Case Report

Volume 16, Number 12, December 2025, pages 475-486

Cecal Involvement of Diffuse Large B-Cell Lymphoma: A Rare Extra-Nodal Presentation

Non-Hodgkin’s lymphoma (NHL) represents a significant portion of hematologic malignancies, accounting for approximately 4% of all cancer diagnoses in the United States. The incidence of NHL has markedly increased, with a reported rise of 168% since 1975 [1]. NHL is characterized by its heterogeneity, comprising a multitude of subtypes, among which diffuse large B-cell lymphoma (DLBCL) is the most prevalent which constitutes approximately 25% of all NHL cases in the United States [1]. Several risk factors have been identified in association with DLBCL, including prior exposure to radiation, obesity, tobacco use, and certain infectious agents such as human immunodeficiency virus (HIV) and human herpes virus 8 (HHV-8). A notable feature of NHL is its propensity for extra-nodal involvement, which occurs in up to 40% of patients [2], with the gastrointestinal (GI) tract being a common site for such manifestations [3, 4].

Primary GI lymphoma is uncommon, with colonic involvement seen in only ∼1.3% of all lymphoma cases, making primary colonic DLBCL, especially in the cecum, rare [5, 6]. In contrast, secondary colonic involvement from systemic DLBCL occurs in only 2-3% of cases, reflecting its rarity as an extranodal site [7]. Within the colon, the cecum is frequently identified as the primary site of involvement. The clinical presentation of colonic lymphoma can often be insidious, leading to delays in diagnosis due to the absence of early symptoms. This delay can result in significant complications, including disease progression, perforation, and an overall poorer prognosis. Patients with advanced-stage DLBCL have a favorable response to treatment, with more than 60% achieving remission or potential cure through the R-CHOP regimen, which combines rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone [8]. This case report details a patient diagnosed with aggressive DLBCL localized to the cecum, who initially presented with an enlarging neck mass.

A 56-year-old male with a past medical history of hypothyroidism due to Hashimoto thyroiditis presented to the office with a 6-week history of sore throat and an enlarging neck mass. The patient reported associated symptoms of throat swelling, odynophagia, and dysphagia, which significantly impacted his ability to swallow. Additionally, he experienced a notable 10-pound weight loss over this period and night sweats, raising concerns for a possible underlying malignancy. A computed tomography (CT) scan of the neck was performed, revealing a moderately enlarged thyroid gland with well-defined lesions bilaterally: a larger lesion on the right measuring 5.5 × 4.9 cm and a smaller lesion on the left measuring 3.0 × 1.8 cm. The imaging also demonstrated moderate prominence of the left tonsillar and peritonsillar soft tissues, accompanied by cervical lymphadenopathy and multiple prominent mediastinal lymph nodes indicative of possible lymphoproliferative disease.

Subsequently, the patient underwent a biopsy of the left tonsillar mass. Histopathological examination showed an atypical lymphoid infiltrate predominantly composed of small-to-medium-sized lymphocytes (Fig. 1). Immunophenotyping confirmed positivity for CD20 (Fig. 2a), a B-cell marker. Immunophenotyping and fluorescent in situ hybridization (FISH) were negative for CD10, CD3, B-cell lymphoma 6 (BCL6), B-cell lymphoma 2 (BCL2), C-MYC and multiple myeloma oncogene 1 (MUM-1) (Figs. 2b, c and 3a-d). Epstein-Barr virus-encoded small RNA in situ hybridization (EBER-ISH) was positive (Fig. 2d). The Ki-67 proliferation index was notably high, ranging from 80% to 90%, which indicated a high-grade lymphoma (Fig. 3e). Based on these findings, the patient was diagnosed with aggressive DLBCL. To assess the extent of the disease, a whole-body positron emission tomography (PET) scan combined with CT imaging was conducted.

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Figure 1. Tonsil mass biopsy histology: high-grade lymphoid neoplasm with necrosis (H&E, × 40). H&E: hematoxylin and eosin.

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Figure 2. Tonsil mass biopsy histology. (a) CD 20 immunostain (× 40): positive in the abnormal infiltrate, confirming B-cell lineage. (b) CD3 immunostain (× 40): negative in the neoplastic B cells. Admixed CD3+ small T cells. (c) CD10 immunostain (× 40): negative in the neoplastic B cells. (d) EBER-ISH (× 40): positive in the neoplastic B cells. EBER-ISH: Epstein-Barr virus-encoded small RNA in situ hybridization.

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Figure 3. Tonsil mass biopsy histology. (a) BCL6 immunostain (× 40): negative in the neoplastic B cells. (b) BCL2 immunostain (× 40): negative in the neoplastic B cells. (c) C-MYC immunostain (× 40): negative in the neoplastic B cells. (d) MUM1 immunostain (× 40): negative in the neoplastic B cells. (e) Ki-67 immunostain (× 40): elevated proliferative index in the large cell infiltrate. BCL2: B-cell lymphoma 2; BCL6: B-cell lymphoma 6; MUM-1: multiple myeloma oncogene 1.

The PET scan revealed F-fluorodeoxyglucose (FDG)-avid lymphadenopathy with central necrosis in bilateral cervical lymph nodes as well as hypermetabolic lymphadenopathy in the left IIa and IIb lymph node stations. Importantly, focal wall thickening at the base of the cecum and the proximal portion of the ascending colon was identified, which demonstrated hypermetabolic activity suggestive of possible colonic involvement. A bone marrow biopsy was done which did not show any evidence of involvement with lymphoma. Considering the above findings, the patient commenced combination chemotherapy with R-CHOP.

Gastroenterology consultation was requested for evaluation of the colonic abnormalities noted on the PET scan. A colonoscopy was performed, which revealed a solitary 15 mm ulcer in the cecum that was biopsied with cold forceps for histology (Fig. 4). Biopsy of the ulcerated colonic mucosa demonstrated infiltration by sheets of large atypical lymphoid cells (Fig. 5a, b). Immunohistochemical analysis confirmed B-cell lineage, with the neoplastic cells showing positive staining for PAX5 and CD79a (Fig. 5c, d). CD20 was negative, consistent with prior anti-CD20 (rituximab) therapy (Fig. 6a). Ki-67 immunostaining revealed a markedly elevated proliferative index within the large cell infiltrate (Fig. 6b). Immunostaining for CD3 was negative (Fig. 6c). The neoplastic cells were also positive for Epstein-Barr virus latent membrane protein 1 (EBV-LMP1), CD10, BCL6, and MUM1 (Fig. 7a-d). Additionally, co-expression of C-MYC and BCL2 was demonstrated, indicating a “double-expressor” phenotype, which is typically associated with a more aggressive clinical course (Fig. 6d, e). Based on these findings, and according to the Hans algorithm, the lesion was classified as DLBCL, germinal center B-cell (GCB) subtype.

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Figure 4. Solitary 15 mm ulcer in cecum on colonoscopy. Arrows indicate the extent and dimensions of ulcer. Circle indicates distortion of ileocecal valve from the ulcer.

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Figure 5. Cecal tumor histology. (a) H&E (× 40): cecal mucosa involved by a large atypical lymphoid infiltrate. No Hodgkin/HRS-like morphology seen. (b) H&E (× 10): cecal mucosa involved by a large atypical lymphoid infiltrate. (c) PAX5 immunostain (× 40): positive in the abnormal infiltrate, confirming B-cell lineage. (d) CD79a immunostain (× 40): positive in the abnormal infiltrate confirming B-cell lineage. H&E: hematoxylin and eosin.

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Figure 6. Cecal tumor histology. (a) CD20 immunostain (× 40): negative in the B-cell infiltrate, consistent with anti-CD20 therapy. (b) Ki-67 immunostain (× 40): elevated proliferative index in the large cell infiltrate. (c) CD3 immunostain (× 40): negative in the neoplastic B cells. Admixed CD3+ small T cells. (d) BCL2 immunostain (× 40): positive in the neoplastic B cells. (e) C-MYC immunostain (× 20): positive (> 35%) in the neoplastic B cells. BCL2: B-cell lymphoma 2.

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Figure 7. Cecal tumor histology. (a) BCL6 immunostain (× 40): positive in the neoplastic B cells. (b) MUM1 immunostain (× 40): positive in the neoplastic B cells. (c) EBV-LMP1 immunostain (× 40): positive in the neoplastic B cells. (d) CD10 immunostain (× 40): positive in the neoplastic B cells. BCL6: B-cell lymphoma 6; EBV-LMP1: Epstein-Barr virus latent membrane protein 1; MUM-1: multiple myeloma oncogene 1.

Six cycles of R-CHOP chemotherapy were given over a period of 3 months. His clinical course was complicated by the development of deep venous thrombosis, requiring initiation of rivaroxaban.

A repeat PET scan was done to determine the response to chemotherapy. The PET scan showed a complete response of the lymphadenopathy in the head and neck region, with persistent significant uptake in the cecal mass (standardized uptake value 23.2, previously 27.3). Since the cecal lymphoma did not respond appropriately to chemotherapy, second line treatment options, including chimeric antigen receptor T-cell therapy (CAR-T therapy) and autologous stem cell transplant, were considered. The patient declined CAR-T therapy due to its potential neurological side effects.

The patient sought a second opinion from a different oncologist and was given the option of repeating the PET-CT scan with surveillance if his disease remained stable. The patient opted for surveillance. Therefore, a repeat PET-CT was performed, which showed metabolically active diffuse cecal wall thickening with slightly increased activity. Necrotic conglomerate lymphadenopathy in the right neck exhibited decreased FDG activity. Interval development of right hydroureteronephrosis was noted.

Due to the persistent abnormality noted on the PET scan, a repeat colonoscopy was performed. An infiltrative and ulcerated obstructing large mass was found in the cecum, measuring 14 mm, which was biopsied (Fig. 8a-c). There was an appearance of an ulcerated fistula in the rectum; biopsies were obtained (Fig. 8d). Both the cecal mass and rectal biopsies confirmed the diagnosis of recurrent DLBCL.

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Figure 8. Infiltrative and ulcerated obstructing large cecal mass and rectal fistula. (a) Infiltrative cecal mass. (b) Partially obstructive cecal mass (arrows). (c) Ulcerated cecal mass. (d) Ulcerated fistula in rectum (arrow).

The patient was then hospitalized for severe diarrhea due to Clostridium difficile colitis and was treated with vancomycin. During this hospitalization, a CT scan of the abdomen with an oral and intravenous contrast was obtained. This revealed a markedly distended cecum with thick-walled changes (Fig. 9a), significant inflammatory stranding, and overt fistulization to the bladder. Dense oral contrast material was noted within the bladder (Fig. 9b, c). Unfortunately, due to the mass effect and colovesical fistula, the patient developed obstructive uropathy, necessitating the placement of a right-sided nephrostomy tube. He developed a urinary tract infection with E. coli as well, which was treated with antibiotics.

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Figure 9. Computed tomography (CT) scan with oral and IV contrast findings. (a) Markedly distended cecum with thick-walled changes (arrows). (b) Oral contrast noted in bladder indicating a presence of a colovesical fistula (arrow). (c) Dense oral contrast material traversing colovesical fistula (arrow).

The patient was then re-hospitalized due to worsening renal function. Due to progression of lymphoma with cecal involvement eroding into adjacent structures and associated urological complications, and given prior failure of R-CHOP therapy, the patient was started on salvage chemotherapy with rituximab, ifosfamide, carboplatin, and etoposide (R-ICE). He received two cycles of R-ICE. A diverting loop ileostomy was performed.

Unfortunately, the patient did not respond to R-ICE chemotherapy. Given the lack of response to prior chemotherapy regimens, the decision was made to initiate treatment with rituximab and polatuzumab on a 6-week cycle, administered every 21 days.

Radiation therapy was not recommended due to concerns about exacerbating the colovesical fistula and the proximity of the mass to the bowel.

Despite these interventions, the patient’s disease continued to progress. Unfortunately, he passed away due to complications related to his underlying lymphoma. An autopsy was not performed.

This case highlights the importance of thorough evaluation for extranodal involvement in patients with NHL, especially when atypical symptoms or imaging findings are present. In this case, lymphoma involving the colon was refractory to chemotherapy and resulted in complications culminating in fatality.

Table 1 shows the brief summary of the clinical course.

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Table 1. Timeline of Clinical Course

We report a rare case of a 56-year-old male with cecal involvement of DLBCL who initially presented with a neck mass, B-symptoms, and weight loss. Histopathology confirmed a GCB subtype DLBCL with a high Ki-67 proliferation index (80-90%) and a double-expressor phenotype (MYC/BCL2 co-expression). Despite frontline R-CHOP chemotherapy and subsequent salvage R-ICE regimen, the patient exhibited primary refractory disease and ultimately developed a colovesical fistula, complicated by recurrent urinary tract infections (UTIs) and renal failure. Radiotherapy was withheld due to the presence of the fistula, given the risk of worsening fistulation. This constellation of features, cecal involvement, double-expressor status, primary chemotherapy refractoriness, and fistula formation, makes this case clinically unique and highlights several important diagnostic and therapeutic challenges.

DLBCL is the most common type of NHL, accounting for approximately 40% of all cases. R-CHOP remains the standard first-line therapy and cures about 60% of patients, while roughly 40% are either refractory or relapse [9]. Chemo refractoriness, as observed in our patient, represents a high-risk clinical scenario.

Double-expressor lymphoma (DEL) is known for aggressive clinical characteristics, including high Ki-67 proliferation indices, elevated International Prognostic Index (IPI) scores, involvement of multiple extranodal sites, and a higher prevalence of non-germinal center B-cell (non-GCB) subtypes. Our patient exhibited several of these high-risk features, including GCB phenotype, markedly elevated Ki-67 (80-90%), and cecal involvement, which aligns with the aggressive disease patterns as reported by Riedell and Smith (2018) [10] and Green et al (2012) [11].

DEL has been consistently associated with poor outcomes when treated with standard R-CHOP therapy. Green et al (2012) [11] and Hu et al (2013) [12] reported 5-year progression-free survival (PFS) of only 27-32% and overall survival (OS) of 30-36% in DEL patients. In our case, the disease remained refractory to both R-CHOP and salvage R-ICE regimens, which aligns with these prior findings. Furthermore, Zhang et al (2019) [13] demonstrated that intensive regimens such as DA-EPOCH-R do not significantly improve survival in DEL patients, which is consistent with the poor response observed in our patient. These findings highlight the challenges in managing DEL. Thus, our case underscores the high-risk nature of DEL and the limitations of conventional therapy. As Ning et al (2012) [14] suggested, novel therapeutic strategies, including histone deacetylase inhibitors and other targeted agents, may be required to improve outcomes in this high-risk population.

Recent evidence suggests that chemotherapy refractoriness in GI DLBCL may result from a complex interplay between gut microbiota dysbiosis and alterations in the tumor microenvironment (TME). Disruption of microbial diversity and enrichment of pro-inflammatory taxa can compromise mucosal integrity, promote systemic inflammation, and impair immune-mediated tumor control, collectively diminishing chemoimmunotherapy efficacy [15]. Simultaneously, immune escape mechanisms within the TME, such as downregulation of major histocompatibility complex (MHC) class I and II molecules, and dysregulation of macrophage phagocytic signaling through TMEM30A mutations or CD47 overexpression further hinder effective antitumor responses [16]. These microenvironmental and microbial factors may synergistically contribute to the aggressive course and limited treatment response observed in primary cecal DLBCL, highlighting the need for integrated approaches that consider host-microbiome-tumor interactions in therapeutic planning.

DLBCL pathogenesis involves genetic and molecular alterations such as BCL6 overexpression, TP53 inactivation, and dysregulation of BCL2 and MYC, leading to genomic instability, immune evasion, and aggressive tumor behavior [17, 18]. Resistance to R-CHOP in DLBCL is frequently driven by genetic and molecular abnormalities. Double-hit lymphomas (DHLs), harboring concurrent MYC and BCL2 rearrangements, and triple-hit lymphomas (THLs), involving MYC, BCL2, and BCL6, are consistently associated with poor outcomes and limited response to standard therapy [19, 20]. Similarly, double protein expression lymphoma (DPL), defined by high MYC and BCL2 protein levels without detectable gene rearrangements, also predicts inferior survival, though slightly better than DHL [19, 21]. Isolated MYC or BCL2 alterations, as well as specific MYC mutations, have variable prognostic significance [22-25]. These findings underscore the need for early molecular screening using FISH for gene rearrangements and immunohistochemistry for protein overexpression, as conventional prognostic tools, including the IPI, often fail to identify patients at high risk of treatment resistance [19, 20].

Tumor-associated bowel fistulas, including enterovesical, enterocolic, and less commonly splenocolic or gastrosplenic fistulas, are rare but serious complications of primary GI lymphoma, particularly DLBCL [26-34]. These fistulas may result from transmural tumor invasion, local inflammatory changes, adherence to adjacent organs, or treatment-related cytotoxic injury, including post-chemotherapy tumor regression leading to wall weakness [28-30, 32]. Clinical manifestations are often nonspecific, ranging from abdominal pain, diarrhea, and weight loss to acute complications such as GI bleeding or partial bowel obstruction, which may delay diagnosis [26, 27, 33, 34]. Imaging modalities including CT, CT angiography, and CT enterography are crucial for early detection, localization of fistulas, and surgical planning, while endoscopy may fail to reveal lesions in some cases [28, 29, 31, 33]. Literature reviews indicate that fistulas can rarely present as the initial manifestation of primary intestinal lymphoma, with the small intestine and colon being the most commonly involved sites, and DLBCL being the predominant histologic type [26, 27, 33]. Management often requires a multidisciplinary approach, combining surgery for resection or drainage with chemotherapy, including R-CHOP regimens, which has been associated with improved survival and functional outcomes [26-29, 30, 32, 34]. While long-term prognosis remains variable, early recognition and timely intervention are pivotal in reducing morbidity and mortality in these patients [26, 27, 33, 34].

In summary, DLBCL typically presents as an enlarging symptomatic mass, often as a growing nodule in the neck or abdomen. Patients frequently report systemic “B” symptoms, including fever, weight loss, and night sweats, which are indicative of advanced disease [35]. As in this case, the presence of “B” symptoms, advanced disease stage, and the patient’s age (greater than 58 years) are recognized as poor prognostic factors for colon lymphoma [36]. In the context of GI involvement, particularly colon lymphoma patients may present with abdominal pain, diarrhea, and GI bleeding, with bowel obstruction occurring in rare instances. The absence of extra-nodal symptoms, as in this case, highlights the importance of recognizing primary symptoms and utilizing imaging modalities such as CT scans for comprehensive evaluation of potential lymphoma sites. The diagnosis is best made by excisional tissue biopsy which allows for definitive histopathological assessment [37].

Management of GI DLBCL involves a multidisciplinary approach, with surgery reserved for large or obstructive tumors and standard chemotherapy consisting of six cycles of R-CHOP [38]. Ongoing monitoring is essential to assess remission, manage treatment related complications, and facilitate early detection of extracolonic malignancies through age-appropriate screening colonoscopies. In older patients, treatment should be individualized based on fitness rather than age: fit patients may receive standard R-CHOP, unfit patients can benefit from dose-reduced regimens such as R-Mini CHOP or anthracycline alternatives (R-CEOP/gemcitabine), while frail patients may not tolerate chemotherapy [39]. Geriatric assessments, prephase corticosteroids, primary granulocyte colony-stimulating factor (G-CSF) prophylaxis help optimize outcomes and minimize toxicity. These observations highlight the need for tailored treatment strategies for high-risk DLBCL and integrating molecular and genetic profiling with conventional and novel therapies may improve precision medicine approaches and patient outcomes [38, 39].

In conclusion, this case highlights that the GI tract involvement of DLBCL, especially metastatic spread to cecum, is a rare occurrence. Early diagnosis of extra-nodal involvement - particularly colonic lesion as seen in our case - is crucial, and clinicians should maintain a high index of suspicion for GI extra-nodal disease in patients presenting with atypical or nonspecific symptoms, even in the absence of clear GI manifestations. Screening colonoscopy could play a pivotal role in diagnosing these lesions ahead of time. Early recognition, especially in tumors with high-risk or chemo-refractory features, may allow for timely surgical intervention and help prevent significant local complications and morbidity. Once suspected, the excisional biopsy of incidental mass is confirmatory. However, treatment options are limited given the scarcity of data. In short, it is imperative for physicians to maintain a high level of suspicion of this clinical entity in NHL-DLBCL patients presenting without any primary GI symptoms as early diagnosis and management can lead to potentially favorable outcomes.

Early identification and diagnosis of extranodal involvement in DLBCL through imaging modalities such as PET-CT, especially in patients without gastrointestinal symptoms, is crucial. This facilitates timely decisions regarding chemotherapy and, when necessary, early surgical intervention, thereby preventing significant morbidity and local complications.

Screening colonoscopy also plays a vital role, not only in detecting polyps and colonic adenocarcinoma but also in identifying atypical lesions, that may lead to the diagnosis of rare malignancies. In our case, age-appropriate colon cancer screening might have led to an earlier diagnosis and identification of extranodal colonic involvement, potentially preventing significant complications, enabling timely treatment, and reducing morbidity.

It is essential to recognize aggressive tumor features and remain vigilant about the potential for chemo-refractory disease.

Management of such difficult-to-treat tumors requires a comprehensive, multidisciplinary approach involving specialists from urology, surgery, hematology-oncology, and gastroenterology.

Acknowledgments

This article was previously presented as a meeting abstract at the 2022 ACG Annual Scientific Meeting on October 21-26, 2022.

Financial Disclosure

The authors received no financial support for the research, authorship, or publication of this article.

Conflict of Interest

The authors declare no conflict of interest.

Informed Consent

Informed consent was obtained from the patient for the publication of this case report and any accompanying images.

Author Contributions

Usama Sakhawat, primary author, contributed to all parts of the report from collecting data, writing abstract, case presentation, literature review, discussion, and finalizing/reviewing the final version. Ahmed Shehadah and Usman Mazhar contributed to literature review and discussion. Miranda Gonzalez contributed to case presentation, abstract, and conclusion. Fahad Malik and Leslie Bank contributed to discussion and conclusion. James Van Gurp contributed to case presentation, discussion, and conclusion.

Data Availability

The authors declare that data supporting the findings of this study are available within the article.

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