Abstract
Ancillary studies for primary nodal lymphomas have been well documented; however, studies of primary thyroid lymphoma (PTL) are limited. Here, we aimed to clarify the clinicopathological, flow cytometric, gene rearrangement, and karyotypic characteristics of PTL by investigation of a large series at a single institute. We performed flow cytometric, IgH rearrangement, and karyotypic analyses of 110 PTL tissues surgically resected at Kuma Hospital between January 2012 and April 2017. All PTLs were of B-cell origin, including mucosa-associated lymphoid tissue lymphoma (MALTL; 89 patients, 80.9%), diffuse large B-cell lymphoma (DLBCL; 18 patients, 16.4%), and follicular lymphoma (FL; three patients, 2.7%). In 96 (87.3%) patients, anti-thyroid antibodies were positive. For flow cytometry using aspirated and resected materials, light chain restriction was observed in 73.7% and 69.2% of examined cases, respectively. Heavy chain JH DNA rearrangement was observed in 65.4% of PTLs (58.1% of MALTL cases, 100% of DLBCL cases, and 100% of FL cases). Chromosomal abnormalities were detected in 49.0% of PTLs, and translocation was most frequently detected (24.0%), followed by addition (20.8%) and trisomy (18.8%). The most frequent (9.4%) karyotype was t(3;14)(q27;q32). Both FLs harbored t(14;18)(q32;q21), and the karyotype was not detected in patients with MALTL and DLBCL. The negative rate for all three examinations was 3.8%. We concluded that thyroid MALTL was cytogenetically different from that in other organs. Our results suggested that pre-operative flow cytometry analysis using aspirated materials was as reliable as that using resected materials.
PRIMARY THYROID LYMPHOMA (PTL) is an uncommon neoplastic disease, accounting for 0.5–5% of all thyroid malignancies [1-3]. PTL typically occurs in older women, with a female to male ratio ranging from 1.4:1 to 6:1 [2, 4-7], and is frequently accompanied by chronic thyroiditis, which is known to increase the risk of PTL [8-10]. Nearly all cases of PTL are B-cell-derived non-Hodgkin’s lymphoma, particularly diffuse large B-cell lymphoma (DLBCL) and mucosa-associated lymphoid tissue lymphoma (MALTL) [1, 11]. DLBCL may be transformed from MALTL or can occur as de novo disease [12-14].
PTL can usually be diagnosed by histological and immunohistochemical examination. In addition, ancillary studies including flow cytometry, immunoglobulin heavy chain (IgH) rearrangement, and karyotypic analyses, can provide important information for determination of the classification and biological behaviors of lymphomas [15-19]. Such analyses for primary nodal lymphomas have been well documented [15-18]. For PTL, however, a few sporadic reports have been published [19-23].
In our institution, Kuma Hospital in Japan, we have identified 110 cases of PTL within the last 6 years. In this study, we report the clinicopathological, flow cytometric, gene rearrangement, and karyotypic characteristics of PTL in this large series of cases at our institute.
Materials and Methods
Patients
The study protocol was reviewed and approved by the Institutional Review Board of Kuma Hospital (170706-3), and was in accordance with the 1964 Helsinki declaration and its amendments or comparable ethical standards. We reviewed 5,979 patients with primary thyroid malignancies that underwent thyroidectomy or incisional biopsy at Kuma Hospital between January 2012 and April 2017. Among these patients, 110 patients with PTL (1.8%) were extracted. The diagnosis of thyroid lymphoma was made based on histological examination in conjunction with immunohistochemical results.
Questionable or suspected PTL cases were not included. PTL was defined as a lymphoma that only involves the thyroid (stage IE under the Ann Arbor staging system) or the thyroid gland with its adjacent lymph nodes (stage IIE under the Ann Arbor staging system). In the latter cases, the lesions in the thyroid were larger than or appeared before those in the lymph nodes.
Diagnostic criteria
The diagnostic criteria for DLBCL were diffuse proliferation of large lymphoid cells with an immunoreactivity for CD20, and the diagnosis of MALTL required either packing, lymphoepithelial lesions, follicular colonization, or light chain restriction. The packing and lymphoepithelial lesions were confirmed by the presence of CD20-positive lymphoid cells within cytokeratin AE1/AE3-positive thyroid follicles. Follicular colonization was confirmed by the absence of CD23-positive follicular dendritic cell processes. When lymphoid cells showed plasma cell differentiation, light chain restriction was confirmed by the presence of lymphoid cells that predominantly expressed either κ or λ chain. Lesions with nodules composed of CD10-positive and BCL-2-positive lymphoid cells were diagnosed as FLs.
Clinical data
Clinical data were obtained from medical records of Kuma Hospital. The normal ranges of free thyroxine and thyrotropin levels were 0.70–1.60 ng/dL and 0.30–5.00 μIU/mL, respectively. Anti-thyroid antibodies were defined as positive when anti-thyroglobulin antibody and anti-thyroperoxidase antibody titers were more than 39.9 IU/mL and/or more than 27.9 IU/mL, respectively.
Study methods
In 99 patients who underwent fine needle aspiration cytology (FNAC), flow cytometry analysis using aspirated materials was performed. The presence of light chain restriction was assumed in cases with kappa lambda ratios of less than 0.33 or more than 3.0 [19]. For tissues surgically resected from 104 patients, flow cytometry based on CD45 and side scatter-based gating, karyotypic analysis (G-banding chromosomal examination), and IgH rearrangement analysis using southern blotting were performed. In eight (7.7%) patients, karyotypic analysis failed because of a lack of metaphase cells. Based on the International System for Human Cytogenetic Nomenclature (ISCN) 2013, the clonality of karyotyping was defined as structural abnormality or trisomy in at least two metaphases or loss of a single chromosome in at least three metaphases [24].
Statistical analysis
We assessed the statistical significance of the data using Fisher’s exact probability tests and independent t-tests. P values of less than 0.05 were considered statistically significant. In addition, during the same period, 49 patients, in whom lymphoma was diagnosed or suspected by FNAC, were referred to other hospitals without histological examination in order to receive chemical and/or radiation therapy. Among these patients, cytological diagnosis of 22 patients was DLBCL.
Results
Clinical findings
Table 1 shows the clinical findings of 110 patients with PTL. All PTL cases were of B-cell origin, including MALTL (89 patients, 80.9%), DLBCL (18 patients, 16.4%), and follicular lymphoma (FL; three patients, 2.7%). One of 18 DLBCLs (5.6%) was positive for CD10. All subtypes showed a female predilection. The mean ages of patients with MALTL, DLBCL, and FL were 69.4, 71.0, and 54.0 years, respectively. The mean age of patients with FL was significantly lower (p < 0.05). Free thyroxine was within normal limits, except for in one case in which a low free thyroxine level was detected. In 14 (12.7%) patients, thyrotropin levels were elevated. In 96 (87.3%) patients, anti-thyroid antibodies were positive. The incidence (92.1%) in patients with MALTL was significantly higher than that in the patients with DLBCL (66.7%; p < 0.05). In seven cases of MALTL (7.9%), six cases of DLBCL (33.3%), and one case of FL (33.3%), anti-thyroid antibodies were negative. Out of 14 patients with negative anti-thyroid antibodies preoperatively, all 10 patients with evaluable non-neoplastic thyroid tissue revealed pathological findings consistent with Hashimoto’s thyroiditis. In four patients with negative anti-thyroid antibodies, anti-thyroid antibodies were measured postoperatively. Three of these patients underwent lobectomy or partial resection and showed positive conversion. In the remaining patient, total thyroidectomy was performed, and anti-thyroid antibodies remained negative.
Table 2 shows the results of flow cytometric, gene rearrangement, and karyotypic examination of PTL. For flow cytometry using aspirated and resected materials, light chain restriction was observed in 73.7% and 69.2% of examined cases, respectively. There were no significant differences in diagnostic accuracies. Heavy chain JH DNA rearrangement was observed in 65.4% of PTL cases (58.1% of MALTL cases, 100% of DLBCL cases, and 100% of FL cases). The incidence in patients with MALTL was significantly lower than that in patients with DLBCL (p < 0.001). For karyotypic analysis, eight cases could not be examined because of proliferation disorder or the absence of mitogenic figures. Chromosomal abnormalities were detected in 47 of 96 patients with PTL (49.0%). Moreover, 10 patients with PTL (9.6%) did not exhibit any abnormalities in the three examinations, and all had MALTL. In six of these cases, light chain restriction was demonstrated pre-operatively. The overall negative rate of the three ancillary examinations in patients with PTL was 3.8% (4/104). Table 3 shows the types and incidences of chromosomal abnormalities. Translocation was most frequently detected (24.0%), followed by addition (20.8%) and trisomy (18.8%). Table 4 shows karyotypes of chromosomal translocation. The most frequently detected karyotype was t(3;14)(q27;q32), and the incidences were 8.5% in MALTL cases and 16.7% in DLBCL cases. 3q27 was the most frequent breakpoint (11.5%). All FLs harbored t(14;18)(q32;q21), and the karyotype was not detected in patients with MALTL and DLBCL. Attached additional materials of unknown origin are shown in Table 5. The incidences were rare, and no regions specific to PTL were detected. Table 6 shows the types of trisomies. Trisomy X was most frequently detected (7.3%), followed by trisomy 5 (5.2%), trisomy 7 (4.2%), and trisomy 8 (4.2%). For patients with MALTL, the incidences of trisomy 3 and 18 were 1.2% and 0%, respectively. One of two patients with FL exhibited four trisomies (2, 7, 18, and 21).
Table 3
Types and incidences of chromosomal abnormalities in primary thyroid lymphoma
|
Total (96) |
MALTL (82) |
DLBCL (12) |
FL (2) |
| Trisomy |
18 (18.8%) |
16 (19.5%) |
1 (8.3%) |
1 (50.0%) |
| Monosomy |
5 (5.2%) |
3 (3.7%) |
1 (8.3%) |
1 (50.0%) |
| Addition |
20 (20.8%) |
17 (20.7%) |
3 (25.0%) |
0 (0%) |
| Translocation |
23 (24.0%) |
17 (20.7%) |
4 (33.3%) |
2 (100%) |
| Deletion |
15 (15.6%) |
13 (15.9%) |
2 (16.7%) |
1 (50.0%) |
| Insert |
3 (3.1%) |
3 (3.7%) |
0 (0%) |
0 (0%) |
| Other |
14 (14.6%) |
11 (13.4%) |
2 (16.7%) |
1 (50.0%) |
| Total |
47 (49.0%) |
37 (45.1%) |
8 (66.7%) |
2 (100%) |
MALTL, mucosa-associated lymphoid tissue lymphoma; DLBCL, diffuse large B cell lymphoma; FL, follicular lymphoma
Table 4
Karyotypes of chromosomal translocation in primary thyroid lymphoma
|
Total (96) |
MALTL (82) |
DLBCL (12) |
FL (2) |
| t(?;1)(?;q21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(1;9)(q21;q34) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(1;14)(q21;q32) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(1;19)(q25;p13) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(2;3)(p12;q27) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(3;14)(q27;q32) |
9 (9.4%) |
7 (8.5%) |
2 (16.7%) |
0 (0%) |
| t(3;18)(q27;q21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(5;11)(q33;p15) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(6;12)(p21;q24.1) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| t(6;19)(p21;p13) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(6;22)(p21;q11.2) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| t(8;22)(q24;q11.2) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| t(14;17)(q32;q23) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(14;18)(q32;q21) |
2 (2.1%) |
0 (0%) |
0 (0%) |
2 (100%) |
| t(14;19)(q32;q31.1) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(X;2)(p11.2;p23) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| t(X;3)(p22.1;p21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| Total |
23 (24.0%) |
17 (20.7%) |
4 (33.3%) |
2 (100%) |
MALTL, mucosa-associated lymphoid tissue lymphoma; DLBCL, diffuse large B cell lymphoma; FL, follicular lymphoma
Table 5
Attached additional materials of unknown origin in primary thyroid lymphoma
|
Total (96) |
MALTL (82) |
DLBCL (12) |
FL (2) |
| add(2)(p11.2) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(3)(p21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(3)(q27) |
2 (2.1%) |
2 (2.4%) |
0 (0%) |
0 (0%) |
| add(5)(p11) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(6)(q21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(7)(q32) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(9)(p11) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(9)(q11) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(9)(p13) |
4 (4.2%) |
3 (3.7%) |
1 (8.3%) |
0 (0%) |
| add(10)(q22) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(11)(q13) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| add(13)(q22) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(14)(q22) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(14)(q24) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(15)(p11.2) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| add(16)(p13.1) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(17)(q21) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(19)(q13.1) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| add(19)(q22) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(21)(p11.2) |
1 (1.0%) |
0 (0%) |
1 (8.3%) |
0 (0%) |
| add(X)(q11) |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| add(X)(p11.2) |
3 (3.1%) |
3 (3.7%) |
0 (0%) |
0 (0%) |
| Total |
20 (20.8%) |
17 (20.7%) |
3 (25.0%) |
0 (0%) |
MALTL, mucosa-associated lymphoid tissue lymphoma; DLBCL, diffuse large B cell lymphoma; FL, follicular lymphoma
Table 6
Types of trisomies in primary thyroid lymphoma
|
Total (96) |
MALTL (82) |
DLBCL (12) |
FL (2) |
| Trisomy 2 |
2 (2.1%) |
0 (0%) |
1 (8.3%) |
1 (50.0%) |
| Trisomy 3 |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| Trisomy 5 |
5 (5.2%) |
5 (6.1%) |
0 (0%) |
0 (0%) |
| Trisomy 7 |
4 (4.2%) |
3 (3.7%) |
0 (0%) |
1 (50.0%) |
| Trisomy 8 |
4 (4.2%) |
4 (4.9%) |
0 (0%) |
0 (0%) |
| Trisomy 10 |
1 (1.0%) |
1 (1.2%) |
0 (0%) |
0 (0%) |
| Trisomy 12 |
3 (3.1%) |
3 (3.7%) |
0 (0%) |
0 (0%) |
| Trisomy 15 |
2 (2.1%) |
2 (2.4%) |
0 (0%) |
0 (0%) |
| Trisomy 18 |
1 (1.0%) |
0 (0%) |
0 (0%) |
1 (50.0%) |
| Trisomy 21 |
3 (3.1%) |
2 (2.4%) |
0 (0%) |
1 (50.0%) |
| Trisomy X |
7 (7.3%) |
7 (8.5%) |
0 (0%) |
0 (0%) |
| Total |
18 (18.8%) |
16 (19.5%) |
1 (8.3%) |
1 (50.0%) |
MALTL, mucosa-associated lymphoid tissue lymphoma; DLBCL, diffuse large B cell lymphoma; FL, follicular lymphoma
Discussion
PTLs are almost exclusively non-Hodgkin’s B cell type. According to some reports from Western countries, the most common subtype is DLBCL (>50%), followed by MALTL (10–30%) and FL (2–10%) [10, 11, 25]. In contrast, in China, the incidences of MALTL, DLBCL, and FL were 50–80%, 20–30%, and 12%, respectively [26]. In our study, MALTL was the most frequent subtype (80.9%), followed by DLBCL (16.4%) and FL (2.7%). The incidences we reported here were based on surgically resected cases, and 49 patients, whose diagnoses were suspected by FNAC and were not confirmed by histological examination, were not included. Even if the excluded patients were added, the order of MALTL and DLBCL would not be reversed. Hirokawa et al. suggested that earlier sonographic detection and more accurate cytological diagnosis increased the proportion of MALTL [19] because DLBCLs could be transformed from pre-existing MALTL [11]. The incidence of CD10-positive DLBCLs, indicating a germinal center phenotype, was low (5.6%) in our study, suggesting a transformation from MALTL to DLBCL. Overall, the incidences of MALTL in recent reports have been higher than those in older reports [10, 11, 25-27]. Improved diagnostic accuracy and racial or environmental factors may be involved in these discrepancies.
Most PTLs arise in a background of chronic thyroiditis, which is estimated to occur in approximately 60–90% of PTLs [12, 14, 28, 29]. The transformation from chronic thyroiditis to PTL occurs in 0.5% of cases [9, 12]. In our study, 96 (87.3%) of 110 PTL cases harbored anti-thyroid antibodies. The incidence (92.1%) in MALTL cases was significantly higher than that (66.7%) in DLBCL cases. Out of 14 patients with negative anti-thyroid antibodies preoperatively, all 10 patients with evaluable non-neoplastic thyroid tissue showed histological findings consistent with Hashimoto’s thyroiditis. Thus, we believe that almost all PTLs are associated with chronic or Hashimoto’s thyroiditis. Interestingly, out of four patients who were negative for preoperative anti-thyroid antibodies and measured anti-thyroid antibody postoperatively, three underwent lobectomy or partial resection and showed positive conversion. At present, this phenomenon still cannot be explained.
Ancillary studies, including flow cytometric, IgH rearrangement, and karyotypic analyses, are useful in the diagnosis of lymphoma. For PTLs, no studies have reported the use of these tools in a large series of cases, and this is the first report to carry out flow cytometric, gene rearrangement, and karyotypic examinations of a large series of PTLs.
Flow cytometry is a rapid technique for determination of surface antigens on cells obtained from lymphoproliferative lesions and has been used to distinguish between reactive lymphoid hyperplasia and lymphoma [19, 30, 31]. When the κ/λ light chain ratio is greater than 3–4:1 or less than 1:2–3, it is thought that clonal proliferation may be present [32-35]. Boonyaarunnate et al. demonstrated the occurrence of light chain restriction in nine (69.2%) of 13 PTLs [31]. However, light chain restriction has been reported in a minority of patients with Hashimoto’s thyroiditis [36-38]. According to a study using fine needle aspiration materials, light chain restriction was observed in 75.0% of PTL cases [19]. In this study, there was no significant difference in the detection rates of light chain restriction by flow cytometry using aspirated (73.7%) and resected materials (69.2%). Additionally, we demonstrated that aspirated materials were adequate to identify light chain restriction by flow cytometry. The results will contribute to making preoperative flow cytometric examination more common in lymphoma-suspected cases.
IgH rearrangements have been identified in half of non-Hodgkin’s B-cell lymphomas [39-41], but the detection rates vary with the technique used. Bernicot et al. identified these rearrangements in 74% of non-Hodgkin’s B-cell lymphomas [41]. Moreover, Matsuzuka et al. reported that 85% of PTLs showed IgH rearrangements, whereas no patients with Hashimoto’s thyroiditis harbored this abnormality [29]. In our study, IgH rearrangements were present in 65.4% of PTL cases. All patients with DLBCL and FL harbored IgH rearrangements, whereas the incidence of IgH rearrangement in patients with MALTL was lower (58.1%). We do not believe that 40% of patients with MALTL do not have IgH rearrangements. Notably, the lesions of MALTL are geographically distributed in the thyroid. Therefore, it is possible that there was some sampling error in our study. In any case, the incidence of IgH rearrangements in PTL seemed to depend on the proportion of subtypes in PTL cases examined, and the MALTL-high proportion group could show a low incidence.
Few studies have reported chromosomal abnormalities in PTL. In this study, chromosomal abnormalities were detected in 49.0% of PTLs, and translocation was the most frequent (24.0%), followed by addition (20.8%) and trisomy (18.8%). Many types of translocation were detected, and no single type was found to be specific to PTL subtypes, except for FL. The most frequently detected karyotype was t(3;14)(q27;q32), and 3q27 was the most frequent breakpoint. In general, MALTLs mainly harbor four chromosomal translocations, i.e., t(1;14)(p22;q32), t(11;18)(q21;q21), t(14;18)(q32;q21), and t(3;14)(p14;q32), which are associated with MALTL pathogenesis [42]. Among these translocations, t(11;18)(q21;q21) is the most commonly observed by fluorescence in situ hybridization (FISH) studies, occurring in 15–40% of all anatomic MALTL sites [43, 44]. However, we did not detect any of the four abnormalities in thyroid MALTLs in G-banding chromosomal examination. This discrepancy may suggest that MALTLs arising in the thyroid and other organs are cytogenetically different. In fact, there is no association between thyroid MALTLs and Helicobacter pylori infection, which has been related to gastric MALTLs [45]. To confirm the hypothesis, FISH and/or G-banding chromosomal examinations should be carried out for MALTLs arising in both the thyroid and other organs. Streubel et al. reported that three of six thyroid MALTLs harbored t(3;14)(p14.1;q32), although this was not detected in our series [46]. t(14;18)(q32;q21) is characteristic to FL at any site [47], and we detected this translocation in both cases of FL examined. Thus, FLs in the thyroid and other sites seemed to be cytogenetically similar.
Trisomies 3, 12, and 18 have been frequently demonstrated in MALT lymphoma [44, 48-50]. Trisomy 3 is the most common aberration in gastrointestinal MALTL with a frequency of up to 35% [48]. Trisomies 3 and 18 seem to be related to the transformation from MALTL to DLBCL [51]; however, we could not obtain data for this phenomenon in PTL. For PTL, Yoshimoto et al. reported a case of thyroid MALTL with trisomy 21 [21]. In our study, trisomy was observed in 18.8% of PTL cases, and the incidence of trisomy 21 was 3.1%; disease-specific trisomy was not identified. Other chromosomal abnormalities, such as monosomy, deletion, and insertion, have not been reported frequently in PTLs. In our study, the incidence was low, and the clinical significance is still unclear. Based on chromosomal abnormalities, the tumorigenesis of PTLs was diverse and did not seem to be related to the abnormalities.
In summary, in this study, we described flow cytometry, karyotypic, and IgH rearrangement analyses for 110 cases of PTL. Almost all cases of PTLs exhibited some abnormities in the three analyses, and negative cases may have been due to sampling error. Because the detection of light chain restriction using flow cytometry was not different between aspirated and resected materials, we suggest that pre-operative flow cytometry analysis using aspirated materials is as reliable as that using resected materials. Chromosomal abnormalities characteristic to PTL were not identified, except for t(14;18)(q32;q21) in FL. Thus, we conclude that thyroid MALTL might be cytogenetically different from that in other organs because the former does not harbor the chromosomal abnormalities that have been reported in the latter.
Acknowledgements
We thank Professor Yuko Hashimoto of the Department of Pathology, Fukushima Medical University for her helpful comments on this manuscript.
Disclosure
None of the authors have any potential conflicts of interest associated with this research.
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