. Common symptoms include upper abdominal discomfort, pain, indigestion, etc. Histopathologically, the condition is characterized by the disruption of follicular architecture, accompanied by the hyperplasia of central cells, and may optionally exhibit the “starry sky” phenomenon. The main treatment for DFL is observation and waiting due to the lack of symptoms and slow progression. The article reviews recent insights into DFL’s epidemiology, symptoms, treatment, and prognosis.

Keywords: Duodenal follicular lymphoma, Clinical characteristics, Pathological manifestations, Treatment advances, Prognosis

Duodenal-Type Follicular Lymphoma (DFL) is a rare non-Hodgkin's lymphoma (NFL), which mainly occurs in the duodenum [1]. Follicular lymphoma (FL) is the most prevalent B-cell non-Hodgkin lymphoma in Western countries, but DFL is rarer, occurring in about 1 in 3000 to 7000 gastroduodenoscopies [2, 3]. It was first identified in the 2016 WHO classification update and remained in the 2022 5th edition. FL categories include FL, in situ follicular B-cell tumor, pediatric FL and DFL. The latter three types have no significant changes in WHO-HAEM5, but FL has been greatly revised. FL is further divided into four types: Classic FL (cFL), FL with abnormal cytological features (uFL), FL with diffuse proliferation growth pattern and follicular large B-cell lymphoma. DFL is a recognized entity akin to classic FL, characterized by an immune profile that overexpresses CD10, CD20, Bcl-2, and the t(14;18) (q32;q21) translocation [4]. This subtype typically affects the distal duodenum and occurs equally in both genders [5]. DFL is typically diagnosed early and confined to the small intestine, particularly the second part of the duodenum, unlike most other FLs, which are often advanced at diagnosis [6]. Most DFL patients are asymptomatic at diagnosis, often in early stages with a favorable prognosis, leading many doctors to opt for a watch-and-wait approach [7].

Epidemiological characteristics of DFL

Gastrointestinal lymphoma is the most common type of extranodal lymphoma. More than 90% of gastrointestinal lymphoma belongs to the B cell line, covering mucosal-related tissue lymphoma and follicular lymphoma (FL) [8]. DFL is a rare lymphoma subtype with a relatively low incidence in non-Hodgkin's lymphoma (NHL) [3]. DFL mostly occurs in middle-aged people. The average diagnosis age is around 53, but it can occur in any age group and affects both males and females equally [9]. Follicular lymphoma accounted for just 4% of gastrointestinal tract lymphomas [10–12]. DFL typically appears as one or more nodular lesions in the duodenum, mainly in its descending section [4]. The second part of the duodenum, especially the peri-ampullary area, is most commonly affected (81%), followed by the jejunum (40%) [13, 14]. The lesion mainly involves the intestines, occasionally affecting the stomach and colon, with rare distant metastasis. Consequently, the prognosis for DFL is generally favorable due to its indolent nature [15]. Five-year progression-free survival exceeds 70%, with overall survival between 80 and 94% [16].

Clinical manifestations of DFL

DFL, an inert lymphoma, usually does not present with systemic lymph node disease, bone marrow infiltration, or spleen enlargement, unlike cFL (Table 1). It is often discovered incidentally during routine endoscopies, as most patients are asymptomatic [17, 18]. Diagnosis relies on endoscopy, histological, and immunohistochemical analysis due to the lack of distinct clinical signs [19]. Some patients may experience mild digestive issues, while less common symptoms include anemia, fatigue, fever, diarrhea, loss of appetite, and swollen lymph nodes [20]. Lesions in confirmed DFL cases typically appear as multiple small polyps or nodules, sometimes with ulcers under endoscopy (Fig. 1) [21, 22]. In rare cases, when lesions are in the pancreatic or hepatic abdominal cavity, obstructive jaundice may occur as the primary symptom [23]. Sato et al. [24] highlight that obstructive jaundice can arise from distant lesions, not just those near the liver or pancreas, necessitating differentiation from pancreatic head cancer or bile duct stones. Older patients with these symptoms should consider the possibility of DFL and undergo prompt testing for accurate diagnosis.

Table 1.

comparison of DFL and cFL

DFL cFL
Lymph node involves Almost no enlarge lymph nodes Always enlarge lymph nodes
Location Small intestine, particularly the second part of the duodenum Lymph node or extra-node sometimes
Neoplastic involvement Duodenal villi submucosa and subserosa
Lesion manifestations Multiple small polyps or nodules Enlarge lymph-nodes
Grade I or II I or II
Bcl-6  +   + (part -)
CD10  +   + (part -)
Bcl-2  +   + 
CD21 In the germinal center, less than 10% of the neoplastic germinal center At other extranodal sites, more than 2/3 of the neoplastic germinal center
CD27  +  –
AID –  + 
T(14;18)  +   + 
Ki-67  ±   ± 
IgVH use V4, V5 V3, most cases
TNFRSF14/HVEM  +   + 
CREBBP  +   + 
KMT2D/MLL2 – High mutation frequency in advanced systemic FL
Genes associated with inflammatory processes  +   + in early-stage low-grade systemic FL
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Fig. 1.

Fig. 1

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Numerous nodules scattered in the descending duodenum observed via endoscopy

Endoscopy has unique advantages in the diagnosis of duodenal follicular lymphoma. Ordinary endoscopic lesions have a variety of manifestations, including submucosal bulge, ulcer type, infiltration type and other forms. The surface of the lesion is covered with normal or congested mucosa, and white granular changes can be seen in some cases. Magnifying endoscopy can observe changes in the microvascular network on the surface of the tumor, and narrowband imaging technology enhances the display of disease boundary. Endoscopy ultrasound accurately evaluates the infiltration depth of the lesion, measures the tumor size, and guides the selection of biopsy sites [25].

Systematic endoscopic examination combined with imaging evaluation provides an accurate basis for disease staging. The Ann Arbor staging system combines Lugano to revise the standard to make clinical staging more accurate. Early cases are limited to the duodenal wall, and the late stage can involve distant lymph nodes and other organs [26].

Pathogenesis and genetic characteristics of DFL

The exact cause of DFL is unknown, but research suggests it is part of the follicular lymphoma (FL) group, sharing genetic markers like the t(14;18)(q32;q21) translocation common in systemic FL. DFL often shows IgVH gene rearrangements, mainly VH4 and VH5, more frequently than in lymph node FL [18]. Hellmuth et al. [17] found high mutation rates in the TNFRSF14/HVEM and CREBBP genes in both systemic FL and DFL, indicating a genetic link. The mutation rate of the CREBBP gene reaches 60%, which encodes histone acetyltransferase to regulate chromatin remodeling and gene expression. The KMT2D/MLL2 gene, frequently mutated in mature B-cell lymphoma, shows high mutation rates in advanced systemic FL but lower rates in early-stage FL and DFL, suggesting DFL is genetically closer to early-stage FL.

In contrast to most FL, DFL has a distinct pathogenesis that is closely linked to inflammation and antigen stimulation. This pathogenesis also reflects similarities with MALT lymphoma, which may account for DFL's potential regression following Helicobacter pylori eradication. DFL and MALT lymphomas exhibited robust expression of genes associated with inflammatory processes at the molecular level, notably CCL20, CCR6, and MADCAM-1, whose expression was corroborated by corresponding protein levels [14]. While its genetic characteristics more closely resemble those of early-stage low-grade systemic follicular lymphoma. Recent studies have shown that other inflammatory-related proteins, such as CCL21, TNFSF15, CCL11, CXCL1, and CXCL6, also exhibit a high expression state in addition to CCL20, indicating that chronic inflammation may promote the development of DFL [27]. Takata K et al. [28] posited that duodenal reactive lymphoid hyperplasia (D-RLH) is associated with frequent methylation of CDKN2B/P15 and DAPK1 in DFL, suggesting that DFL may originate from D-RLH. DNA methylation spectrum analysis [29] shows that high methylation occurs in the tumor-inhibiting gene promoter region, resulting in gene silencing. The mutation rate of EZH2 gene is about 25%, which affects the epigenetic regulation network by changing histone modification. The change of histone modification mode affects the open state of chromatin and interferes with the normal gene expression regulation. Abnormality of non-coding RNA expression spectrum also participates in the occurrence of disease, and the upregulation of micro RNA miR-155 expression promotes tumor cell proliferation.

Histological characteristics of DFL

The foci of duodenal follicular lymphoma are white or grayish-white raised lesions, with a smooth surface and different sizes, and a diameter usually between 0.2–2.0 cm. Microscope observation shows that tumor cell infiltration is mainly limited to the intrinsic layer of the mucosa and the submucosal layer, and rarely invades the muscle layer. The lesion area has a typical follicular-like structure. The follicle varies in size and irregular in shape, and the follicular interval is separated by fibrous tissue [30].

DFL is marked by clustered germinal centers with centrocytes and few or no centroblasts, lacking visible tingible body macrophages and mantle zones. Small lymphoid cells with irregular nuclei are usually outside the follicles, and the lymphoma often impacts the mucosa and submucosa. Despite the removal of the histological classification of follicular lymphoma from the The WHO Classification of Haematolymphoid Tumours (5th Edition, 2022), the majority of duodenal follicular lymphomas are categorized as grade 1–2 under the histological classification system, accounting for about 85% [31]. The lesion area is often accompanied by reactive lymphatic follicular hyperplasia, which needs to be distinguished from benign lymphatic tissue hyperplasia.

Villi atrophy is prevalent on the mucosal surface with disordered gland structures. Tumor cells infiltrate diffusely, disrupting the original tissue. Notable angiogenesis occurs in the lesion, with thin, fragile new blood vessel walls. The interstitial area shows varying levels of inflammatory cell infiltration, primarily small lymphocytes and plasma cells [21]. The pathological analysis of biopsy samples, including HE staining (Hematoxylin–Eosin staining, Fig. 2 and Fig. 3) and immunohistochemistry staining, is necessary for the diagnosis [24].

Fig. 2.

Fig. 2

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Hematoxylin–Eosin staining(original magnification × 40)

Fig. 3.

Fig. 3

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Hematoxylin–Eosin staining(original magnification × 100)

Immunohistochemistry analysis of DFL

DFL shares an immunophenotype akin to low-grade nodal FL (NFL), marked by the expression of CD20 (Fig. 4), CD79a (Fig. 5), CD10 (Fig. 6), BCL-6 (Fig. 7), BCL-2 (Fig. 8) and PAX5 (Fig. 9), while lacking CD3 (Fig. 10), CD5 (Fig. 11), CD23, CD43, BCL-1, or T-cell markers, and exhibit a low Ki-67 (Fig. 12) proliferation rate. DFL differs from NFL in that it exhibits unique CD21 (Fig. 13) and CD23 expression patterns in follicular dendritic cells, with these cells making up less than 10% of the neoplastic germinal center, unlike the more than two-thirds seen in NFL and other extranodal FLs. DFL's low-grade nature may be partly due to its restricted interaction with FDC. There are significant differences in the expression of immune markers between DFL and gastrointestinal follicular lymphoma (GI-FL). Specifically, CD27 is positive in DFL, while AID is negative, which is completely opposite to the performance of GI-FL. As a type I glycoprotein, CD27 belongs to the tumor necrosis factor receptor family and is an important marker of memory B cells. AID belongs to the RNA-encoded cytosine deaminase family, which is specifically expressed in the B cell within the germinal center, which is essential for the transformation of B cells and high mutation processes [32]. The abnormal expression of members of the BCL2 gene family changes the apoptosis threshold and gives tumor cells a survival advantage. The tumor microenvironment plays a key role in the progression of DFL. In the microenvironment, follicular dendritic cells secrete CXCL13 chemokine, attracting abnormal B cells to gather into the follicle [33]. The increased proportion of regulatory T cells inhibits the body's anti-tumor immune response, and M2 macrophages secrete inhibitory factors such as IL-10 to jointly build an immunosuppressive microenvironment.

Fig. 4.

Fig. 4

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Diffuse expression of tumor cells CD20 (original magnification × 100)

Fig. 5.

Fig. 5

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CD79a positive for dyeing(original magnification × 100)

Fig. 6.

Fig. 6

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Tumor cell CD10 positive (original magnification × 100)

Fig. 7.

Fig. 7

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Abnormal expression of Bcl-6 on tumor cells(original magnification × 100)

Fig. 8.

Fig. 8

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Abnormal expression of Bcl-2 on tumor cells(original magnification × 100)

Fig. 9.

Fig. 9

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Tumor cell PAX5 positive (original magnification × 100)

Fig. 10.

Fig. 10

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CD3 staining negative (original magnification × 100)

Fig. 11.

Fig. 11

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CD5 staining negative (original magnification × 100)

Fig. 12.

Fig. 12

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The Ki‐67 proliferation index of tumor cells is about 10%(original magnification × 100)

Fig. 13.

Fig. 13

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CD21 positive for dyeing(original magnification × 100)

Notably, DFL and MALT lymphoma share significant similarities in the expression of genes, such as CCL20, CCR6, and MADCAM-1, with increased levels of CCL20 and MADCAM-1 indicating their crucial role in tumor development. And the gene expression maps such as PCDHGA3, PCDHGA8 and PCDHGB4 are also similar in DFL and NFL.

Treatment of DFL

There is no agreed-upon treatment for DFL. Treatment decisions should consider the patient's overall health, tumor size and extent, symptoms, and complications. Recent international reports indicate a preference for a Watch and Wait (W&W) approach [7]. The Watch and Wait (W&W) approach is the most common treatment for DFL, particularly for patients without any symptoms. In this situation, frequent monitoring and endoscopic exams are crucial. If psychological or social stressors are significant, radiotherapy or medication may be more appropriate.

For small tumors confined to the mucosal layer, endoscopic resection is a minimally invasive option with quick recovery, though it may only be suitable for smaller tumors. Luo S et al. [34] were the first to report using ESD endoscopy to treat DFL, located in the mucosal layer of the duodenum's descending segment, allowing for complete lesion removal. Zhang W et al. [35] reached a similar conclusion for ovarian-type follicular lymphoma. Endoscopy is crucial for duodenal follicular lymphoma, improving symptoms like intestinal and biliary obstruction [36]. Surgery may be needed for larger tumors or plasma layer invasion, but it often reduces postoperative quality of life without clear benefits [37]. Local duodenectomy has an 8.5% complication rate, mainly anastomotic fistula and bleeding, while pancryodenectomy has a higher 15.7% rate, requiring close monitoring for pancreas fistula and abdominal infection [38].

For locally advanced or recurrent cases, chemotherapy may be combined with radiotherapy. Radiotherapy is the standard treatment for early mucosal-related lymphoid tissue extranodal marginal lymphoma (EMZL) and gastric follicular lymphoma or DFL, aiding in local tumor control, particularly post-surgery or chemotherapy. It serves as the primary treatment for patients who are not surgical candidates [39, 40]. Lee H et al. [41] found that 95% of patients experienced complete relief after receiving 24–36 Gy of radiotherapy. Choi KH et al. [8] reported no difference in local control between duodenal follicular lymphoma treated with 24 Gy and gastric MALT lymphoma treated with 30.6 Gy. However, Baek JY et al. [40] indicated that radiotherapy for duodenal follicular lymphoma might damage the pancreas, raising the risk of diabetes.

The most common chemotherapy regimen is R-Chemo, which includes RCVP (rituximab, cyclophosphamide, vincristine, prednisone), RCHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone), or BR (Rituximab + bendamustine) [18]. Rituximab can also be administered alone [42]. Kiesewetter B et al. [43] documented a patient who entered lasting remission with four cycles of clarithromycin alone, showing no symptoms or progression during follow-up. Advancements in understanding lymphoma’s molecular mechanisms have led to the clinical use of targeted therapies, like B-cell receptor inhibitors (e.g., ibrutinib) and apoptosis regulators (e.g., venetoclax). For refractory or recurrent DFL, hematopoietic stem cell transplantation (both autologous and allogeneic) may be an effective treatment [44].

Stroma cells secrete vascular endothelial growth factors that enhance tumor angiogenesis and support tumor growth. Studies suggest that targeting the microenvironment could be a future treatment strategy. PD-1/PD-L1 inhibitors with rituximab have proven effective in trials, and the microenvironmental regulator lenalidomide shows potential for application [33].

The prognosis of DFL

Research indicates that patient age significantly affects prognosis, with those over 60 experiencing poorer outcomes due to increased immune status and complication risks [9]. The extent of lesions also plays a crucial role; patients with limited lesions fare better than those with extensive ones. Specifically, patients with duodenal involvement alone have a better prognosis due to lower tumor load and treatment complexity. Additionally, immune phenotypic characteristics impact prognosis, as patients expressing CD10 and BCL-2 respond more favorably to chemotherapy [17].

The patient's physical condition and genetic mutations are key for prognosis. The study showed that patients with an ECOG score of ≤ 1 had better outcomes, and those with BCL2 rearrangement responded well to rituximab [27]. A high Ki-67 proliferation index in tumor cells indicates a higher risk of disease progression, necessitating more aggressive treatment.

Compared to other non-Hodgkin lymphomas, DFL generally has a favorable prognosis due to its slow progression as an indolent lymphoma [15]. However, predicting its course is difficult, and it doesn't fit well into existing prognostic indices [45]. Although DFL rarely transforms into more aggressive lymphomas, when it does, it becomes highly aggressive. Saburi M and colleagues [46] found that 2 out of 23 DFL patients developed diffuse large B-cell lymphoma; one improved temporarily with R-THP-COP treatment but worsened, while the other was successfully treated with allogeneic stem cell transplantation.

A study by Kamijo K et al. [1] found that among 26 DFL patients, only one developed diffuse large B-cell lymphoma and died. Few cases of DFL histological transition are documented, with limited research available. Patients with histological changes have lower survival rates. Therefore, strict follow-up is essential, despite DFL's slow progression [47]. Long-term monitoring is needed to detect recurrence or progression. Prognosis varies and may improve with new treatments, so a qualified medical team should manage patient care [47].

Look ahead

DFL usually occurs in the small intestine, especially the distal duodenum, often without obvious symptoms. It shares a similar cell structure and immune phenotype with low-grade FL, despite a unique follicle dendritic cell distribution. Its low incidence makes systematic research challenging, and the cause remains unknown with no ideal treatment. Early identification is crucial due to the poor prognosis of histological transition. There are no effective prognostic systems or biomarkers for predicting transformation. Further studies using various omics are needed to uncover DFL’s cause and transformation. Future treatment strategies will focus on individualized and precise approaches. Immunocheckpoint inhibitors and CAR-T cell therapy show promise for relapsed patients. Treatment choices and efficacy prediction models guided by molecular typing may help reduce histological transformation. Early assessment and timely treatment can enhance patient outcomes. More retrospective studies with global case data are needed.

Acknowledgements

We would like to thank the participants who made this study possible.

Author contributions

All of the authors participated in designing this study. L W wrote the first draft of the manuscript. W Y S and L X helped pathological staining and provided pathological pictures. Finally, the manuscript was reviewed by BL H and XY Z, who also provided further contributions and suggestions. The author(s) read and approved the final manuscript.

Funding

The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

All authors have given consent for publication.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

No datasets were generated or analysed during the current study.

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