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ORIGINAL ARTICLE  
Year : 2012  |  Volume : 55  |  Issue : 1  |  Page : 66-71
Morphological spectrum of leukemic mantle cell lymphoma


1 Hematopathologist, Rajiv Gandhi Cancer Institute and Research, New Delhi, India
2 Hematopathology Lab, TMH, Mumbai, India
3 Cancer Cytogenetics Lab, TMH, Mumbai, India
4 Medical Oncology, TMH, Mumbai, India

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Date of Web Publication11-Apr-2012
 

   Abstract 

Background: Leukemic involvement in mantle cell lymphoma (MCL) is common, and can be secondary to nodal or extranodal disease or can be de-novo. There is paucity of literature that describes the morphological spectrum. Aim: This study was aimed at studying the morphological spectrum of leukemic MCL and to correlate the morphology with other features. Materials and Methods: Twenty six such cases diagnosed over a period of four years were studied. Peripheral blood and bone marrow aspiration smears stained with Wrights stain were examined by three hematopathologists. Immunophenotyping was done using multicolor flow cytometry. Fluorescence in situ hybridization (FISH) done in 12 cases showed t(11;14)(q13:q32). Results: Six cases had de-novo leukemic involvement; while 20 cases had secondary involvement. Morphologically, the cells were small (less than twice the size of red blood cell) or large. Small cell morphology in turn showed irregular nuclear border (n=13) or round nuclear contour (n=6). Large cells had blastic morphology (n=5) or had central prominent nucleoli resembling prolymhphocytes (n=2). Twenty cases showed characteristic immunophenotype of CD5+/CD19+/CD20+/FMC7+/CD10-/CD23- and light chain restrictions. Three cases expressed CD23 and two cases were negative for FMC7. Five out of 12 cases, where FISH was done, showed cytogenetic abnormalities in addition to t(11;14)(q13;q32). Conclusion: Morphological spectrum of leukemic MCL ranges from small cells resembling chronic lymphocytic leukemia (CLL) or follicular lymphoma (FL) to large cell mimicking prolymphocytic leukemia (PLL) or acute leukemia. Large cell morphology was associated with more frequent additional cytogenetic abnormality as well as a poorer outcome.

Keywords: De novo leukemic involvement, mantle cell lymphoma, morphological spectrum

How to cite this article:
Rahman K, Subramanian P G, Kadam PA, Gadage V, Galani K, Mittal N, Ghogale S, Badrinath Y, Ansari R, Kushte S, Nair R, Sengar M, Menon H, Gujral S. Morphological spectrum of leukemic mantle cell lymphoma. Indian J Pathol Microbiol 2012;55:66-71

How to cite this URL:
Rahman K, Subramanian P G, Kadam PA, Gadage V, Galani K, Mittal N, Ghogale S, Badrinath Y, Ansari R, Kushte S, Nair R, Sengar M, Menon H, Gujral S. Morphological spectrum of leukemic mantle cell lymphoma. Indian J Pathol Microbiol [serial online] 2012 [cited 2020 Feb 21];55:66-71. Available from: http://www.ijpmonline.org/text.asp?2012/55/1/66/94860



   Introduction Top


Mantle cell lymphoma (MCL) is a B cell non-Hodgkin lymphoma (NHL) generally composed of monomorphic small to medium sized lymphoid cells with irregular nuclear contour and a a cyclin D1 (CCND1) translocation. [1] It occurs in elderly and comprises approximately 2-10% of NHL. [1],[2] Lymph nodes are the most commonly involved site. Spleen, gastrointestinal tract and Waldeyer's ring are the other common sites of involvement.

Peripheral blood and bone marrow involvement is seen in 53 to 93% of the cases. [3],[4],[5] It may be secondary to the nodal or extranodal disease or de novo without any primary tissue diagnosis. Patients who present primarily with bone marrow (BM) and peripheral blood (PB) involvement present with lymphocytosis as a chronic lymph proliferative disorders (CLPD). There is paucity of literature that describes the morphological spectrum of MCL either as PB or BM involvement. Few available reports describe the cells to range from small cell morphology mimicking chronic lymphocytic leukemia to large blastic morphology masquerading acute leukemia. Large nucleolated cell and blastic morphology have been regarded as high grade morphologic subtypes and have been associated with poor prognosis. [2],[6],[7]

In order to fill this lacuna in the description of morphological variants of leukemic MCL, 26 cases have been studied along with their clinical and immunophenotypic profile.


   Materials and Methods Top


Inclusion Criteria

A total of 26 consecutive cases of MCL with PB or BM involvement diagnosed over a period of four years were selected. These cases were diagnosed as MCL based on morphology, substantiated with flow cytometric immunophenotyping and Immunohistochemistry (IHC) (CD20 and Cyclin D1 expression). Fluorescence in situ hybridization (FISH) was available in 12 cases.

The characteristic immunophenotype was defined as CD5 + /CD19 + /CD20 + /FMC7 + /Light chain restriction (LCR) and CD23 negative or occasionally weak positive. [1]

Morphological Examination

Slides were retrieved from the archives of hematopathology laboratory. Morphological examination was carried out using air dried Wright's stained PB smears or BM aspiration slides. The slides were reviewed individually by three hematopathologists and features like cell size (smaller or larger than twice the size of red blood cell [RBC]) and nuclear characteristics such as nuclear contour, chromatin pattern and presence of nucleoli were taken into account. Based on this, the cells were broadly classified into small and large cell groups. Small cells were further grouped into (a) small cell having irregular nuclear contour with notching or cleaving; and (b) small cell with round nuclei. Similarly, large cells were classified as (c) large cells with immature blastic nuclei or (d) large cells with central prominent nucleoli mimicking prolymphocytes. If there was difference in the morphological interpretation between the three hematopathologists, then slides were seen together and a consensus for the morphological type was reached.

Immunophenotypic Analysis

Immunophenotyping was performed on ethylene diamine tetra-acetic acid (EDTA) anticoagulated PB or BM aspirate using standard lyse wash technique in 25 cases. In one case, the sample was not sent for flow cytometry. The diagnosis of MCL in this case was based on IHC of the bone marrow biopsy. Antibodies tagged to different flurochromes like Fluoroisothiocyanate (FITC), phycoerythrin (PE) Peridinin Chlorophyll (Per CP) Peridinin Chlorophyll-cyanin 5.5 (PerCP- Cy 5.5), Phycoerythrin- Cyanin 5 (PE cy 5) , Allophycocyanin (APC), and Allophycocyanin H 7 (APC H7) were used to stain the cells. Antibodies used were CD45, CD3, CD4, CD5, CD8, CD10, CD19, CD20, CD22, CD23, CD38, FMC7, CD79, IgM, IgD Kappa, and lambda light chains. A three color combination was used until March 2010 (n= 19), after which a six color combination of antibodies was used (n=6). Sample was acquired with 10,000 to 30,000 ungated events.

Immunohistochemistry for cyclin D1 was done on the bone marrow biopsy sample (n=8), lymph node biopsy (n =3), and GIT lesion biopsy specimen (n=2).

Cytogenetic Studies

Cytogenetic preparation was obtained by short term culture of BM or PB cells and standard harvesting method. FISH studies were performed in 12 cases using LSI dual color fusion translocation probe for IgH/CCND1.

Follow-up and Survival

Patients follow-up and survival was noted with the help of electronic medical record, patients file, and personal communications. A complete follow-up was available in 13 patients.


   Results Top


There were 22 males and 4 females with age ranging from 41 to 80 years (median age of 64 years). Twenty cases had secondary involvement of PB and BM. Lymph node was the most common primary site of involvement (n=17) followed by gastrointestinal tract (n=2) and nasopharynx (n=1). Six cases had de novo BM and PB involvement and presented as chronic lymphoproliferative disorder. Only one of these patients had peripheral lymphadenopathy, but that too was a small (1.2 cm) axillary node which was not biopsied.

Fever was the most common presenting symptom (n=22) followed by swelling or lump and abdominal pain. On examination, lymphadenopathy (n=17) and splenomegaly (n=14) were common findings. At baseline, the median hemoglobin was 9.5 gm/dl(5.4gm/dl to 13.6gm/dl), total leukocyte count was 21.65×10 3 /μl (7.1×10 3 /μl to 264×10 3 /μl), absolute lymphocyte count was 10.25×10 3 /μl(4.3×10 3 /μl -200.2×10 3 /μl), and platelet counts was 138×10 3 /μl (29×10 3 /μl to 264×10 3 /μl).

The percentage of atypical lymphoid cells in the differential count ranged from 33 to 95%. Commonest morphological variant was small cells having angulated, notched and/or cleaved nucleus morphologically resembling follicular lymphoma (n=13) [Figure 1]a. Small cells with round nucleus and scant to moderate amount of cytoplasm resembling the CLL was second common subtype (n=6) [Figure 1]b. Large cell with round nucleus and immature chromatin resembling blast was the third common type (n=5) [Figure 1]c. Large cells with prominent single nucleoli, resembling prolymphocytic leukemia (PLL) were seen in two cases only [Figure 1]d. Cases with small cell morphology had a more overt involvement, with greater percentage of atypical lymphoid cells (median 71 %) as compared to cases with large cell morphology (median 42%).
Figure 1: Photomicrographs showing different morphological variants of leukemic mantle cell lymphoma. Small cells showing irregular nuclear contour with notching and cleaving of nucleus and mature chromatin (compare the size with RBC and adjacent myelocyte) (a). Small cells with round nuclear contour mimicking CLL (b). Large cells more than twice or thrice the size of RBC with immature chromatin resembling blast (c). Large cells with central prominent nucleoli and moderate to abundant amount of cytoplasm resembling prolymphocyte (d) (Wright's stain, ×100 oil immersion)

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Eighty percent of the cases (n=20) had classical immunophenotype of MCL with expression of CD5, CD19, CD20, FMC7, light chain restriction; and CD23 negativity [Figure 2]. Three cases expressed CD23 weakly and two cases revealed FMC 7 negativity. All these five cases with aberrant phenotype had small cell morphology and were confirmed as MCL based on expression of cyclin D1 on BM biosy (n=1) and LN biopsy (n=1) by IHC; and t(11;14)(q13:q32) by FISH (n=2). The single remaining case where FISH or IHC could not be performed was best regarded as MCL based on morphology and immunophenotypic character.
Figure 2: Multicolor flow cytometric immunophentyping with atypical lymphoid cells gated in FSC vs SSC plot expressing CD45, CD5, CD19, CD20, FMC7, CD79 and Lambda light chain restriction; while these cells are negative for CD 10, CD23

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FISH could be carried out in 12 cases only (large cell=2, small cell =10) and all of them showed reciprocal IgH/CCND1 translocation. Additional cytogenetic aberrations were noted in five cases (large=2, small cell= 3). The two cases with large cell morphology revealed three copies of IgH/CCND1 due to duplication of derivative 14 [Figure 3]. Additional abnormalities in small cell morphology group were 11q and 13q deletion (n=1); trisomy 19 (n=1); and duplication of der 14 (n=1).
Figure 3: Florescence in situ hybridisation (FISH) on interphase cells showing 1 green signal of IgH, 2 orange signals of CCND1 and 3 orange/ green signals of IgH-CCND1 indicating duplication of IgH-CCND1

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IHC for cyclin D1 was available in 13 cases. Among these, six cases were diagnosed as MCL based on IHC only as FISH could not be performed on them. Two cases with large cell morphology and prominent nucleoli resembling prolymphocyte was very unusual for this type of lymphoma. Both these cases had characteristic immunophenotype of mantle cell lymphoma, CD5/CD19/CD20/FMC7 positive, light chain restriction; and CD23 negative. One case showed t(11;14) by FISH with duplication of der 14. FISH could not be performed on second case, but it was positive for cyclin D1 on IHC.

All those cases (n=8) where t(11;14) (q13:q32) by FISH or CCND1 over-expression on IHC could not be proved, MCL was the best possible diagnosis based on clinical, morphological, and immunophenotypic analysis.

Follow-up was available in 13 patients, 3 from the large cell morphology group and 10 from the small cell morphology group. The median duration of follow-up was five months (two to seven months) in the large cell group and eight months (four to 60 months) in small cell morphology group. Treatment with curative intent was offered to 11 patients; while 2 patients were advised palliative treatment because of old age (68 and 75 years) and poor cardiac functions. Different treatment regimen offered were cyclophosphamide, hydroxydaunorubicin, oncovin, prednisolon (CHOP), cyclophosphamide, vincristine, prednisolone (CVP), cyclophophamide, etoposide, oncovin, prednisolone (CEOP) and bendamustine, with or without rituximab, depending upon the feasibility.

There were a total of five deaths, two from the large cell morphology and three from the small cell morphology group. Median duration from the diagnosis to the death was seven months in small cell morphology group (n=3) and three months in large cell morphology group (n=2). Median absolute lymphocyte count in the patient who died was 44.25×10 3 /μl (11.23-106.9× 10 3 /μl) as compared with 8.3×10 3 /μl (4.3-200.2×10 3 /μl) in the patients who were alive at follow-up.

A comparison of clinical and laboratory findings of small and large cell morphology is presented in [Table 1]. Important findings of our study and that of Schlettes et al.,[6] the only study we could find in literature that has addressed the morphological variants of leukemic MCL, is compared in [Table 2].
Table 1: Comparison of clinical and laboratory finding between small and large cell morphological groups of 26 cases of mantle cell lymphoma with bone marrow and peripheral blood involvement.

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Table 2: Comparison of present study with that of Schlette et al11

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   Discussion Top


MCL is a B cell NHL with distinct morphological, immunophenotypic and genetic feature. In early 1990, the association between t(11;14) and this tumor was noted, and subsequently in 1992, a group of American and European pathologists proposed the term 'mantle cell lymphoma' for these group of NHL. [8] It occurs predominantly in adults and older individuals with a median age of 60 years and a definite male preponderance who present with fever, lymphadenopathy, and hepatoslenomegaly. [1] MCL has a distinct immunophenotype of pre-germinal centre naïve B cell that express CD5, but lack CD10 and CD 23. A diagnosis of MCL is confirmed by the presence of t(11;14)(q13:q32) which can be demonstrated by FISH or nuclear positivity for Cyclin D1 on IHC. However, several cases of Cyclin D1 negative MCL have been reported in literature with the frequency as high as 15% in some case series. [9] Thus, a diagnosis of MCL is based on a combination of morphology, imunophenotyping and cytogenetic findings in a correct clinical setting.

Leukemic involvement in MCL is a common finding and the reported incidence in literature varies from 53 to 93%. [1],[3],[4],[5] It occurs mostly secondary to the nodal or extranodal disease. However, de novo leukemic involvement is also well documented. [4],[10] Six (23%) cases in our study presented as CLPD and a diagnosis of de novo leukemic MCL was based on flow cytometric immunophenotyping and cytogenetic studies, a figure similar to earlier reported from our lab. [2] The presence of lymphadenopathy may be variable in patients presenting with de novo MCL. [11] Similar finding was noted in our study.

The finding of a high total leukocyte count (median of 21.65×10 3 /μl) and a high absolute lymphocyte count (median of 10.25×10 3 /μl) was in concordance with those reported in literature. [5],[6] Peripheral blood involvement with absolute lymphocyte count greater than 10×10 3 /μl has been regarded as an independent poor prognostic factor that heralds shorter patient survival. [3],[4] Our data also supports the premise as the patients who died had higher median lymphocyte count (44.25×10 3 /μl) as compared with those who were alive (8.3×10 3 /μl).

World Health Organization (WHO) defines two major morphological variants of MCL, 'Aggressive variant', including the blastoid and pleomorphic or nucleolated variant, and 'Other variants' that include small cell and the marginal zone like cells, based on histopathological findings. However, morphological spectrum of MCL cells in bone marrow or peripheral blood presenting as CLPD are not described well. [1] Few studies have tried to classify leukemic MCL into various morphological subtypes based on cell size and nuclear features. [6]

In the present study, small cell morphology with angulation, notching and cleaving of the nucleus was the most common type (50% cases), followed by the small cells with round nucleus (23%). Similar finding was noted by Schlettes et al[6] in their study of 23 cases of leukemic MCL. They found 9 (40%) cases with small cells and irregular nuclear contour and 6 (26%) cases with round nuclear contour.

Large cells with blastic morphology have been described by some workers. [7],[11] Blastic morphology, which is considered as a high grade variant, may be the original morphology at presentation or may be the morphology after transformation of a low grade variant during the course of disease. Cases described by Singleton et al.[7] as well as Vishwanatha et al.[11] had blastic morphology since the time of presentation. In contrast to them, Argatoff et al.[3] and Schlette et al.[6] described cases that showed transformation with increase in the number of lymphoblast like cells in the peripheral blood or bone marrow. This high grade blastic or PLL like transformation is reported in 32% of the cases, and in one study it has been reported to be as high as 70%. [6],[12] We had only one case with high grade transformation. Peripheral blood of this 62-year-old patient came to us as a referral material for immunophenotyping, with a history of MCL diagnosed on lymph node biopsy 5 years back at a private hospital. PBS showed lymphoid cells with high grade blastic morphology. Immunophenotypic pattern of CD5, CD19, CD20, and FMC7 positivity with CD10 and CD23 negativity and lambda light chain restriction labeled the case as a blastic transformation of MCL.

Cases with single central prominent nucleoli resembling prolymphocytes is the least common variant and is described in literature as case reports and small case series. [6],[10],[13],[14] Ruchlemer et al.[13] reviewed eight cases of B Prolymphocytic leukemia with t(11;14) diagnosed over a period 18 years and suggested that these cases represent MCL evolving into leukemia with a prolymphocytoid morphology. Wong et al[10] had also described four cases of MCL morphologically mimicking PLL. Similarly, in our study, there were only two cases with this morphologic subtype and they were diagnosed as MCL based on FISH in one case and IHC for cyclin D1 on BM biopsy in the other one.

Immunophenotypically MCL expresses CD19, CD20, CD5, FMC 7, and CD43; while negative for CD 10 and BCL 6. CD 23 is negative or is weakly expressed. These cell express surface IgM/IgD, and more frequently lambda than kappa light chain restriction. [1] Although CD5 positivity is observed both in CLL and MCL, CD 23 is regarded as a useful marker of CLL and is generally negative in MCL. [15] The intensity of CD20 and light chain expression has also been described as useful for distinguishing MCL from CLL, which are brighter in MCL as compared to CLL. Our study showed five cases with aberrant phenotype in the form of CD 23 positivity (n=3) and FMC7 negativity (n=2). Similar findings have been reported in literature. [3],[6],[16] Schlettes et al.[6] were not able to find any correlation between immunophenotypic aberrancy and morphological subtype of MCL in their study. In contrast, all the five cases in our study with unusual phenotype were of small cell type. This could be the result of a selection bias.

The t(11;14)(q13:q32) is regarded as primary genetic event in MCL. It brings about juxtapositioning of CCND1 gene on chromosome 11 to IgH gene at chromosome 14q32. This leads to deregulated expression of CCNDI, which in turn caused over-expression of cyclin D1 both at mRNA as well as protein level in MCL. This genetic abnormality can be demonstrated by FISH or indirectly by cyclin D1 positivity on IHC. [1],[17] Earlier several case reports of cyclin D1 expression in NHLs other than MCL like CLL and PLL has been described. But later on, many of these cases were reviewed and were finally labelled as morphological variant of MCL only. [6],[13],[18] Similarly Schellets et al.[6] opined that presence of t(11;14) in either PB or BM, in conjunction with compatible immunophenotypic features, supports the diagnosis of MCL, even in absence of biopsy proven lymph node.

Additional cytogenetic abnormalities seen in MCL as described in literature are chromosome 17p abnormalities with p53 mutation, trisomy 12, gains of 3q26, 7p21, 8q24 and losses of 1p13- p31, 6q 23-q27, 13q11-q13, 11q22-23 etc. [1],[6] Five of our cases also showed additional cytogenetic abnormalities where duplication of IgH-CCND1 signal was most frequent. In addition, deletion of 11q22-23-ATM and 13q was found in one case, which has been reported in other series. [19],[20],[21] Schlettes et al.[6] in their review of 23 cases of MCL in leukemic phase found additional abnormalities in 22 cases with chromosome 17 involvement as the most frequent abnormality. This frequency of additional cytogenetic abnormality was less in present study because conventional karyotyping was not carried out. Schlettes et al.[6] were not able to find any correlation between the additional genetic aberration and morphological subtype. However, in our study, it was found to be more frequent with the large cell morphology (2/2) as compared to small cell type (3/10).

Follow-up was available in fewer number of patients and also for a shorter duration as compared with other studies. [6],[11],[22] Proportion of death was more (66%) in patients with large cell morphology as compared with those with small cell morphology (30%). In addition, median time from initial diagnosis to death was shorter (3 months) for the patients with large cell morphology as compared to those with small cell morphology (7 months). This shows that patients with small cell morphology had better survival than cases with large cell morphology. Similar findings have been described in literature. [6],[7],[11],[22]

In conclusion, leukemic involvement in MCL can be secondary to nodal or extranodal sites (77%) or can be de novo (23%) where patient may not have any peripheral lymhpadenopathy. Morphological spectrum of leukemic MCL ranges from small cells resembling CLL or FL to large cell mimicking PLL or acute leukemia. Small cells with angulated, notched, or cleaved nuclei are the most common variants (50%). Large cell morphology is associated with more frequent cytogentic abnormalities in addition to t(11;14)(q13:q32) and predict a poor prognosis with shorter survival. A high absolute lymphocyte count of more than 10×10 3 /μl is associated with poor prognosis in the patients with leukemic MCL. There is paucity of literature discussing morphology of tumour cells in cases of leukemic mantle cell lymphoma. More studies with a longer follow-up of the patients are required to establish the survival benefits of the different morphological variants.

 
   References Top

1.Swerdlow SH , Campo E, Seto M, Muller Hermelink HK. Mantle cell lymphoma. In. WHO classification of hematopoietic and lymphoid tissue. Lyon, France: WHO blue book published; 2008. p. 229-37.   Back to cited text no. 1
    
2.Gujral S, Agarwal A, Gota V, Nair R, Gupta S, Pai SK, et al. A clinicopathological study of mantle cell lymphoma in single centre study in India. Ind J Pathol Microbiol 2008;51:315-22.   Back to cited text no. 2
    
3.Argatoff LH, Connors JM, Klasa RJ, Horsman DE, Gascoyne RD. Mantle cell lymphoma: A clinicopathologic study of 80 cases. Blood 1997;89:2067-78.  Back to cited text no. 3
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6.Schlette E, Lai R, Onciu M, Dohetry D, Beuso-Ramos C, Medieross LJ. Leukemic mantle cell lymphoma: Clinical and pathologic spectrum of twenty-three cases. Mod Pathol 2001;4:1133-40.  Back to cited text no. 6
    
7.Singleton TP, Anderson MM, Ross CW, Schnitzer B. Leukemic phase of mantle cell lymphoma, blastoid varian. Am J Clin Pathol 1999;111:495-500.  Back to cited text no. 7
    
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10.Wong KF, Chi Chiu So, Chan JK. Nucleolated variant of Mantle cell lymphoma with leukemic manifestation mimicking prolyphocytic leukemia. Am J Clin Pathol 2002;117:246-51.  Back to cited text no. 10
    
11.Viswanatha DS, Foucar K, Berry BR, Gascoyne RD, Evans HL, Leith CP. Blastic mantle leukemia: An unusual presentation of blastic mantle cell lymphoma. Mod Pathol 2000;13:825-33.  Back to cited text no. 11
    
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13.Ruchlemer R, Parry- jones N, Brito V, Attolico I, Wotherspoon AC, Matutes E, et al. B- prolymhpocytic leukemia with t(11;14) revisited: A splenomegalic form of Mantle cell lymphoma evolving with leukemia. Br J Hemat 2004;125:330-6.  Back to cited text no. 13
    
14.Smith MD, Singleton TP, Balaraman S, Jayesimi I, O'malley B, Saadi AA, et al. Case report: Mantle cell lymphoma, prolymphocytoid variant, with leukostasis syndrome. Mod Pathol 2004;17:879-83.  Back to cited text no. 14
    
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16.Dorfman DM, Pinkus S. Distinction between small lymphocytic and mantle cell lymphoma by immunoreactivity for CD23. Mod Pathol 1994;71:32-6.  Back to cited text no. 16
    
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18.Dascalescu C, Gressin R, Callanan M, Sotto JJ, Leroux D. t(11;14)(q13;q32): Chronic lymphocytic leukemia or mantle cell leukemia. Br J Haemat 1996;95:572-3.   Back to cited text no. 18
    
19.Chagant RS, Nanjangud G, Shmidt H, Teruya-Feldstein J. Recurring chromosomal abnormality in Non Hodgkin Lymphoma. Bioogic and clinical significance. Semin Hematol 2000;37:396-411.  Back to cited text no. 19
    
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Correspondence Address:
Khaliqur Rahman
Consultant Hematopathologist, Rajiv Gandhi Cancer Institute & Research Centre, Sector V, Rohini, New Delhi - 110 085
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.94860

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