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Multiple myeloma (MM) is incurable and the second most common hematologic malignancy in plasma cells. Multiple myeloma stem cell-like cells (MMSCs), a rare population of MM cells, are believed to be the major cause of drug resistance and high recurrence rates in patients with MM. Therefore, developing novel strategies to eradicate MMSCs may favor myeloma treatment. In this study, based on the drug repositioning strategy, we found that albendazole (ABZ), a broad-spectrum antiparasitic drug, selectively suppresses the proliferation of multiple myeloma cells in vitro and in vivo and decreases number of aldehyde dehydrogenase (ALDH)-positive MMSCs in MM. Furthermore, RNA-seq of MM cells after ABZ treatment revealed that inhibition of the nuclear factor kappa-B (NF-κB) pathway is a key mediator of ABZ against MM. Moreover, we demonstrated that ABZ can resensitize cells resistant to bortezomib and overcome MMSCs-induced bortezomib resistance by decreasing ALDH1+ MMSCs numbers. Our findings provide preclinical evidence for utilizing the previously known pharmacologically active drug albendazole for the treatment of multiple myeloma.

Icaritin is an active prenylflavonoid derived from Epimedium genus, a traditional Chinese medicine. Icaritin has a wide range of pharmacological and biological activities, including cardiovascular function improvement, hormone regulation and antitumor activity. Here, we investigated the effect of icaritin on multiple myeloma (MM) in vitro and in vivo. Icaritin inhibited cell growth of MM cell line and primary MM cells. In contrast, icaritin had low or no cytotoxic effect on normal hematopoiesis. We also demonstrated that in MM xenograft mouse models, icaritin suppressed tumor growth and decreased serum IL-6 and IgE levels, but did not show adverse reactions such as body weight loss. The anti-MM activity of icaritin was mainly mediated by inhibiting IL-6/JAK2/STAT3 signaling. We suggest that icaritin can be further tested in clinical trials in MM.

Thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease characterized by microvascular platelet deposition and thrombus formation with resulting microangiopathic hemolytic anemia. Deficiency of the von Willebrand factor cleavage protease, also known as ADAMTS 13, has been implicated as an important etiological factor in TTP. Little studies were obtained on Chinese patients with TTP until now. Our aim was to analyze the clinical features, outcome and laboratory characteristics of Chinese TTP patients, and determine whether plasma ADAMTS 13 activity is decreased in TTP and its diagnostic value for TTP. Forty-two TTP patients (29 females; 13 males) admitted to our hospital from 1998 to 2010 were analyzed. There were 34 patients (81%) with the triad of TTP, including hemolytic anemia, thrombocytopenia and neurologic abnormalities; 7 (16.7%) had the classical pentad of TTP. Major etiologic factors were acquired autoimmunological abnormalities (31%); no familial TTP was identified in this series. The schistocytes of peripheral blood smears were present in all cases with a mean frequency of 4.6% (range from 0.3% to 13.4%). Plasma ADAMTS 13 activity was determined in 22 patients with the FRET-vWF86 assay. Only 4 idiopathic TTP patients (18.2%) had severe ADAMTS 13 deficiency (activity10%); 9 (40.9%) had moderate decrease of ADAMTS 13 activity (activity: 10-40%); another 9 (40.91%) had normal ADAMTS 13 activity (40%). T lymphocyte subpopulation was measured in 23 TTP patients with FACS Calibur; 14 of the 23 (60.9%) had significantly decreased CD4 cells count and CD4/CD8 ratio, suggesting cellular immune dysfunction may be involved in the pathogenesis of TTP. In the studies, plasmapheresis is the main therapeutic method. 26 of 31 patients (83.9%) accepting plasmapheresis achieved complete remission; those patients who only underwent plasma infusion had low remission rate (18.2%) and high mortality (9/11; 81.8%). Four patients with packed RBC infusion manifested transient exacerbation of neurologic or psychiatric symptoms. In conclusion, the diagnosis of TTP in China is still based on clinical features including evidence of microangiopathic hemolysis. Severe ADAMTS 13 activity deficiency might be a valuable indicator for idiopathic TTP diagnosis. Further studies are needed to determine the real value of ADAMTS 13 activity for TTP diagnosis and whether T lymphocytes subset dysregulation plays important role in TTP pathogenesis.

Objective To evaluate the clinical efficacy and safety of arsenic trioxide, retinoic acid and thalidomide combination therapy in higher risk MDS. Methods Twenty-one patients diagnosed with higher risk MDS were administered 10 mg/day arsenic trioxide intravenously for 10 days, 40 mg/day retinoic acid orally for 2 weeks and 100 mg/day thalidomide orally for 4 weeks per cycle. Results After at least two treatment cycles, 10 patients showed hematologic responses. One achieved CR, one achieved PR, three patients achieved major hematological improvements. The efficacy rate was 24% (5/21), and the response rate was 48% (10/21). The schedule was tolerated well by all patients and toxicities were moderate and reversible. Conclusion The combination of arsenic trioxide, retinoic acid and thalidomide could have therapeutic benefit in higher risk MDS with safety.

A rare case of a 46-year-old man who underwent myelodysplastic syndrome, acute monocytic leukemia with FLT3-ITD mutation and splenic disruption following orthotopic liver transplantation is reported. The study of this case may be helpful to understand both the pathogenesis of acute leukemia and new complication of liver transplantation.

Characterization of an acquired factor VIII inhibitor and plasmapheresis therapy in a patient with bullous pemphigoid

Chemotherapy resistance is still the main clinical limitation to the successful treatment of leukemia. The underlying mechanisms of drug resistance are not fully understood. Recently, research on m...

To screen phosphopeptide specific for acute leukemia.Mononuclear cells from bone marrow were collected from 16 newly diagnosed acute lymphoblastic leukemia (ALL) and 20 acute myeloid leukemia (AML) patients. Peptides were extracted and purified, analyzed by immunoprecipitation and liquid chromatography coupled with tandem mass spectrometry (LC-MS).(1) Non-receptor tyrosine kinase family members Fyn, Yes, Src widely expressed in acute leukemia; (2) Some phosphopeptides, including non-receptor tyrosine kinase family members Abl/iso1 and Abl, non-receptor Ser/Thr protein kinase family members Bcr, JNK2, JNK2 iso2, Adaptor/scaffold members Cas-L, Cbl, CrkL CENTD1 (Centaurin delta1) ZO2, transcriptor GFR-1 and phosphatase SHIP-2 were detected in Ph positive ALL, but not in other kinds of ALL. (3) Hck, Lyn and Fgr selectively expressed in AML (except AML-M(3)).Some phosphopeptides were specific for ALL and AML, and may be useful for diagnosis and therapy of acute leukemia.

Purpose To explore the effects of Icaritin on chronic myeloid leukemia (CML) cells and underlying mechanisms. Method CML cells were incubated with various concentration of Icaritin for 48 hours, the cell proliferation was analyzed by MTT and the apoptosis was assessed with Annexin V and Hoechst 33258 staining. Cell hemoglobinization was determined. Western blotting was used to evaluate the expressions of MAPK/ERK/JNK signal pathway and Jak-2/Phorpho-Stat3/Phorsph-Akt network-related protein. NOD-SCID nude mice were applied to demonstrate the anti-leukemia effect of Icaritin in vivo. Results Icaritin potently inhibited proliferation of K562 cells (IC50 was 8 µM) and primary CML cells (IC50 was 13.4 µM for CML-CP and 18 µM for CML-BC), induced CML cells apoptosis and promoted the erythroid differentiation of K562 cells with time-dependent manner. Furthermore, Icaritin was able to suppress the growth of primary CD34+ leukemia cells (CML) and Imatinib-resistant cells, and to induce apoptosis. In mouse leukemia model, Icaritin could prolong lifespan of NOD-SCID nude mice inoculated with K562 cells as effective as Imatinib without suppression of bone marrow. Icaritin could up-regulate phospho-JNK or phospho-C-Jun and down-regulate phospho-ERK, phospho-P-38, Jak-2, phospho-Stat3 and phospho-Akt expression with dose- or time-dependent manner. Icaritin had no influence both on c-Abl and phospho-c-Abl protein expression and mRNA levels of Bcr/Abl. Conclusion Icaritin from Chinese herb medicine may be a potential anti-CML agent with low adverse effect. The mechanism of anti-leukemia for Icaritin is involved in the regulation of Bcr/Abl downstream signaling. Icaritin may be useful for an alternative therapeutic choice of Imatinib-resistant forms of CML.

To explore the relationship between microRNA and drug resistance in leukemia treatment by screening and identifying the microRNAs which differentially express in K562 cell line and its adriamycin resistant cells-K562/A02 cell line.The drug resistance potency of K562/A02 cells was evaluated by MTT assay. P-gp expression of K562 and K562/A02 cells were detected by flow cytometry (FCM). The differentially expressed microRNAs in K562 and K562/A02 cells were analyzed by microarray technique and Real Time RT-PCR.The resistance to adriamycin (ADM) of K562/A02 cells was 180 fold greater than that of K562 cells. P-gp expression rate of K562 and K562/A02 cells was 0.2% and 86%, respectively. Twenty-two microRNAs expressed differentially in K562 and K562/A02 cells (P0.01). As compared to K562 cells, expressions of miR-221, miR-155 and miR-451 were up-regulated by more than two fold, while expression of miR-98, miR-181a, let-7f, let-7g, miR-424 and miR-563 down-regulated by more than two fold in K562/A02 cells. The results of real time RT-PCR were consistent with that of microarray. Of note, differential expressions of miR-451, miR-155, miR-221, let-7f and miR-424 were remarkable.K562/A02 cells show a different microRNA expression profile as compared to its parental K562 cells, suggesting microRNAs including miR-221, miR-155, miR-451, let-7f and miR-424 may be involved in the mechanism of drug resistance in leukemia. These differentially expressed microRNAs provide potential novel targets for overcoming drug-resistance.

In the present study, 90 patients with newly diagnosed acute promyelocytic leukemia (APL) were studied for all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) combination treatment in remission induction and postremission therapy. In addition, 20 APL patients who had achieved complete remission (CR) with an ATRA-based regimen received ATRA/As2O3 combination for consolidation and maintenance were also enrolled. The results showed that ATRA/As2O3 combination therapy yielded a high CR rate of 93.3% and a significantly shorter time to enter CR (median: 31 days; range: 18–59 days) compared to the ATRA-based regimen (n = 72; median: 39 days; range: 25–62 days). With the ATRA/As2O3 combination for CR maintaining, regardless of the way by which CR was attained, the relapse-free survival was significantly better than with an ATRA plus cytotoxic chemotherapy regimen (92.9 ± 3.2% vs. 72.4 ± 7.6%, for the 3-year Kaplan-Meier estimate of relapse-free survival). The drug toxicity profile showed that with the use of As2O3, the incidence of hepatotoxicity was obviously high during remission induction but decreased significantly during postremission treatment. We conclude that APL patients may benefit from the early use of the combination of ATRA and As2O3, in either remission induction or consolidation/maintenance.

Aim To assess the expression level of fms-like tyrosine kinase 3 (FLT3), the incidence of FLT3/internal tandem duplications (ITD) mutation, and prognostic value of FLT3 changes in different types of adult leukemia. Methods Bone marrow mononuclear cells were isolated from 147 adult patients with leukemia. Reverse transcriptase polymerase chain reaction (PCR) was used to screen FLT3/ITD mutation and quantitative PCR was performed to evaluate the expression of the FLT3 transcript. Flow cytometry was used for detection of FLT3 receptor protein expression on bone marrow mononuclear cells. Pearson correlation analysis was performed to estimate the significance of FLT3. Results FLT3 expression was higher in acute myeloid leukemia and Bacute lymphoid leukemia than in T-acute lymphoid leukemia (P = 0.006, P = 0.001) and chronic myelogenous leukemia (P < 0.001). In chronic myelogenous leukemia, FLT3 expression in blast transformation phase was higher than in acceleration phase (P = 0.023). Surface expression of FLT3 protein was correlated with high percentage of bone marrow blasts and with FLT3 mRNA expression (r = 0.366, P < 0.001) in acute leukemia. FLT3/ITDs in the juxtamembrane domain were found in 25% of patients with acute myeloid leukemia and 7% of patients with acute lymphoid leukemia. FLT3/ITD positive sequences had 36, 42, and 57 nucleotides. FLT3/ITD mutation was associated with a higher white blood cell count, higher marrow blast percentage, and elevated serum lactate dehydrogenase (P = 0.045, P = 0.014, P < 0.001, respectively) and not associated with a higher FLT3 mRNA and FLT3 protein expression, and lower complete remission (P = 0.091, P = 0.060, P = 0.270, respectively). Conclusion FLT3 expression levels differed in different types of adult leukemia. Overexpression of FLT3 and presence of a positive FLT3/ ITD mutation in acute leukemia were associated with unfavorable clinical characteristics and poor prognosis.

To study the clinical features and molecular genetics of acute monocytic leukemia (AML) after orthotopic liver transplantation and significance thereof.The clinical manifestations, laboratory findings, development, diagnosis, treatment, and prognosis of the first case of AML after orthotopic liver transplantation in the world, a Chinese, male, aged 46, were observed. RT-PCR was used to analyze the mRNA expression of FLT3, Pim-1, and Hsp-70 in the bone marrow mononuclear cells (BMMCs) of the patient. Nucleotide sequence analysis was used to detect the mutation of FLT3-ITD. Flow cytometry was used to examine the protein expression of C-kit, a stem cell factor receptor, and platelet derived growth factor receptor-alpha (PDGFRalpha).(1) Three months after the orthotopic liver transplantation the patient manifested symptoms and signs of anemia and thrombocytopenia. Laboratory tests found increase of white blood cells and myeloblasts with Auer's rods. Cytogenetic analysis showed a genotype of 46XY/47XY with an extra chromosome 8. Bone marrow examination revealed increased promonocytes. The diagnosis of chronic myelomonocytic leukemia was made. Five months after the liver transplantation the disease developed to AML. The patient underwent combined chemotherapy (HA or DA regimens) for 5 courses and showed a partial remission both hematologically and in bone marrow examination at first, however, became resistant to all chemotherapeutic agents. RT-PCR showed absence of wild type FLT3 allele. At last the patient died of infection. (2) A FLT3-ITD mutation of "insertion" type was identified in the BMMCs. The Pim-1 mRNA was weakly expressed and the expression of Hsp-70 mRNA was upregulated in the BMMCs. (3) The protein expression of C-kit and that of PDGFRalpha were both upregulated in the BMMCs as showed by flow cytometry.Orthotopic liver transplantation may be complicated with acute leukemia heterogeneous in clinical features and hematology. Certain defects in cytogenetics/molecular genetics may attribute to unfavorable prognosis.

To understand the clinical features and histopathology of histocytic necrotizing lymphadenitis (HNL) so as to better recognize the disease.The clinical features, histopathology, and diagnosis of 10 patients admitted to our hospital were retrospectively analyzed.The clinical features of these 10 cases included: young females were the majority; lymphadenopathy and fever were the most common clinical manifestations; some cases were accompanied by connective tissue diseases. Histopathologic examination showed distinctive necrosis and around the necrotic foci, variable proliferations of histocytes but generally without infiltration of neutrophils.HNL has some typical histopathological alterations and relatively fine prognosis,but it tends to be misdiagnosed as lymphoma or lymphoid tuberculosis and may be accompanied by other diseases.

To monitor the changes of hemolysis parameters and endothelial cell markers in thrombotic thrombocytopenic purpura (TTP) and reveal the clinical significance of these changes.vWF-cleaving protease (vWF-CP) activity in 3 cases of TTP was detected by Western blot. The percentages of fragmented red cells (FRC) were counted throughout the entire clinical course. Levels of plasma thrombomodulin were detected by Western blot combined with density screening in TTP and healthy individuals (n = 3). Concentration of plasma VEGF was measured by enzyme-linked immunosorbent assay in TTP and healthy individuals (n = 9). Fundus fluorescein angiography was performed to search the evidence of microvascular thrombosis in one TTP patient with impaired visual acuity.The lower vWF-CP activity was observed in TTP patients; the percentages of FRC in 3 cases of TTP were 1.65%, 2.50%, 3.32% respectively with an average of 2.49% at the onset of and decreased with the improvement of the disease. The levels of plasma TM and VEGF were significantly elevated in TTP than those in healthy individuals, and related to the severity of TTP. Fundus photography in one TTP patient with impaired visual acuity revealed vascular occlusion in fundus arteriole and venulae.A decreased vWF-CP activity is in favour of TTP diagnosis. Dynamic monitoring of plasma TM and VEGF as well as percentages of FRC are useful indexes for reflecting the severity and evaluating therapeutic response of TTP. Selective fundus fluorescein angiography is useful for the judgement of microvascular thrombosis in TTP.

To determine whether JAK/STAT pathway is involved in proliferation of hypereosinophilic syndrome (HES) cells, and reveal the pathogenesis of HES; observe the dynamic change of the clinical phenotype and hematological response, the expression of janaus kinase/signal transducer and activator of transcription (JAK/STAT) protein or FIP1L1-PDGFRA mRNA in one HES patient treated with low-dose imatinib.The granulocytes of peripheral blood of 4 HES patients, including 3 FIP1L1-PDGFRA positive cases and 1 negative case, were collected. The expression of JAK2, STAT3, and phosphorylated STAT (P-STAT5) proteins were detected by western blotting. One FIP1L1-PDGFRA fusion gene positive patient was administered with low-dose imatinib. Retrospective reverse transcription polymerase chain reaction (RT-PCR) analysis of FIP1L1-PDGFRA was performed and the expressions of JAK2, STAT3 and P-STAT5 were detected by western blotting before treatment and 10, 30, and 60 days after the beginning of treatment.Upregulation of JAK2, STAT3, and P-STAT5 proteins was shown in 3 FIP1L1-PDGFRA fusion gene positive HES patients, while all of these proteins were not expressed in one case of FIP1L1-PDGFRA negative HES. Continuous hematological remission was observed in one FIP1L1-PDGFRA fusion gene positive HES patient after low-dose imatinib treatment. The amount of FIP1L1-PDGFRA transcripts in peripheral blood granulocytes was significantly decreased in 30 days after therapy and turned negative 60 days after therapy. JAK2, STAT3, STAT5, and P-STAT5 expressions were all down-regulated time-dependently and were all negative 60 days after.There is excessive activation of JAK/STAT signal pathway in HES patient, which may contribute to the malignant proliferation of eosinophils. Low-dose imatinib, that induces complete hematological and molecular genetic remission, exerts significant effects on FIP1L1-PDGFRA positive HES.

To determine whether FIP1L1-PDGFRA fusion exists in hypereosinophilic syndrome (HES) patients, explore the relationship between FIP1L1-PDGFRA fusion and clinical phenotypes, and observe and reveal the expression of signal transducer and activator of transcription 5 (STAT(5)) in granulocytes of HES and the biological significance thereof.Specimens of peripheral blood were collected from 4 HES patients diagnosed based on the criteria of Chusid et al. Total RNA was extracted from granulocytes and cDNA was synthesized by reverse transcription. Nested-PCR was used to amplify the target fusion gene and the positive PCR fragments were sequenced directly. Total protein of the peripheral granulocytes was extracted. Western blotting was used to detect the expression of STAT(5) protein in the granulocyte lysates.FIP1L1-PDGFRA fusion genes were found in 3 of the 4 HES patients. The break points in PDGFRA were all located at exon 12, while in FIP1L1 the break points were highly variable, located at exon 8a, intron 8a, and exon 8 respectively. The patients with FIP1L1-PDGFRA fusion were susceptible to cardiac involvement. The expression of STAT(5) protein was upregulated in FIP1L1-PDGFRA positive HES patients, while STAT(5) protein expression was negative in HES patients without FIP1L1-PDGFRA fusion.FIP1L1-PDGFRA fusion has a universal significance for HES. The identification of FIP1L1-PDGFRA rearrangement is a useful molecular mark for HES diagnosis and works as the therapeutic target of imatinib. Furthermore, the activation of STAT(5), a downstream signal of the FIP1L1-PDGFRA fusion, indicates that HES is a malignant clonal disease of the hematopoietic tissue.

A nonsteroidal anti-inflammatory drug, indomethacin, has been shown to have anti-leukemic activity and induce leukemic cell apoptosis. This study was to elucidate the mechanism of indomethacin-induced K562 cell apoptosis.K562 cells were grown in RPMI 1640 medium and treated with different doses of indomethacin (0 micromol/L, 100 micromol/L, 200 micromol/L, 400 micromol/L, 800 micromol/L) for 72 hours. The cells were harvested, and cell viability or apoptosis was analyzed using MTT assay and AO/EB stain, combining laser scanning confocal microscopy (LSCM) technique separately. For the localization and distribution of intracellular caspase-3 or caspase-8 protein, immunofluorescence assay was carried out. To reveal the activation of caspase-3 or caspase-8 in indomethacin-treated cells, Western blot detection was used. The change in intracellular free calcium was determined by Fluo-3/Am probe labeling combined with LSCM.Indomethacin could lead to K562 cell apoptosis and inhibit cell viability in a concentration-dependent manner. An increased expression of intracellular caspase-3 or caspase-8 was observed at higher doses of indomethacin (400 - 800 micromol/L). Western blot results showed upregulation and activation in both caspase-3 and caspase-8 protein. Under indomethacin intervention, the levels of intracellular free calcium showed a significant increase. Blocking the activity of cyclooxygenase did not abolish the effects of indomethacin on K562 cell apoptosis.Activation and upregulation of caspase-3 or caspase-8 protein were responsible for Indomethacin-induced K562 cell apoptosis. Variation of intracellular free calcium might switch on the apoptotic pathway and the proapoptotic effect of indomethacin might be cyclooxygenase-independent.

To study the plasma HCII activity and antigen level variations and their relationship with arterial and deep venous thrombotic diseases.Seventy-five patients with brain infarction (BI), 50 myocardial infarction (MI), 36 deep venous thromboembolic disease (DVT) and 50 healthy controls were entered in this study. Plasma HCII activity was measured with chromogenic substrate method and the HCII antigen level by Western blotting assay. Plasma antithrombin (AT) activity was detected for the HCII deficiency individuals with DVT using chromogenic substrate method.There was no significant difference in the mean plasma HCII activity and antigen levels between BI group [(99.97 +/- 21.14)% and 0.96 +/- 0.24], MI group [(98.18 +/- 29.35)% and 0.95 +/- 0.20] and healthy controls [(96.80 +/- 20.11)% and 0.93 +/- 0.19]. The plasma HCII activity and antigen concentrations in patients with DVT [(89.57 +/- 17.12)% and 0.87 +/- 10.18] tended to be decreased as compared with healthy controls, but they were not significant. No significant difference was found for the prevalence of HCII deficiency between patient groups and control group. The HCII deficiency individuals with DVT had normal AT activity and fibrinogen concentration.Plasma HCII deficiency may not be the risk factor for arterial thrombosis in the Han population of Hunan Chinese. It is needed to further confirm if decreased plasma HCII is correlated with venous thrombosis.

To establish a high-performance liquid chromatography (HPLC) assay with an internal standard for determining plasma total homocysteine.The Hcy-mixed disulfides or protein bound Hcy in the plasma were reduced with TCEP. Subsequently, the thiol-compounds in the samples were derivatized with a thiol-specific fluorogenic reagent, SBD-F. The derivate was then separated and detected by HPLC with fluorometric detection.The detection limit was 0.625 mumol.L-1; the rate of recovery was 98.87%; the intra-assay coefficient of variation (CV) was less than 5.5%; and the inter-assay CV was less than 9.0%.The method presented in this paper is simple, sensitive, precise, and stable.

Dear Editor, We present here a case of thyroid diffuse large B cell lymphoma (DLBCL) arising on the background of thyroid medullary cancer, which was treated with thyroid lobectomy 10 years ago, and highlight its excellent response to treatment with rituximab-based CHOP chemotherapy (RCHOP). To our knowledge, this is the first case of primary thyroid lymphoma following thyroid medullary cancer. A 63-year-old Chinese womanwas admitted to our hospital with the complaints of neck mass, slight cough and dyspnea for 2 weeks in Aug 2005. She had a previous history of thyroid mass in the right lobe and received lobectomy 10 years ago. At that time, histopathological examination of the biopsy specimen from the thyroid mass was reported as thyroid medullary cancer (Fig. 1a). Immunohistochemical and special stainings displayed Cal (+), CK (+), Syn (+), TG (−), EMA (−), Congo red (+) and NSE (+) (Fig. 1b), which were consistent with the diagnostic features of thyroid medullary cancer. She had not undergone any chemotherapy or radiotherapy, and kept in a good condition after the surgical operation. Regular examinations including thyroid function tests and ultrasonic scan for thyroid showed no abnormality. Two weeks before admission, she found a mass up to 6 cm in diameter in the thyroid, with slight cough and dyspnea. Physical examination showed III grade enlargement in thyroid with deviation of trachea. No lymphadenopathy and hepatosplenomegaly was found. Laboratory examinations revealed that, blood cell counts, urine routine, stool routine, serum electrolytes, liver function, and renal function were within normal limits; serum lactate dehydrogenase (LDH) was 360 u/L, serum β2-microglobulin (BMG), immunoglobulin, and calcitonin were normal. Thyroid functional profile included a T3 of 0.89 nmol/L (0.7–2.7), T4 of 73.6 nmol/L (58.1–164.8), FT3 of 1.80 pmol/L (2.1– 6.2), FrT4 of 13.7 pmol/L (9.0–23.9), TSH of 3.8 mIU/L (0.35–5.5). The anti-microsomal antibody (MCA) and thyroglobulin antibody (TGA) were detected as negative titers with a radio-immunity (RI) method. Bone marrow smear showed normal cellular morphology and cellular ratio. A computerized tomography (CT) scan of the neck showed a mass in thyroid with trachea compressed. Chest and abdomen CT showed no lymph node or organ involvement. With the dyspnea progressed, a tracheal intubation subsequently a surgical operation was performed. The surgery was palliative just for relieving the airway obstruction and mass biopsy. Histopathological examination from thyroid mass biopsy showed diffuse proliferation of lymphoma cells with large nuclei (Fig. 2a). Immunohistochemically staining indicated MUM1(−), CD45R0(−), EMA(−), LCK(−), CaL(−), TG(−), LCA(++), Bcl-6(+), CD10 (+), and CD20(++) (Fig. 2b). A diagnosis of diffuse large B cell lymphoma (DLBCL), stage IE, was made. The international prognostic index (IPI) portrayed a lowintermediate risk. The patient was treated with CHOP (cyclophosphamide, doxorubicin, vincristin, and prednisolone) combined with rituximab (MabThera). After six courses of R-CHOP regimen, the mass in thyroid completely disappeared and she is still in complete remission after a 34 month follow-up. Non-Hodgkin’s lymphoma (NHL) of the thyroid gland is uncommon, accounting for only 1–5% of all thyroid malignancies, and classified as non-epithelial thyroid tumors [1–3]. In this report, we present the case that developed a DLBCL in the thyroid site where a thyroid Ann Hematol (2009) 88:701–702 DOI 10.1007/s00277-008-0639-9