Cureus · 2026

Редкий случай плазмабластической миеломы с двойным Каппой и Lambda mRNA экспрессией, представляющий себя как одинокая тяжёлая опухоль.

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Tanaka K, Hasegawa M, Katsumi A

Аннотация

Плазмабластическая миелома является агрессивным вариантом миэломы плазменных клеток, которая может имитировать плазмобластную лимфому, когда она представляет собой одиночную массу. Двойное выражение каппы и лямбды светоцепной цепи является исключительно редким и может быть упущено, если оценка основывается только на обнаружении уровня протеина. Мы сообщаем о случае с женщиной в 80 лет, которая подавала опухоль с левым опухолью и перерезала одинокий опухоль и опухоль. Гистология показала, что листы больших плазмбластических клеток являются положительными для CD38, CD138, множественной миэломы онкогене. 1, и иммуноглобулин G, и отрицательный для маркеров B-клеток и Эпштейн-Барр с вирусом RNA. В течение нескольких недель у нее развилась болезнь, тошнота и пэнтикопенсия. Лабораторные исследования выявили повышенную лактатную дегидрогеназу и сыворотку иммуноглобулин G 4,409 мг/дл с иммунопарезом. Свободные от сыворотки слегка возвышенные каппа и заметно повышенная лямбда с соотношением каппа/ламбда 0.02. Позитронный эмиссионный томографический анализ показал диффузное скелетное и селезеночное фтор-деоксиглукоза-позитивное поглощение без дополнительных экстрамульгальных повреждений, что подтверждает, что опухоль жесткого палата является единственным дополнительным местом. Анализ костного мозга показал заметную гиперклеточную стойкость с широкой заменой клетками плазменной плазмы, выражающими циклин D1, в то время как исследования вируса Эпштейн-Барр и анапластической лимфатической киназы были отрицательными. Светоцепная иммунохимия показала отсутствие пятен каппы и лямбды в лишь небольшой поднаборе клеток опухоли, в то время как RNA in situ гибридизация продемонстрировала двойное светоцепное резиновое выражение RNA в большинстве клеток опухоли. Цитогенетический анализ выявил амплификацию 1q21, исключение 17p13, и реструктуризацию тяжёлой цепи иммуноглобулина/МАФ. Несмотря на высокодозированный дексаметазон, последовательный протеозный ингибитор... anti-CD38 :: лечение антитела и иммуномудулятора на основе лекарств, за которым следует антигенная зрелость B-клеток х CD3, диагностика антител, болезнь осталась неизлечимой, и пациент умер. 45 Через несколько дней после диагноза. Это дело подчеркивает, что тесты светоцепных систем на основе транскрипции могут обнаруживать исключительно редкие двойные выражения каппы и лямбды, когда белковые анализы являются отрицательными или вводящими в заблуждение. В случае одиночных плазмбластических повреждений комплексная клинкопатологическая оценка, включая исследования вируса циклина D1, вируса Эпштейна-Барра и гибридизации РНК in situ, имеет решающее значение для точного диагноза и признания этого очень агрессивного подтипа.

Оригинал публикации

A Rare Case of Plasmablastic Myeloma With Dual Kappa and Lambda mRNA Expression Presenting as a Solitary Hard Palate Tumor.

Plasmablastic myeloma is an aggressive variant of plasma cell myeloma that can mimic plasmablastic lymphoma when it presents as a solitary mass. Dual kappa and lambda light-chain expression is exceptionally rare and may be missed if evaluation relies on protein-level detection alone. We report the case of a woman in her 80s who presented with left hard palate swelling and underwent resection of a solitary hard palate and maxillary tumor. Histology showed sheets of large plasmablastic cells positive for CD38, CD138, multiple myeloma oncogene 1, and immunoglobulin G, and negative for B-cell markers and Epstein-Barr virus-encoded RNA. Within weeks, she developed malaise, nausea, and pancytopenia. Laboratory studies revealed elevated lactate dehydrogenase and serum immunoglobulin G of 4,409 mg/dL with immunoparesis. Serum free light chains showed mildly elevated kappa and markedly elevated lambda, with a kappa/lambda ratio of 0.02. Positron emission tomography-computed tomography demonstrated diffuse skeletal and splenic fluorodeoxyglucose uptake without additional extramedullary lesions, confirming the hard palate tumor as the only extramedullary site. Bone marrow examination showed marked hypercellularity with extensive replacement by plasmablastic plasma cells expressing cyclin D1, while Epstein-Barr virus studies and anaplastic lymphoma kinase were negative. Light-chain immunohistochemistry showed absent kappa staining and lambda staining in only a small subset of tumor cells, whereas RNA in situ hybridization demonstrated dual light-chain messenger RNA expression in most tumor cells. Cytogenetic analysis revealed 1q21 amplification, deletion of 17p13, and immunoglobulin heavy chain/MAF rearrangement. Despite high-dose dexamethasone, sequential proteasome inhibitor-, anti-CD38 antibody-, and immunomodulatory drug-based therapies, followed by B-cell maturation antigen × CD3 bispecific antibody treatment, the disease remained refractory and the patient died 45 days after diagnosis. This case highlights that transcript-based light-chain testing can uncover exceptionally rare dual kappa and lambda expressions when protein assays are negative or misleading. In solitary plasmablastic lesions, integrated clinicopathological assessment, including cyclin D1, Epstein-Barr virus studies, and RNA in situ hybridization, is critical for accurate diagnosis and recognition of this highly aggressive subtype.

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This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Introduction

Plasmablastic myeloma is an uncommon and aggressive morphologic variant of plasma cell myeloma. In a classic morphologic series, the plasmablastic subtype accounted for 15% of untreated myeloma cases and was associated with markedly shorter survival than other morphologic subtypes [ 1 ]. Diagnostic difficulty is greatest when plasmablastic morphology presents as a solitary oral or maxillofacial mass, because plasmablastic myeloma and plasmablastic lymphoma share large-cell morphology, loss of pan-B-cell markers, and expression of plasma cell-associated antigens [ 2 - 6 ].

Accurate classification therefore requires integrated clinical, serologic, radiologic, and pathologic assessment. Features favoring plasmablastic myeloma include marrow-based plasma cell disease, a monoclonal serum immunoglobulin, myeloma-associated cytogenetic abnormalities, and cyclin D1 expression in an appropriate context, whereas oral cavity predilection, immunodeficiency, Epstein-Barr virus association, and MYC-related biology more often favor plasmablastic lymphoma, although exceptions and overlap are well recognized [ 2 - 7 ]. Clonal plasma cell neoplasms usually show either kappa or lambda light-chain restriction because of allelic exclusion. Accordingly, dual kappa and lambda expression is exceptionally rare and has been reported only in isolated case reports and small series [ 8 - 10 ].

We report an unusual case of plasmablastic myeloma initially presenting as a solitary hard palate tumor in which protein-level light-chain staining was misleading, whereas RNA in situ hybridization disclosed dual kappa and lambda light-chain messenger RNA expression. The case illustrates how transcript-based light-chain testing can refine diagnosis when a plasmablastic oral lesion raises concern for plasmablastic lymphoma.

Case presentation

A Japanese woman in her 80s with a remote history of cervical cancer treated by total hysterectomy in her forties presented with swelling of the left hard palate. She had no regular medications, no known allergies, no smoking or alcohol history, and no family history of hematologic disease.

She initially noticed a left hard palate and maxillary swelling several months before hospital admission. The symptoms temporarily improved after dental treatment, but subsequently recurred and progressed. She underwent surgical resection of a hard palate and maxillary tumor with multiple tooth extractions at an outside hospital.

Histologic examination of the oral lesion showed diffuse sheets of large plasmablastic cells with prominent nucleoli. Immunohistochemistry demonstrated plasma cell differentiation with CD138 positivity and immunoglobulin G positivity, with loss of B-cell markers. CD20 was negative, and CD79a was negative on subsequent staining. Epstein-Barr virus-encoded RNA (EBER) in situ hybridization was negative. Light-chain immunohistochemistry in the oral lesion was not definitively restrictive, showing only weak lambda staining and negative kappa staining. No additional extramedullary lesions were identified clinically at that time.

Within weeks of surgery, the patient developed malaise, nausea, and rapidly progressive cytopenias and was referred to our institution. On admission, vital signs were stable, chest examination was unremarkable, and the hard palate tumor had already been resected with no apparent residual mass.

Key admission laboratory findings are summarized in Table 1 .

Table 1
Key laboratory findings at admission HHV-8: human herpesvirus 8; HIV-1: human immunodeficiency virus type 1; HTLV-1: human T-cell leukemia virus type 1; Ig: immunoglobulin.

Hemoglobin	6.5 g/dL	14-18 g/dL	Severe anemia
Lactate dehydrogenase	1,739 U/L	124–222 U/L	Markedly elevated
Albumin	3.3 g/dL	4.1–5.1 g/dL	Low
IgG	4,409 mg/dL	861–1,747 mg/dL	Markedly elevated
IgA	10 mg/dL	93–393 mg/dL	Suppressed
IgM	8 mg/dL	50–269 mg/dL	Suppressed
Free kappa light chain	27.1 mg/L	3.3–19.4 mg/L	Mildly elevated
Free lambda light chain	1,137 mg/L	5.7–26.3 mg/L	Markedly elevated
Kappa/lambda ratio	0.02	0.26–1.65	Markedly decreased
Beta-2 microglobulin	7.8 mg/L	0.9–2.0 mg/L	Elevated
HIV-1 serology	Negative	Negative	No evidence of HIV infection
HTLV-1 serology	Negative	Negative	No evidence of HTLV-1 infection
HHV-8 serology	Negative	Negative	No evidence of HHV-8 infection

The patient had pancytopenia, markedly elevated lactate dehydrogenase, hypoalbuminemia, marked IgG elevation with immunoparesis, and striking lambda-predominant free light-chain excess. Viral serologies, including human immunodeficiency virus type 1, human T-cell leukemia virus type 1, and human herpesvirus 8, were negative.

A skeletal survey did not show overt lytic lesions. Positron emission tomography-computed tomography demonstrated diffuse fluorodeoxyglucose uptake throughout the skeleton and diffuse splenic uptake, consistent with systemic myeloma involvement (Figure 1 ).

Figure 1 Positron emission tomography-computed tomography image of the patient. Positron emission tomography-computed tomography demonstrated diffuse fluorodeoxyglucose uptake thr… — Figure 1 Positron emission tomography-computed tomography image of the patient. Positron emission tomography-computed tomography demonstrated diffuse fluorodeoxyglucose uptake throughout the skeleton and diffuse splenic uptake.

Importantly, no additional extramedullary lesions were detected beyond the previously resected hard palate tumor, supporting that the oral tumor represented the only extramedullary site.

Bone marrow aspirate and clot sections showed a markedly hypercellular marrow, with approximately 90% cellularity, extensively replaced by large plasmablastic plasma cells. The neoplastic cells expressed CD38 and CD138 and were positive for multiple myeloma oncogene 1. Cyclin D1 was positive. Epstein-Barr virus-encoded RNA in situ hybridization and anaplastic lymphoma kinase were negative. Flow cytometry demonstrated very low surface immunoglobulin expression overall, with small fractions showing surface light-chain signals, including surface kappa in 0.2% and surface lambda in 6.3% of cells within the relevant gate, consistent with clonal plasmablastic differentiation.

A central diagnostic feature of this case was the discrepancy between light-chain detection at the protein and messenger RNA levels. Protein-level immunohistochemistry showed absent kappa staining in neoplastic plasma cells and lambda positivity in only a small subset of tumor cells, approximately 5%. In contrast, RNA in situ hybridization for immunoglobulin light chains demonstrated dual light-chain messenger RNA expression, with kappa messenger RNA in approximately 70% and lambda messenger RNA in approximately 80% of tumor cells (Figure 2 ). Thus, the tumor showed widespread transcription of both light-chain genes despite minimal detectable light-chain protein by immunohistochemistry.

Figure 2 Bone marrow findings in plasmablastic myeloma with dual kappa and lambda light-chain messenger RNA expression Hematoxylin and eosin staining (A, D) shows marrow infiltrat… — Figure 2 Bone marrow findings in plasmablastic myeloma with dual kappa and lambda light-chain messenger RNA expression Hematoxylin and eosin staining (A, D) shows marrow infiltration by plasmablastic cells. Immunohistochemistry demonstrates absent kappa staining (B) and only focal lambda staining (C). In contrast, RNA in situ hybridization demonstrates widespread kappa (E) and lambda (F) messenger RNA expression in most tumor cells on serial sections, highlighting the discrepancy between protein-level and transcript-level light-chain assessment. Scale bars = 100 μm.

Fluorescence in situ hybridization demonstrated high-risk cytogenetic abnormalities, including 1q21 amplification involving CKS1B in 21%, deletion of 17p13, del(17p13), involving TP53 in 25%, and immunoglobulin heavy chain/MAF rearrangement in 31.5%, while immunoglobulin heavy chain/FGFR3 rearrangement was negative. Conventional karyotyping showed t(7;8)(p12;q24.1) and complex karyotypes. Fluorescence in situ hybridization for MYC was not performed.

The integrated findings favored plasmablastic myeloma rather than plasmablastic lymphoma. Specifically, the patient had extensive marrow replacement by plasmablastic plasma cells, a prominent serum IgG monoclonal component with lambda-predominant free light-chain secretion, cyclin D1 positivity, EBER negativity, and myeloma-associated high-risk cytogenetic abnormalities. These key diagnostic features are summarized in Table 2 .

Table 2
Integrated findings supporting plasmablastic myeloma in the differential diagnosis

Diagnostic domain	Finding in the present case	Interpretation
Clinical pattern	Rapid systemic deterioration after resection of a solitary hard palate lesion	Suggests that the oral lesion was part of disseminated plasma cell disease rather than isolated lymphoma
Serum studies	IgG 4,409 mg/dL with marked immunoparesis and lambda-predominant free light-chain excess	Strongly supports a secretory plasma cell neoplasm
Imaging	Diffuse skeletal and splenic FDG uptake without other soft-tissue lesions	Supports systemic myeloma with a solitary extramedullary oral site
Bone marrow	Markedly hypercellular marrow extensively replaced by plasmablastic plasma cells	Favors marrow-based plasma cell myeloma
Plasma cell markers	CD38+, CD138+, MUM1+	Consistent with plasmacytic differentiation
Lymphoma-associated exclusions	CD20-, CD79a-, ALK-, EBER-ISH negative	Makes classic oral plasmablastic lymphoma less likely in this context
Additional supportive marker	Cyclin D1 positive	Supports plasma cell myeloma in the clinicopathologic setting
Light-chain studies	Kappa IHC absent, lambda IHC focal, but dual kappa/lambda mRNA expression by RNA-ISH	Demonstrates that protein-level staining was misleading and that transcript-based testing added diagnostic value
Cytogenetics	1q21 amplification, del(17p13), IGH/MAF rearrangement	Supports high-risk myeloma biology

Because of rapid clinical and biochemical progression, high-dose dexamethasone was initiated. The patient then sequentially received daratumumab, bortezomib, and dexamethasone, but the disease progressed. Therapy was changed to isatuximab, carfilzomib, and dexamethasone, with carfilzomib dose reduction because of concern for toxicity, but progression continued. Lenalidomide and dexamethasone were then started, again without response. Because the disease was refractory after exposure to a proteasome inhibitor, anti-CD38 antibody therapies, and an immunomodulatory drug, B-cell maturation antigen × CD3 bispecific antibody therapy with elranatamab was initiated with step-up dosing. Cytokine release syndrome was limited to transient grade 1 fever without significant neurotoxicity, but there was no meaningful biochemical or clinical response. Supportive care included transfusions and denosumab for skeletal-related complications and hypercalcemia risk. A central venous port was placed but was complicated by hematoma, limiting its use. The treatment sequence, clinical rationale, response assessment, and toxicities are summarized in Table 3 .

Table 3
Treatment course, rationale, response, and toxicity

Approximate timing	Regimen	Clinical rationale	Response / reason for discontinuation	Toxicity / complication
Immediately after diagnosis	High-dose dexamethasone	Rapid cytoreduction in fulminant plasmablastic disease	Inadequate disease control	No specific major toxicity documented
First myeloma regimen	Daratumumab + bortezomib + dexamethasone	Standard anti-CD38/proteasome inhibitor-based urgent therapy	Progressive disease	No regimen-limiting organ-specific toxicity documented before progression
Second myeloma regimen	Isatuximab + carfilzomib + dexamethasone	Escalation after early progression on prior anti-CD38/proteasome inhibitor-based approach	Progressive disease	Carfilzomib dose reduction for anticipated frailty-related cardiorenal risk; no clear documented severe carfilzomib-specific event before progression
Third regimen	Lenalidomide + dexamethasone	Addition of IMiD class after refractory disease	No meaningful response	No major new regimen-limiting toxicity documented
Salvage immunotherapy	Elranatamab with step-up dosing	BCMA-directed therapy after multi-class refractory disease	No meaningful biochemical or clinical response	Grade 1 cytokine release syndrome with transient fever; no significant neurotoxicity

Despite intensive therapy and supportive measures, the disease remained refractory and rapidly progressive. The patient died 45 days after diagnosis.

The clinical course proceeded as follows. Initial oral symptoms developed several months before admission, and the oral lesion subsequently progressed. The hard palate tumor was resected before referral. Systemic evaluation and bone marrow sampling were performed on postoperative day 21, hospital admission and diagnostic confirmation occurred on postoperative day 23, high-dose dexamethasone began on postoperative day 24, sequential myeloma regimens were administered from postoperative day 27, B-cell maturation antigen-directed bispecific therapy began on postoperative day 52, and the patient died on postoperative day 68.

The postoperative clinical course is summarized in Figure 3 .

Figure 3 Postoperative clinical timeline Chronological postoperative sequence after hard palate/maxillary tumor resection is shown. The timeline highlights rapid postoperative dia… — Figure 3 Postoperative clinical timeline Chronological postoperative sequence after hard palate/maxillary tumor resection is shown. The timeline highlights rapid postoperative diagnostic confirmation, early initiation of anti-myeloma therapy, refractory progression through sequential regimens, elranatamab step-up dosing on POD 52, and death on POD 68. POD: Postoperative day.

Discussion

This case highlights two related diagnostic problems: first, the challenge of distinguishing plasmablastic myeloma from plasmablastic lymphoma when the presenting lesion is a solitary oral mass; and second, the value of RNA-based light-chain testing when protein-level assays are weak or discordant.

The oral cavity is a classic site of presentation for plasmablastic lymphoma, and oral/maxillofacial plasmablastic lesions require careful differential diagnosis [ 5 - 7 , 11 , 12 ]. Prior reports have also documented hard palate plasmablastic myeloma, including an extraskeletal palatal plasmablastic myeloma reported by Kumar et al. [ 13 ]. Compared with that previously reported palatal case, the present patient was substantially older and showed diffuse marrow replacement, secretory IgG-lambda disease, and extremely rapid fatal progression over only 45 days after diagnosis. These features strongly supported systemic plasmablastic myeloma with a solitary extramedullary hard palate manifestation rather than primary oral plasmablastic lymphoma.

RNA in situ hybridization was particularly important in this case because protein-level light-chain staining was misleading. Bright-field RNA-based assays for kappa and lambda transcripts have been shown to improve assessment of B-cell clonality in tissue and cytology specimens, especially when conventional immunohistochemistry is weak or noncontributory [ 14 , 15 ]. In diagnostically difficult plasmablastic neoplasms, demonstration of light-chain expression can materially affect classification, because light-chain-restricted lesions may align more closely with plasma cell neoplasia than with “true” plasmablastic lymphoma in some settings [ 6 ]. In the present case, RNA in situ hybridization did not merely confirm clonality; it disclosed biologically unusual dual kappa and lambda light-chain transcription that was not evident on immunohistochemistry and that helped explain the discrepancy between tissue staining and serum studies.

The adverse clinical course was most likely driven by the aggregate high-risk biology of the disease rather than by lambda predominance itself. Plasmablastic morphology has long been associated with aggressive behavior [ 1 ]. In addition, this patient had extramedullary disease, markedly elevated lactate dehydrogenase, 1q21 amplification, del(17p13), and IGH/MAF rearrangement, all of which are features associated with high-risk multiple myeloma and treatment resistance [ 16 - 20 ]. Recent data further suggest that extramedullary disease, particularly soft-tissue disease independent of bone, confers inferior outcomes even in the era of modern therapy [ 19 ]. Accordingly, the lambda-dominant secretory pattern in this case should be interpreted as a descriptive biologic feature rather than the principal explanation for the poor outcome.

Overall, this case emphasizes that solitary oral plasmablastic lesions should not be diagnosed on morphology alone. Integrated clinicopathological evaluation, including serum monoclonal protein studies, bone marrow assessment, EBV testing, cyclin D1, and, where needed, transcript-based light-chain testing, is critical for correct classification.

Conclusions

Plasmablastic myeloma can present as a solitary hard palate tumor and may closely mimic plasmablastic lymphoma. In this case, light-chain immunohistochemistry was misleading, whereas RNA in situ hybridization demonstrated dual kappa and lambda messenger RNA expression and materially strengthened diagnostic interpretation. When evaluating oral or maxillary plasmablastic lesions, integrated clinicopathological correlation is essential, and RNA-based light-chain testing should be considered when protein-level assays are weak, negative, or discordant with serum findings.

Acknowledgments

Ken Tanaka was supported by the 2023–2024 Quad Fellowship, an initiative of the governments of Australia, India, Japan, and the United States. We thank the Quad Fellowship for its support of this project.

Funding Statement

This study was supported in part by the 2023-2024 Quad Fellowship to KT, the Grant of Japan Health Research Promotion Bureau Project Fund (JHP2025-B-02), JSPS KAKENHI (Grant Number: 22K08518, 25K11680) and the Research Funding for Longevity Sciences (25-11) from the National Center for Geriatrics and Gerontology to AK.

Disclosures

Human subjects: Informed consent for treatment and open access publication was obtained or waived by all participants in this study. National Center for Geriatrics and Gerontology Institutional Review Boards issued approval 1835. This study was conducted in accordance with the ethical principles of the Declaration of Helsinki and approved by the National Center for Geriatrics and Gerontology Institutional Review Boards (No. 1835).

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following:

Payment/services info: This study was supported in part by the 2023-2024 Quad Fellowship to KT, the Grant of Japan Health Research Promotion Bureau Project Fund (JHP2025-B-02), JSPS KAKENHI (Grant Number: 22K08518, 25K11680) and the Research Funding for Longevity Sciences (25-11) from the National Center for Geriatrics and Gerontology to AK.

Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work.

Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Author Contributions

Concept and design: Akira Katsumi, Ken Tanaka, Masaki Hasegawa

Acquisition, analysis, or interpretation of data: Akira Katsumi, Ken Tanaka, Masaki Hasegawa

Critical review of the manuscript for important intellectual content: Akira Katsumi, Ken Tanaka, Masaki Hasegawa

Supervision: Akira Katsumi, Masaki Hasegawa

Drafting of the manuscript: Ken Tanaka

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