Treatment of metastatic pancreatic cancer with concurrent BRAF V600E mutation and germline BRCA2 mutation: a case report
Case Report

Treatment of metastatic pancreatic cancer with concurrent BRAF V600E mutation and germline BRCA2 mutation: a case report

Xiaoting Ma1,2,3, Mei Guan1, Ningning Li1, Ying Liu4, Huanwen Wu5, Yuejuan Cheng1, Yi Ba1,2

1Department of Medical Oncology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; 2Department of Cancer Medical Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; 3Department of Internal Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; 4Beijing Chaoyang Integrative Medicine Rescue and First Aid Hospital, Beijing, China; 5Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

Contributions: (I) Conception and design: X Ma, Y Cheng; (II) Administrative support: M Guan, Y Ba; (III) Provision of study materials or patients: Y Liu, Y Cheng; (IV) Collection and assembly of data: N Li, Y Liu; (V) Data analysis and interpretation: X Ma, H Wu, Y Cheng; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Yuejuan Cheng, MD. Department of Medical Oncology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 41 Damucang Hutong, Xicheng District, Beijing 100032, China. Email: chengyuejuan@pumch.cn.

Background: Pancreatic ductal adenocarcinoma (PDAC) with concurrent somatic BRAF V600E and germline BRCA2 mutations is exceedingly rare. While BRAF mutations define a distinct KRAS-wildtype subset, and BRCA2 mutations are associated with homologous recombination deficiency and sensitivity to platinum-based therapy/PARP inhibitors, the clinical behavior and optimal treatment strategy for tumors harboring both alterations remain unknown. This case report adds to the limited literature by detailing the therapeutic course and inherent challenges in managing this unique molecular subtype.

Case Description: A 61-year-old male underwent distal pancreatectomy for moderately differentiated PDAC (pT2N1M0). Molecular profiling revealed a somatic BRAF V600E mutation and a germline BRCA2 pathogenic mutation (p.F1241Vfs*17) with somatic second-hit inactivation (p.E2953*), indicating biallelic loss. Post-operative adjuvant gemcitabine/nab-paclitaxel was administered. Upon recurrence, platinum-based therapy (S-1/oxaliplatin) was poorly tolerated and ineffective. Subsequent olaparib maintenance achieved a transient partial response (PR) [progression-free survival (PFS): 5.5 months] before progression. Therapy was then switched to dabrafenib/trametinib (BRAF/MEK inhibition), which led to initial tumor shrinkage but was followed by rapid disease progression with malignant ascites. The patient died 22 months post-surgery despite combined targeted therapy and intraperitoneal chemotherapy.

Conclusions: This case highlights that the co-occurrence of BRAF V600E and biallelic BRCA2 mutations may confer a unique clinical phenotype with suboptimal or transient responses to both BRCA-directed therapies (platinum, olaparib) and BRAF/MEK inhibition. It underscores the complexity of precision oncology in PDAC, where genotype does not always predict therapeutic response, potentially due to factors like tumor heterogeneity, stromal barriers, or undiscovered resistance mechanisms. Future large-scale studies are needed to define prognostic implications and explore potential combination strategies (e.g., BRAF/MEK + PARP inhibitors) for this rare molecular cohort.

Keywords: BRAF V600E; BRCA2; case report; pancreatic cancer; targeted therapy

Submitted Oct 13, 2025. Accepted for publication Jan 15, 2026. Published online Feb 09, 2026.

doi: 10.21037/cco-2025-aw-132

Highlight box

Key findings

• This study reports a rare case of pancreatic ductal adenocarcinoma (PDAC) harboring concurrent somatic BRAF V600E mutation and biallelic inactivation of a germline BRCA2 mutation. The patient exhibited poor or only transient responses to standard BRCA-directed therapies (platinum-based chemotherapy and the PARP inhibitor olaparib) as well as to subsequent BRAF/MEK-targeted combination therapy (dabrafenib/trametinib), ultimately resulting in an unfavorable outcome.

What is known and what is new?

• It is known that BRAF V600E mutations are uncommon in PDAC, often associated with KRAS‑wildtype status, and BRAF/MEK inhibitors may show activity. Germline BRCA2 mutations lead to homologous recombination deficiency, sensitizing tumors to DNA-damaging agents (e.g., platinum) and PARP inhibitors. However, clinical data on PDAC with co-occurring BRAF V600E and biallelic BRCA2 mutations are lacking.

• This case provides the first detailed longitudinal treatment course and clinical challenges of such a double-mutant PDAC, suggesting inherent resistance to both classes of targeted therapy and highlighting a genotype-phenotype discrepancy.

What is the implication, and what should change now?

• This case indicates that current single-marker-guided strategies may be insufficient for PDAC with rare co-mutations. Clinicians should be aware of the complexity and potential primary resistance in such tumors. Future multicenter efforts are needed to collect more cases, define prognosis, and explore effective combination strategies. Dynamic molecular monitoring during treatment should be strengthened to uncover resistance mechanisms.

Introduction

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by insidious onset, rapid progression, and poor therapeutic outcomes, with the majority of patients diagnosed at an advanced stage. In recent years, the global incidence and mortality rates of PDAC have shown a consistent upward trend. According to the latest data from the National Cancer Center of China, PDAC currently ranks as the 10th most common cancer in terms of incidence and the 6th leading cause of cancer-related mortality (1). It is estimated that PDAC will become the second leading cause of cancer-related deaths by 2030.

Surgery remains the cornerstone of curative treatment for PDAC; however, only 15–20% of patients are eligible for resection, and even after surgery, the risk of recurrence and metastasis remains substantial (2-4). For patients with locally advanced or metastatic disease who are not surgical candidates, first-line chemotherapy regimens, including FOLFIRINOX (folinic acid, oxaliplatin, fluorouracil, and irinotecan), NALIRIFOX (nanoliposomal irinotecan, fluorouracil, and oxaliplatin), and nab-paclitaxel plus gemcitabine, have demonstrated modest survival benefits, although the overall therapeutic gains remain limited. Despite extensive research efforts, targeted therapies directed at pathways such as vascular endothelial growth factor, epidermal growth factor receptor, MEK, fibroblast growth factor receptor, phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR), and cancer stem cells have not yet achieved significant clinical efficacy. Nonetheless, precision medicine guided by molecular profiling is increasingly emerging as a promising therapeutic paradigm in PDAC management.

In PDAC, KRAS mutations are present in over 90% of cases, driving uncontrolled cell proliferation through the activation of the RAF/MEK/ERK and PI3K/AKT signaling pathways (5). The targeted inhibition of KRAS and its critical downstream effectors represents a promising strategy for the effective clinical management of PDAC. BRAF, another key molecule downstream of KRAS, is mutated in approximately 4% of PDAC patients, with BRAF V600E mutation accounting for 20% to 30% of these cases (6).

In addition to somatic genetic alterations, a subset of PDAC cases is linked to hereditary factors, most notably germline mutations in the BRCA1/2 genes. Pathogenic or likely pathogenic germline mutations in BRCA1/2 are identified in approximately 4% to 7% of PDAC patients (7). Previous studies have demonstrated that PDAC harboring mutations in BRCA1/2 genes exhibit heightened sensitivity to platinum-based chemotherapy and the PARP inhibitor olaparib. Notably, among patients with advanced PDAC receiving platinum-based regimens, those with BRCA1/2 germline mutations show a marked improvement in overall survival (8,9).

Here we present a case of PDAC characterized by concurrent somatic BRAF V600E mutation and germline BRCA2 mutation. The patient demonstrated a suboptimal response to both platinum-based chemotherapy and molecularly targeted therapy. We present this article in accordance with the CARE reporting checklist (available at https://cco.amegroups.com/article/view/10.21037/cco-2025-aw-132/rc).

Case presentation

A 61-year-old male patient presented with epigastric discomfort and had an abdominal contrast-enhanced computed tomography (CT) scan at another hospital on February 2, 2023, which revealed a cystic-solid mass in the pancreatic tail, highly suggestive of malignancy. Serum tumor markers, including carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9), were within normal ranges. On February 23, 2023, he underwent a laparoscopic distal pancreatectomy with splenectomy. Postoperative pathology confirmed moderately differentiated PDAC in the body and tail of the pancreas, measuring approximately 2.7 cm × 2.1 cm × 3.4 cm, with perineural and lymphovascular invasion, as well as lymph node metastasis (4/13). Immunohistochemistry staining demonstrated intact expression of mismatch repair proteins and strong positivity for BRAF V600E in tumor cells. Next-generation sequencing analysis identified a pathogenic germline BRCA2 mutation (p.F1241Vfs*17) and a somatic BRAF activating mutation (p.V600E). The presence of a second, somatic BRCA2-inactivating mutation (p.E2953*) in the tumor indicated complete loss of homologous recombination repair function. The tumor was microsatellite stable and exhibited a low tumor mutational burden (1.08 mutations/Mb).

From March 31, 2023, to September 14, 2023, the patient received six cycles of postoperative adjuvant chemotherapy with gemcitabine and nab-paclitaxel at Peking Union Medical College Hospital, followed by regular follow-up examinations. In December 2023, a contrast-enhanced CT scan detected a nodule in the surgical area with increased uptake on PETCT scan, and disease recurrence was diagnosed. Given the presence of germline BRCA2 mutation, a platinum-based regimen (S-1 plus oxaliplatin) was administered for three cycles. However, the patient exhibited poor tolerance to the treatment, and follow-up CT scans showed no reduction in the size of the tumor. The patient declined further chemotherapy. On March 30, 2024, the treatment was switched to oral olaparib at a dose of 300 mg twice daily (four capsules per day). After two weeks, due to persistent nausea, the dose was reduced to three capsules daily, which alleviated the nausea symptoms. On June 12, 2024, follow-up imaging showed tumor shrinkage, and the therapeutic response was assessed as a partial response (PR). By September 9, 2024, a follow-up CT scan demonstrated significant enlargement of the tumor, measuring approximately 5.6 cm × 3.5 cm. Multiple nodular peritoneal metastases and ascites were also presented. The patient developed abdominal distension and fever with a maximum body temperature of 39 ℃ which did not respond to antibiotic therapy, hence was considered as cancer related. The therapeutic response was assessed as progressive disease (PD). On September 13, 2024, the treatment regimen was switched to dabrafenib combined with trametinib, and the patient’s body temperature normalized afterward. A follow-up CT scan on November 5, 2024, showed a reduction of the tumor size with the largest cross-section measuring 2.8 cm × 1.6 cm. However, abdominal and pelvic effusion had significantly increased (Figures 1,2). Malignant cells were identified in the ascitic fluid. The patient continued treatment with dabrafenib and trametinib, along with intraperitoneal 5-fluorouracil (5-FU) chemotherapy, but no further clinical improvement was achieved. The patient died on December 7, 2024, with an overall survival of 22 months since the surgery (Figure 3).

Figure 1 Changes in CT images. Recurrent disease in the pancreatic surgical area. The red arrows indicate tumor lesions. CT, computed tomography.
Figure 2 Changes in CT images. Progressive increase in abdominal and pelvic fluid accumulation. CT, computed tomography.
Figure 3 Flow chart of treatment. PD, progressive disease; PFS, progression-free survival.

The patient has no history of chronic diseases. In the family history, the father died of esophageal cancer.

All procedures performed in this study were in accordance with the ethical standards of the Ethics Committees of Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, and Peking Union Medical College, and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

In this case report, we present the treatment course of a patient with a rare co-occurrence of somatic BRAF V600E and germline BRCA2 mutations, highlighting the unique molecular characteristics that might lead to the ineffectiveness of standard anti-tumor therapies.

BRCA1/2 gene play a critical role in homologous recombination repair. Germline pathogenic or likely pathogenic mutations in BRCA1/2 significantly elevate the risk of breast, ovarian, pancreatic, and prostate cancers (10-12). Approximately 5% of PDAC patients harbor BRCA1/2 germline mutations. PDAC with BRCA germline mutations are frequently accompanied by loss of heterozygosity (LOH) of BRCA, resulting in homologous recombination deficiency due to the absence of normal BRCA gene product activity, which compromises effective DNA damage repair (DDR) (13). Platinum-based chemotherapeutic agents exert their anti-tumor effects by inducing DNA damage. Previous studies have demonstrated that PDAC patients with BRCA germline mutations exhibit an 83% response rate to platinum-based chemotherapy, establishing it as a highly effective treatment strategy (14). The POLO trial, a randomized, double-blind, placebo-controlled phase III study, evaluated the efficacy of olaparib as maintenance therapy in patients with metastatic PDAC who had received platinum-based first-line treatment for more than 16 weeks without disease progression and who carried BRCA1/2 germline mutations (9). The results revealed that the olaparib maintenance group had a significantly longer median progression-free survival (PFS) compared to the placebo group (7.4 vs. 3.8 months, P=0.004). Consequently, olaparib has been approved by the U.S. Food and Drug Administration as a first-line maintenance therapy for metastatic PDAC patients with pathogenic or likely pathogenic BRCA germline mutations. In this case, the patient carried a definitive pathogenic BRCA2 germline mutation and a somatic second-hit mutation, which genetically constituted biallelic inactivation. However, no significant therapeutic response was observed to first-line platinum-based therapy, with even slight progression of the lesions and poor tolerance. After switching to olaparib, the best therapeutic outcome achieved was a PR, yet the PFS was only 5.5 months.

This phenomenon may be associated with the absence of BRCA LOH, indicating a discrepancy between genotype and functional phenotype. Studies have demonstrated that PDAC associated with pathogenic BRCA germline variants typically exhibits BRCA LOH, resulting in defective DDR due to the loss of normal BRCA gene product activity. In such cases, platinum-based therapies have been shown to be highly effective. Conversely, in patients with pathogenic BRCA germline mutations but without BRCA LOH, the therapeutic efficacy of platinum-based regimens in PDAC is significantly diminished (15,16).

Furthermore, the patient concurrently carried a BRAF V600E mutation, which may serve as a potential contributing factor to the suboptimal therapeutic responses observed above. This case belongs to the rare KRAS wild-type subtype of PDAC. Over 90% of PDAC cases are driven by oncogenic KRAS mutations, while the approximately 5–10% of KRAS wild-type tumors constitute a distinct group characterized by heterogeneity in etiology, molecular features, and potential therapeutic strategies (17). Previous studies have demonstrated that BRAF and KRAS mutations are typically mutually exclusive in PDAC, with BRAF mutations occurring in approximately 30% of KRAS wild-type PDAC patients (18,19). Therefore, the BRAF V600E mutation not only represents a driver molecular event in this case but also serves as a key marker of its KRAS wild-type status.

Due to the rarity of BRAF V600E mutations in PDAC, large-scale studies are lacking. Previous case reports have shown that metastatic PDAC with BRAF V600E mutations exhibited at least a PR to BRAF/MEK inhibitors (20). Based on this, the combination of dabrafenib and trametinib has been incorporated into guidelines as one of the treatment options for patients with BRAF V600E mutation-positive metastatic PDAC who have failed prior therapies. Furthermore, vemurafenib has demonstrated clinical activity in various non-melanoma cancers harboring BRAF V600E mutations (e.g., non-small cell lung cancer, thyroid cancer, hairy cell leukemia), although its efficacy is often limited by resistance mechanisms and tumor heterogeneity (21). A study involving only two PDAC patients, one of whom achieved stable disease for nearly 7 months, provides insufficient evidence to draw definitive conclusions regarding the efficacy of vemurafenib in BRAF V600E-mutated PDAC. In the present case, the patient received two cycles of dabrafenib combined with trametinib. Follow-up CT scans revealed a significant increase in abdominal and pelvic effusion, with malignant cells identified in the fluid. Overall, the disease was assessed as progressive, indicating limited efficacy of the dabrafenib and trametinib combination therapy.

Resistance to the combination of dabrafenib and trametinib may arise not only from common mechanisms such as reactivation of the MAPK pathway or activation of alternative signaling pathways (e.g., PI3K-AKT-mTOR) to sustain cell proliferation but also from the intrinsic biological features of PDAC. Firstly, PDAC is characterized by a highly fibrotic stroma, which can hinder drug delivery and reduce the effective concentration of dabrafenib and trametinib within tumor tissues (22). Secondly, PDAC demonstrates pronounced intratumoral heterogeneity, with the BRAF V600E mutation potentially confined to a subset of tumor cells. Other tumor cell populations may depend on alternative driver mutations, limiting the efficacy of targeted therapy against the entire tumor (23). Furthermore, PDAC cells may develop new mutations or undergo phenotypic changes during prior treatments, contributing to resistance against the combination therapy (23). However, given the limited data, the therapeutic efficacy of BRAF/MEK inhibitors in BRAF V600E-mutated PDAC require further exploration in larger cohorts.

For patients with concurrent BRAF V600E and BRCA2 mutations, combined therapy with BRAF V600E-targeted therapy and PARP inhibitors may represent a potential therapeutic strategy. However, this approach is associated with high costs, and its efficacy remains unknown. Given this patient’s compromised general condition, the combined regimen was not deemed appropriate. Currently, the development of multi-target combination therapies guided by tumor molecular profiling has emerged as a significant research focus in precision oncology, though further clinical data accumulation remains imperative.

Conclusions

Currently, there is limited data on malignancies with concurrent BRAF V600E and germline BRCA2 mutations. Large-scale studies are warranted to elucidate the prognostic significance and therapeutic implications of co-occurring BRAF and BRCA mutations. Potential effective treatment strategies for these patients may include single or combination therapies targeting BRAF, MEK, and PARP inhibitors. However, the underlying mechanisms require further validation through preclinical research.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://cco.amegroups.com/article/view/10.21037/cco-2025-aw-132/rc

Peer Review File: Available at https://cco.amegroups.com/article/view/10.21037/cco-2025-aw-132/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cco.amegroups.com/article/view/10.21037/cco-2025-aw-132/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the Ethics Committees of Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, and Peking Union Medical College, and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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Cite this article as: Ma X, Guan M, Li N, Liu Y, Wu H, Cheng Y, Ba Y. Treatment of metastatic pancreatic cancer with concurrent BRAF V600E mutation and germline BRCA2 mutation: a case report. Chin Clin Oncol 2026;15(1):13. doi: 10.21037/cco-2025-aw-132

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