Mantle Cell Lymphoma

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Primary Author(s)*

  • Mahsa Khanlari, MD
  • Zhenya Tang, MD, PhD

The University Of Texas MD Anderson Cancer Center, Department of Hematopathology, Houston, Texas

Cancer Category/Type

Cancer Sub-Classification / Subtype

Definition / Description of Disease

  • Clinically aggressive, mature B cell lymphoma
  • Small to medium sized lymphoid cells (monomorphic, except in pleomorphic variant)
  • Associated with t(11;14)(q13;q32) and cyclin D1 overexpression in over 95% of cases

Synonyms / Terminology

Obsolete names:

  • Centrocytic malignant lymphoma (obsolete) [1]
  • Lymphocytic lymphoma of intermediate differentiation [2]
  • Mantle zone lymphoma [3]
  • Malignant lymphomatous polyposis
  • in situ mantle cell lymphoma (for in situ mantle cell neoplasia)

Epidemiology / Prevalence

  • ~ 7% of B cell lymphomas [4]
  • 2.5%-10% of non-Hodgkin lymphomas [5]
  • Age adjusted incidence: 0.7/100,000 person years in white population in USA [6]
  • Median age: 60 years[7]
  • M:F = 3:1 (range, 1.6-6.8 :1)[8]

Clinical Features[9]

  • Approximately 70% with stage IV disease at presentation
    • Generalized lymphadenopathy, hepatosplenomegaly and bone marrow involvement
    • 40-50% with B symptoms
    • Two subtypes based on clinical presentation:
      • More aggressive, with SOX11 overexpression (SOX11+disease), nodal presentation (the most common subtype)
      • More indolent, without SOX11 expression (SOX11-disease), leukemic presentation, and non-nodal disease
  • Peripheral blood:
    • Atypical lymphoid cells: present virtually in all cases by flow cytometry [10]
      • Atypical lymphoid cells can be detected in the peripheral blood in the absence of lymphocytosis
      • Leukemic involvement: 20 - 70% of patients at diagnosis
      • Leukemic involvement is usually a the sign of disease progression
    • Blastoid morphology of the circulating lymphoma cells may mimic acute leukemia
    • A leukemic phase with no or minimal lymph node involvement is possible, Leukemic Non-Nodal Mantle Cell Lymphoma
      • Asymptomatic for long period
      • Splenomegaly
    • Anemia and thrombocytopenia (10%- 40%)
  • Multiple intestinal polyps (lymphomatous polyposis)
  • Progress to blastoid / pleomorphic variant
    • At the time of relapse (~22%)

Sites of Involvement

  • Lymph node
  • Bone marrow involvement independent of peripheral blood (50 - 90%), peripheral blood (20 - 70%), spleen (~50%), liver (~20%) [11][12][13]
  • Frequent extranodal site involvement : gastrointestinal tract, Waldeyer ring, lungs, pleura, skin, CNS
    • CNS involvement may occur mostly at the time of relapse[14]
  • Extranodal involvement without lymphadenopathies: 4 - 15%

Morphologic Features

  • Architectural pattern: Diffuse > nodular > mantle zone growth patterns
    • Nodal (> 50% nodular), diffuse growth pattern (< 50% nodular)
  • Cytologic variants: Classic, blastoid, pleomorphic, small cell, marginal zone-like
  • Blastoid and pleomorphic cytologic variants are known as aggressive variants of MCL
  • Classic variant:
    • Small to medium monomorphic lymphoid neoplasm
    • Irregular nuclear border, clumped chromatin and inconspicuous nucleoli
    • No proliferation centers
    • No centroblasts, immunoblasts or paraimmunoblasts
    • Hyalinized vessels
    • Epithelioid histiocytes
    • Follicular dendritic cell (FDC) meshwork
      • Nodular pattern
        • Primary follicle-like pattern
        • Germinal center-like pattern
      • Diffuse pattern
  • Aggressive variants
    • Blastoid: lymphoblast-like in appearance, monomorphic
      • >20 - 30 mitoses per 10 high power fields
      • Resemble lymphoblastic lymphoma
    • Pleomorphic: large cells with irregular nuclear border, cerebriform nuclei, multinucleation, lack of monomorphism
      • Prominent nucleoli and abundant pale cytoplasm
      • Resemble DLBCL
  • Other variants
    • Small cell: small round lymphocytes with more clumped chromatin
      • Resemble CLL
    • Marginal zone-like: abundant pale cytoplasm
      • Resembling marginal zone or monocytoid B cells
    • Lymphoplasmacytic differentiation, some cases [15]
  • Bone marrow
    • Nodular, interstitial or paratrabecular or combination
  • Peripheral blood (see below)
    • Similar spectrum seen in tissue sample
    • Nucleoli are sometimes more prominent
  • Spleen
    • White pulp nodules involved (enlarged)
    • Variable involvement of the red pulp
    • Residual naked germinal centers
    • Tumor cells: similar monotonous morphology
    • Some cases may show a marginal zone-like area [16]
  • Gastrointestinal
    • May mimic lymphoepithelial lesions in marginal zone lymphoma [17]
  • Relapse
    • Loss of a mantle zone growth pattern
    • Increase in nuclear size
    • Pleomorphism and chromatin dispersal
    • Increase in mitotic activity and Ki67
    • Cases that are blastoid at diagnosis may relapse with classic morphology [18]


Finding Marker
Positive (>95%) cyclin D1
Positive (>90%) Sox-11
Positive (100%) B-cell associated markers (CD19, CD20, CD22, CD79a/b)
Positive (>95%) CD5
Positive CD43
Positive IgM+/- IgD
Positive BCL-2
Positive (flow cytometry) FMC-7
Positive (50% in small subset of cells) MUM1 / IRF4
Positive (subset) MYC
Positive (subset) p53
Positive/ Negative CD10
Positive/ Negative BCL-6
Negative T-cell associated markers (except CD5)
Negative CD200
Negative LEF-1
  • Ki67 count [19]
    • Five independent high power fields count
    • Avoidance of residual germinal centers, hot spots and proliferating T cells
    • Note: Ki67 index is not sufficient to classify as blastoid or pleomorphic subtype
    • Classical mantle cell lymphoma might also show high cell proliferation[20]
  • p53 in subset; intense expression correlates with TP53 gene mutation
    • Note: no protein expression; on the other hand, cannot predict the homozygous deletions of the locus [21]
  • MYC in subset
    • High expression correlates with MYC translocation [22]
  • CD10+ MCL more associated with diffuse growth pattern, blastoid/pleomorphic morphology, and BCL6 expression[23]
  • CD23: small subset of cases [24]
  • CD200: May be positive in a subset of SOX11 negative mantle cell lymphomas[25] Leukemic Non-Nodal Mantle Cell Lymphoma
  • LEF-1: positive in 4 - 9% of mantle cell lymphomas [26][27]
  • Cyclin D1-negative MCL
    • Morphology, phenotype, gene expression, clinical presentation and evolution similar to cyclin D1-positive MCL [28]
    • Positive for Sox-11
    • Frequently express cyclin D2 or cyclin D3 (IG-mediated translocations) [29]
    • cyclin E in cases with negative expression of cyclin D and aggressive behavior [30]

Chromosomal Rearrangements (Gene Fusions)[31]

Chromosomal Rearrangement Genes in Fusion (5’ or 3’ Segments) Pathogenic Derivative Prevalence
t(11;14)(q13;q32) IGH/CCND1 der(11) and der(14) >90%
t(2;12)(p12;p13) IGK/CCND1 der(2) and der(12) NA
t(12;22)(p13;q11) IGL/CCND2 der(12) and der(22) NA
t(12;14)(p13;q32) IGH/CCND2 der(12) and der(14) NA
t(6;14)(p21;q32) IGH/CCND3 der(6) and der(14) NA

Characteristic Chromosomal Aberrations / Patterns

  • CCND1 rearrangement; t(11;14)(q13;q32)
    • FISH is convenient because it can be performed on fixed tissue sections
    • Conventional cytogenetics if fresh material available
    • Most PCR assays usually detect 1 major breakpoint region in mantle cell lymphoma
  • Cyclin D2 (CCND2) rearrangements by FISH in 55%-70% of cyclin D1-negative cases
  • Almost all cyclin D1-negative mantle cell lymphomas carry CCND2/CCND3 rearrangements with immunoglobulin genes (including a novel IGK/L enhancer hijacking mechanism)
  • A broad spectrum of secondary chromosomal aberrations have been reported, especially in MCL with bone marrow and peripheral blood involvement[32].
  • Tetraploidy is more frequent in pleomorphic (80%) and blastoid (36%) variants than in classic MCLs (8%) [33]
  • t(8;14)(q24;q32)/MYC-IGH in small subset of cases [34][35]
Parameter n %
CCND2 translocation
IGH-CCND2 3/40 8
IGK-CCND2 10/40 25
IGL-CCND2 5/40 13
CCND2-break 2/40 5
CCDND2-? 2/40 5
Negative 18/40 45

Genomic Gain/Loss/LOH

Secondary chromosomal aberrations[36]

Chromosome Number Gain/Loss/Amp/LOH Region Possible target gene/s Frequency Functional process
3 Gain q26 ? 31 - 50% ?
7 Gain p21 ? 16 - 34% ?
8 Gain q24 MYC 16 - 36% Cell growth, proliferation, apoptosis
11 Gain q13.3-q21 CCND1 4-14% Cell cycle
12 Gain q14 CDK4, MDM2 3-7% Cell cycle, DNA damage response, apoptosis
13 Gain q31 MIR17HG 24% Cell cycle, apoptosis
18 Gain q21.33 BCL2 18-55% Apoptosis
1 Loss p32.3-p33 CDKN2C, FAF1 18-52% Cell cycle, apoptosis
2 Loss q13 BCL2L11 3-17% Apoptosis
2 Loss q37.1 SP100-SP140 15-33% DNA damage response
6 Loss q23.3 TNFAIP3 19-36% NF-κB inhibitor
6 Loss q25 LATS1 19-36% Hippo signaling pathway
8 Loss p21.3 MCPH1 17-34% DNA damage response
9 Loss p21.2 MOBKL2B 10-36% Hippo signaling pathway
9 Loss p21.3 CDKN2A, ARF1 10-36% Cell cycle, DNA damage response
9 Loss q22.2-q22.31 CDC14B, FANCC, GAS1 17-31% ?
10 Loss p14-p13 ? 18-28% ?
11 Loss q22.3 ATM 11-57% DNA damage response
13 Loss q13.3-q34 DLEU1, DLEU2, RB1 25-70% Cell cycle, apoptosis
13 Loss q34 CUL4A, ING1 16-54% DNA damage response
17 Loss p13 TP53 21-45% DNA damage response
19 Loss P13.3 MOBKL2A 10-24% Hippo signaling pathway

Gene Mutations (SNV/INDEL)[37]

Gene Oncogene/Tumor Suppressor/Other Prevalence (COSMIC/TCGA/Other)
BIRC3 Apoptosis regulator/ NF-KB pathway 8.6-16.2%
MYC Apoptosis regulator 11.2-20.8%
CARD11 B-cell receptor signaling 8.5-16.3%
TRAF2 B-cell receptor signaling 4.5-15.7%
BTK B-cell receptor signaling 5.5-17.1%
MAP3K14 B-cell receptor signaling 2.4-14.2%
CCND1 CDK kinase regulator 20.2-27.7%
CDKN2A CDK kinase regulator 23.9-29.5%
SMARCA4 Chromatin modification 14.9-18.7%
ARID2 Chromatin modification 6.8-16.3%
ARID1B Chromatin modification 17.2-18.3%
CHD2 Chromatin modification 4.0-14.1%
ATM DNA damage response 43.5-57.6%
KMT2D Histone modification 18.4-21.8%
NSD2 Histone modification 15.0-22.8%
KMT2C Histone modification 17.6-19.1%
KMT2A Histone modification 8.9-21.4%
BCOR Histone modification 13.6-14.2%
IGH Immune response 21.5-38.4%
MEF2B Immune response 9.3-13.8%
SP140 Immune response 8.4-14.3%
TLR2 Immune response 4.3-14.3%
S1PR1 Immune response 8.6-13.9%
TET2 Myelopoiesis 5.6-14.1%
NOTCH1 NOTCH signaling pathway 10.8-14.8%
NOTCH2 NOTCH signaling pathway 5.8-14.3%
UBR5 Protein ligases 17.8%
TP53 Tumor suppressor 26.8-43.0%
RB1 Tumor suppressor 24.5%

Genes and Main Pathways Involved

Please refer to Gene Mutations (SNV/INDEL)

Diagnostic Testing Methods

  • Tissue biopsy (lymph node / extranodal sites): monomorphic proliferation of small to intermediate sized B cells with overexpression of cyclin D1 or SOX11
  • t(11;14)(q13;q32) IGH/CCND1
  • MRD is defined as the minimal traceable persistence of lymphoma cells after a successful treatment.
  • Many methods to monitor MRD have been published
  • The most sensitive and the most commonly used and best standardized approach in MCL: allele-specific oligonucleotide (ASO) quantitative polymerase chain reaction (qPCR) method [38]

Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)

  • Median survival: 5 - 7 years
    • Mantle cell lymphoma international prognostic index (clinical), MIPI [39]
    • Age, performance status, lactate dehydrogenase, leukocyte count
    • 3 morphologic groups with significantly different prognoses
  • Adverse outcome (histopathology / molecular)
    • High mitotic rate (> 50/mm2) [40]
    • Ki67 or MIB1 IHC stains (> 30%) [41]
    • Blastoid and pleomorphic variants [42]
    • MYC rearrangement [43][34]
    • TP53 mutation / overexpression / loss (17p) [44]
    • Either TP53 mutations or deletions or both associates with poor prognosis[45]
      • Elevated Ki-67
      • Higher MIPI-c classes
      • Blastoid morphology
      • Impact on survival independent of these risk factors
      • Higher levels of MRD positivity after allo-stem cell transplant
    • CDKN2A deletion (9p) [44]
    • Gains in 3q, deletions of 9q [46]
    • Patients with KMT2D mutation [45]
      • Chemo-immunotherapy failure
      • High-risk patients based on MIPI-C

Familial Forms

  • Family history of leukemia may elevate risks particularly among men with mantle-cell lymphomas (OR = 3.1, 95% CI = 1.6-6.2)[47]

Other Information

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Leukemic Non-Nodal Mantle Cell Lymphoma

In Situ Mantle Cell Neoplasia

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