髓系／NK前体细胞急性白血病1例的诊断分析

目的 分析1例髓系／NK前体细胞急性白血病（M／NKPAL）的诊断过程,提高对M／NKPAL的认识。方法 对1例M/NKPAL采用细胞涂片染色、细胞化学染色方法和流式细胞术进行细胞形态学和免疫表型分析,并应用细胞遗传学和PCR技术进行染色体核型分析及T细胞受体、白血病融合基因的检测,同时结合相关文献进行分析。结果骨髓原始细胞为90.4％,绝大部分白血病细胞形态学类似急性淋巴细胞白血病L2型,过氧化物酶染色阴性,偶见Auer小体。免疫表型为CD34、HLA-DR、CD33、CD7、CD56、CD38阳性和cyCD3弱表达,而cyMPO、CD3、CD4等阴性。存在染色体核型异常,未检测到克隆性T细胞受体基因重排和白血病相关的融合基因。结论M/NKPAL临床少见,诊断复杂,仅依据形态学难以诊断,应注意与伴有髓系抗原表达的T淋巴细胞白血病、急性髓细胞白血病微分化型、T／髓系混合表型急性白血病和母细胞性NK细胞白血病／淋巴瘤等相鉴别。     

急性白血病伴CD56阳性的临床意义

目的：探讨CD56在急性白血病中的表达及其临床意义。方法：就近2年来应用流式细胞仪检测了CD56的92例急性白血患者中发现的CD56阳性病例,分析细胞形态学、免疫表型和临床特点。结果：92例急性白血病中15例（16．3％）表达CD56,其中1例急性前髓系／NK细胞白血病（Myeloid/NK cell precursor acute leukemia),1例原始NK细胞白血病（Blastic NK cell leukemia),1例NK样T细胞淋巴瘤／白血病（NK－like T-cell lymphoma/leukemia),12例急性髓细胞白血病伴NK细胞抗原表达或急性髓系／NK细胞白血病。结论：伴CD56阳性急性白血病,其细胞形态学、免疫表型及临床表现各有特点,见于M2、M5、L2,髓外浸润多见,多预后不良。     

35例急性白血病免疫表型特征

 目的 分析急性白血病（AL）免疫表型诊断意义并对急性白血病各亚型CD抗原表达进行比较。方法 对35例AL患者进行形态学检查,并用流式细胞仪检测白血病细胞免疫表型。结果 35例AL患者中,形态学分型：急性髓细胞白血病（AML）M1 2例,M2 4例,M3 6例,M4 7例,M5 8例,不能分型AL 1例,急性混合细胞白血病1例,急性淋巴细胞白血病（ALL）L1 4例,L2 2例。免疫表型检查结果在AML各亚型中CD13、CD33、MPO均阳性,CD+34 18例,CD+14 5例。其中2例伴有CD+19,6例ALL患者中,CD19、CyCD79a均阳性,CD+10 4例,CD+20 2例,1例不能分型AL表达CD10、CD19、CD34、CyCD79a诊断为B-ALL,1例混合细胞白血病有淋系和髓系表达,故诊断为混合细胞白血病。结论 白血病免疫表型检测能使AL的诊断率提高,因此对形态无法鉴别的AL,应进一步进行免疫表型检测。     

髓系/自然杀伤细胞祖细胞急性白血病(附1例报道并文献复习)

目的：提高对髓系／自然杀伤细胞祖细胞(myeloid／Datural killer cell precursor,M／NKP)急性白血病的认识。方法：报告1例M／NKP急性白血病并复习相关文献。结果：M／NKP急性白血病起源于髓系和NK细胞共同的祖细胞。白血病细胞形态学特征类似急性淋巴细胞白血病L型．胞体大小不等,核圆或不规则,核仁明显,胞质苍白,无嗜天青颗粒,髓过氧化物酶(MPO)染色阴性,免疫表型特征为表达CD7,CD33,CD34,CD56和HLA-DR,其他NK细胞及T、B细胞分化抗原阴性。临床特征为髓外浸润较常见,急性髓系白血病化疗方案疗效相对较好,但预后差。结论：M／NKP急性白血病具有独特的临床和实验室特征,是有别于其他NK细胞及髓系细胞恶性疾病的一类独立疾病。     

急性髓系及混合型白血病流式细胞术免疫分型检测结果

 目的　研究流式细胞术（FCM）检测在急性髓系白血病（AML）及混合型白血病（MAL）诊断中的意义。方法　采用四色FCM对52例AML和7例MAL患者进行免疫表型检测。结果　52 例AML患者以系列专一表达为主,主要表达 CD13（94.2 %）,CD117（90.4 %）,cMPO（90.4 %）CD33（86.5 %）,CD34（57.7 %）,HLA-DR（53.8 %）。7例MAL中髓系／B系（M／B）混合3例,均表达CD13,CD34,CD117,CD10,CD19,cMPO,cCD79a;髓系／T系（M／T）混合2例,均表达CD13,CD117,CD33,CD34,CD5,CD7,cMPO;B系／T系（B／T）混合2例,均表达CD5,CD7,CD10,CD19,CD20,CD34。且与形态学和组织化学诊断具有高符合率。结论　FCM能够提高AML和MAL的确诊率,对该类白血病的明确诊断及分型具有重要的临床指导意义。     

132例初发儿童急性淋巴细胞白血病免疫表型及细胞遗传学特征分析

目的：探讨儿童急性淋巴细胞白血病（ALL）的免疫表型及细胞遗传学特征,为其诊断及治疗提供依据。方法：采用多参数流式细胞术（FCM）对132例初发儿童 ALL 患者进行免疫表型分析,并应用荧光原位杂交（FISH）技术检测其细胞遗传学特点。结果：132例 ALL 患者中,12.9%（17/132）为 T 淋巴细胞急性淋巴细胞白血病（T - ALL）,87.1%（115/132）为 B 淋巴细胞急性淋巴细胞白血病（B - ALL）。46.2%（56/132）的ALL 患者表达髓系抗原,CD13是 ALL 中最常见的髓系抗原,其阳性率为28.0%。T - ALL 髓系相关抗原表达阳性率为47.1%,与 B - ALL 的46.1%比较,差异无统计学意义（χ2=0.006,P =0.940）。可供核型分析的96例 ALL 中,核型异常者50例（52.1%）,其中染色体数目异常26例,染色体结构异常24例。96例 ALL 患者中,TEL/ AML1融合基因阳性21例（21.8%）,BCR/ ABL 融合基因阳性14例（14.6%）,TCF3/ PBX1融合基因阳性5例（5.2%）,MLL 重排3例（3.1%）。对不同免疫分型患者细胞遗传学异常检出率进行比较,差异均无统计学意义（P >0.05）。结论：儿童 ALL 免疫表型和细胞遗传学具有一定的特点,两者联合检测对 ALL 的诊断及分型具有重要的价值。     

儿童急性白血病免疫表型及临床意义

 目的　探讨儿童急性白血病的免疫表型特征和临床意义。方法　应用10种单克隆抗体,采用免疫酶标技术ABC-AP染色对76例白血病患者骨髓涂片进行免疫表型测定。结果　各型白血病主要表达该系列特异抗原,形态学与免疫学检查符合率为97.6 %（74／76）,1例形态学误诊被免疫分型纠正,1例形态学诊断不明经免疫分型确诊;淋系可见髓系抗原表达,髓系也可见淋系抗原表达,T-ALL与M3不表达HLA-DR。结论　白血病细胞免疫表型具有高度异质性;FAB与免疫分型同时结合可互相补充,提高诊断的准确率。     

双表型急性白血病流式细胞术免疫分型检测结果

 目的　应用流式细胞术（FCM）检测双表型急性白血病（BAL）的免疫表型。方法　采用四色FCM检测23例BAL患者的免疫表型。结果　23例BAL患者中有10例（43.4 %）表达cCD3,16例（69.6 %）表达cCD79a,20例（87.0 %）表达cMPO,14例（60.9 %）表达TdT,19例（82.6 %）表达CD34,20例（87.0 %）表达CD117,同时表达髓系和B系抗原者13例（56.5 %）,均共同表达cCD79a和cMPO;同时表达髓系和T 系抗原者7 例（30.4 %）,均共同表达cCD3和cMPO;同时表达T系和B系抗原者3例（13.04 %）,均共同表达cCD3和cCD79a。结论　cCD3、cCD79a、cMPO为系列特异性抗原标志,对诊断及鉴别BAL具有重要意义,FCM是目前诊断BAL特异可靠的方法,在临床白血病治疗和预后方面有重要的指导意义。     

成人急性双表型白血病的临床和生物学特征研究

目的：分析成人急性双表型白血病（BAL）的临床和生物学特征.方法：采用流式细胞术检测22例成人BAL患者治疗前骨髓细胞的免疫表型,染色体R显带技术对其中的16例进行核型分析.结果：在同期急性白血病496例患者中BAL发生率为4.4%（22/496）,16例（72.7%）为髓系和B系抗原共表达,5例（22.7%）为T系和髓系 抗原共表达,T系、B系和髓系均表达者1例 （4.5%）.BAL患者CD34阳性率为86.4%,高于同期ALL（60.3%）和AML（62.9%）（P＜0.05）.BAL患者中位年龄大于ALL患者（P＜0.05）.BAL组肝、脾、淋巴结肿大例数明显高于AML组（P＜0.01）.BAL组异常核型占56.3%,Ph染色体阳性率（25%）明显高于AML组（0%）（P＜0.01）.结论：成人BAL发病率低,以髓系和B淋巴系抗原共表达为主.BAL患者发病中位年龄高,高表达CD34,Ph染色体阳性者多见,肝、脾、淋巴结浸润发生率高.     

新疆地区450例急性白血病的免疫分型研究

 目的　研究新疆地区急性白血病（AL）患者免疫表型分布特点。方法　采用间接免疫荧光法对450例AL患者进行免疫表型分析。结果　106例急性淋巴细胞白血病（ALL）,334例急性髓系白血病（AML）,10例为FAB不能分类的急性白血病（UAL）;ALL中髓系抗原的表达15 %,AML中淋系抗原的表达25 %,表达最频繁的是CD7;研究了295例AL患者MPO mRNA基因表达,81例ALL中有1例表达MPO基因;所有髓系均不同程度地表达MPO基因,9例UAL有6例表达MPO基因;ALL免疫分型特点在汉族和维吾尔族（简称维族）中差异无统计学意义（P＞0.05）,在AML中,汉族髓系抗原的表达率依次为CD33＞CD13＞CD15,维族髓系抗原的表达率依次为CD15＞CD33＞CD14。结论　免疫表型的检测对AL更精确地诊断和分型有重要意义。联合分析AL形态学、细胞化学、免疫学及MPO mRNA表达等特点,对于AL的诊断和指导治疗均有重要意义。     

112例淋巴系统恶性肿瘤骨髓免疫表型分析

背景与目的:淋巴细胞白血病和淋巴瘤骨髓侵犯的诊断以细胞形态学为基础,而免疫分型可通过获得肿瘤细胞分化和发育阶段的信息使淋巴系统恶性肿瘤的诊断更为准确,为临床合理治疗和预后判断提供重要的科学依据.本研究应用多参数流式细胞术(flow cytometry,FCM)探讨淋巴细胞白血病和非霍奇金淋巴瘤(non-Hodgkin's lymphoma,NHL)骨髓侵犯的免疫表型特点.方法:收集112例病理确诊NHL并伴骨髓侵犯和淋巴细胞白血病患者的骨髓标本.应用FCM检测肿瘤细胞的免疫表型.结果:45例前驱B淋巴母细胞白血病/淋巴瘤(precursor B lymphoblastic lymphoma/leukemia,B-ALL/LBL)主要表达CD19、CD10、TdT、CD34、HLA-DR和CD20;32例前驱T淋巴母细胞白血病/淋巴瘤(precursor T lymphoblastic lymphoma/leukemia,T-ALL/LBL)主要表达胞内CD3(cytoplasmic CD3,CyCD3)、CD7、CD5、TdT、膜表面CD3(surface CD3,sCD3)和HLA-DR.77例前驱淋巴细胞肿瘤中,28例(36%)有髓系抗原CD13、CD33的表达;9例(20%)B-ALL/LBL病例有CD20与CD34共同表达,28例(87.5%)T-ALL/LBL病例有CyCD3与TdT共同表达.成熟淋巴细胞肿瘤35例,其中17例慢性淋巴细胞白血病/小淋巴细胞淋巴瘤主要表达CD19、CD20、CD5和HLA-DR,并有CD19与CD5共同表达.4例弥漫大B细胞性淋巴瘤主要表达CD19、CD20、CD10和HLA-DR.3例伯基特淋巴瘤主要表达CD19、CD10、CD20、SIgM.1例套细胞淋巴瘤表达CD5、CD19、CD20、HLA-DR.5例外周T细胞淋巴瘤(PTCL)主要表达sCD3、CD5、CD7、CD4或CD8.1例间变性大细胞淋巴瘤主要表达sCD3、HLA-DR.4例NK/T细胞肿瘤表达CD56、HLA-DR,也表达CD7或CD4或CD8.成熟淋巴细胞肿瘤不表达早期抗原如CD34、TdT.成熟淋巴细胞肿瘤可伴有髓系抗原CD13、CD33的表达.结论:淋巴系统恶性肿瘤侵犯骨髓采用形态学结合FCM免疫学分型可获得T、B细胞来源、肿瘤细胞分化阶段和异常抗原表达等参数,有助于临床诊断和微小残留病灶的检测.     

Secondary myeloid/natural killer cell acute leukemia following T-cell lymphoma

A 56-year-old woman was treated with combination chemotherapy and radiation therapy for peripheral T-cell lymphoma. Following complete remission for a period of 6 months, she returned again with marked leukocytosis. Leukemic cells were characterized by scanty cytoplasm with fine azurophilic granules, and were highly positive for myeloperoxidase and sudan black-B. Immunophenotypic analysis revealed that blast cells were positive for myeloid antigens (CD13, CD33), and natural killer (NK) cell antigen (CD56), but negative for T-cell antigens (CD2, CD5, CD7), B-cell antigens (CD19, CD20), CD34, and HLA-DR. The case was diagnosed as secondary myeloid/NK cell acute leukemia following non-Hodgkin's lymphoma. Despite aggressive chemotherapy against leukemia, she died of multiorgan failure 7 months following onset of leukemia. We present, to the best of our knowledge, the first published report of what seems to be a secondary myeloid/NK cell acute leukemia following T-cell lymphoma.     

Clinicopathological features of myeloid/natural killer (NK) cell precursor acute leukemia

Four patients (three males and one female) were diagnosed as myeloid/natural killer (NK) cell precursor acute leukemia in our department. Two patients showed the extramedullary involvement at initial presentation. Leukemic cells expressed CD7, CD33, CD45 and CD56 in all patients. Additionally, CD13, CD34, HLA-DR, cytoplasmic CD3 and myeloperoxidase were expressed in some patients. Trisomy 10 was found in two patients, which has not been reported in this disease. Therefore, myeloid/NK cell precursor acute leukemia might be rather heterogeneous especially in chromosomal abnormality though it seemed to constitute the distinct clinical entity among acute myeloid leukemia of M0 subtype.     

急性髓细胞白血病微分化型流式细胞术免疫分型分析

目的探讨流式细胞术（FCM）检测免疫表型在诊断急性髓细胞白血病微分化型（AML—M0）中的意义。方法采用多色FCM分析14例AML—M0病例的各相关抗原表达情况。结果14例AML—M0中,仅1例依据骨髓细胞形态学作出诊断,其余13例均依靠FCM作出明确诊断。在AML—M0中,髓系抗原CD33 14例（100％）表达阳性,CD13和CD117 9例（64％）表达阳性,CD34和HLA—DR12例（86％）表达阳性,一般成熟髓系相关抗原如CD16、CD10、CD14等均阴性,B和T淋巴细胞特异抗原如CD79a和CD3均为阴性,少数原始细胞表达细胞内髓过氧化物酶（MPO）、TdT。常常表达一些淋系但并不特异的抗原如CD7、CD2或CD19,但比淋巴细胞白血病表达的荧光强度弱。结论FCM免疫分型在AML—M0诊断中至关重要。     

Karyotypic patterns in acute mixed lineage leukemia

We performed cytogenetic and immunologic studies of blast cells from 13 children with acute mixed lineage leukemia (AMLL) to discern patterns of chromosome alteration and antigen expression that would assist in classification of this disease entity. Six patients with 11q23 translocations--including four with the t(11;19), one with the t(9;11), and one with the t(1;11)--were characterized by a young age and hyperleukocytosis. A B cell-associated antigen (CD19) and HLA-DR antigens were expressed by blast cells from all patients; only one case was positive for the common acute lymphocytic leukemia antigen (CALLA, CD10). A myeloid-associated antigen (CD13) was expressed by blast cells from one patient at diagnosis and from another at relapse; it was also expressed by cells from the remaining four patients after brief in vitro culture without addition of differentiating agents. Four patients with t(9;22)(q34;q11) were characterized by an older age and hyperleukocytosis. Each of these cases was positive for CD13, CD19, and HLA-DR, and three were positive for CALLA. The 11q23 translocation was associated with CALLA- ALL marked by a myeloid phenotype, whereas the t(9;22) occurred in cases of acute myeloid leukemia with a CALLA+ lymphoid phenotype. One case had a 7q35-q36 translocation, which involves the region of the T cell receptor beta-chain gene. Our results suggest that karyotypic alterations can be used to refine the classification of AMLL.     

Pediatric acute blastic natural killer cell leukemia

The goal of this report is to describe a rare case of pediatric blastic natural killer (NK) cell leukemia and to compare pediatric blastic NK cell leukemia/lymphoma to other reported cases of pediatric NK cell leukemia. The patient, a 9-year-old girl, presented with acute leukemia with a phenotype similar to adult blastic NK cell leukemia/lymphoma. The blasts were agranular and expressed CD7, 45, 56, and HLA-DR, but not CD3, 11c, 13, 33, or TdT. She had a complete response to ALL-directed chemotherapy, but had multiple relapses involving the cerebrospinal fluid, nasal sinus, lymph node and skin. In addition to the reported case, a review of the literature identified 9 previously reported cases of NK cell leukemia in patients 18 years of age or less. Cases were subdivided into blastic, acute/aggressive, and myeloid precursor NK cell leukemia based upon CD13/33 expression and morphologic characteristics. Compared to pediatric acute/aggressive NK cell leukemia, children with blastic NK cell leukemia showed greater variation in age and race. Prognosis was poor for all groups. Pediatric blastic NK cell leukemia is a distinct clinicopathologic entity which differs from other types of pediatric NK cell leukemia.     

Significance of aberrant immunophenotypes in childhood acute lymphoid leukemia

Leukemic cells from 51 pediatric patients (younger than 18 years) diagnosed with acute lymphoid leukemia by standard morphologic and cytochemical methods were subjected to flow cytometric studies using a panel of monoclonal antibodies against T-cell (CD1, 2, 3, 4, 5, 7, 8), B-cell (CD10, 19, 20, 21), myeloid (CD13, 14, 15, 33), and HLA-DR antigens. Cases of "conventional" acute lymphoid leukemia (leukemic cells with a normal configuration of B-cell or T-cell differentiation antigens) were observed in 26 of 51 (51%) cases, whereas cases of "aberrant" acute lymphoid leukemia (cells with abnormal patterns of B-cell or T-cell antigens or with concomitant myeloid antigens) were noticed in 25 (49%) cases. Myeloid antigen-positive acute lymphoid leukemia was observed in the leukemic cells of eight (16%) individuals. No significant differences were observed between conventional and aberrant ALL in the distribution of sex, age, leukocyte count, hemoglobin concentration, platelet count, blast count, French-American-British (FAB) type, lymphadenopathy, organomegaly, rate or duration of remission, or survival. When only myeloid antigen-positive cases were compared with myeloid antigen negative-cases, no significant correlations were observed except for duration of first remission (myeloid antigen positive, 26+ +/- 22 months; myeloid antigen negative, 40+ +/- 18 months; P less than 0.001), and duration of survival (myeloid antigen positive, 27+ +/- 24 months; myeloid antigen negative, 62+ +/- 17 months; P = 0.001). These data suggest that pediatric patients with ALL blasts possessing myeloid antigens may represent a high-risk group for length of remission and survival.     

Malignancies of natural killer (NK) cell precursor: myeloid/NK cell precursor acute leukemia and blastic NK cell lymphoma/leukemia.

Malignant hematolymphoid disorders arising from natural killer (NK) cells have become widely recognized in the past decade. Recently, we as well as others have drawn attention to some neoplasms of conceivable NK cell precursor origin that might represent two distinct entities, i.e. myeloid/NK cell precursor acute leukemia and blastic NK cell lymphoma/leukemia. Both of these diseases were characterized by remarkable extramedullary involvement and lymphoblastoid morphology, although the sites of involvement differed. Myeloid/NK cell precursor acute leukemia exhibited more frequent involvement of bone marrow (BM) and lymph nodes, whereas blastic NK cell lymphoma/leukemia affected extranodal sites, mainly the skin/subcutis. Tumor cells of these two diseases shared the CD16-, CD56+ and CD57- phenotype, but differed in other phenotypic profiles. Indeed, myeloid/NK cell precursor acute leukemia was immunophenotypically characterized by the expression of CD34 and blastic NK cell lymphoma/leukemia by that of CD4. On the theoretical level in the NK cell differentiation pathway, myeloid/NK cell precursor acute leukemia might be derived from a myeloid antigen-positive precursor preceding a NK cell committed precursor as a conceivable counterpart of blastic NK cell lymphoma/leukemia. Most cases with either disease lacked cytotoxic activities or molecules, a finding which seems to support their precursor origin. Notably, Epstein Barr virus (EBV) was negative in all cases, which contrasted with its high level associated with mature NK cell malignancies. Chemotherapy for acute myeloid leukemia was generally effective for myeloid/NK cell precursor acute leukemia, while the regimen for lymphoid malignancy was effective for blastic NK cell lymphoma/leukemia. These data suggests that each of these two diseases constitutes a distinct entity, which is also different from mature NK cell malignancies.     

Pediatric leukemia/lymphoma with t(8;14)(q24;q11).

A variety of chromosomal translocations occur in pediatric T-cell acute lymphoblastic leukemia (T-ALL) in which a cellular oncogene or growth-related gene is translocated to the alpha/delta locus of the T-cell receptor gene. The t(8;14)(q24;q11) has been described at the cytogenetic and molecular level, but the disease associated with this translocation has not been defined clinically. Fifteen pediatric cases of leukemia/lymphoma with a t(8;14)(q24;q11) chromosomal translocation were collected from previous publications and institutional records. The estimated prevalence of this abnormality among all cases of ALL was 1%. The t(8;14)(q24;q11) disease was characterized by male predominance (10/15), a median age of 5.5 years (range 1.8-17 years), high white blood cell count (median 95 x 10(9)/l), central nervous system infiltration (4/11), bulky extramedullary leukemia (10/11), and T-cell immunophenotype (12/15). The median event-free survival was 4 months, and the median survival, 11 months. Seven cell lines with t(8;14)(q24;q11) were established from six of the cases; four were T-lymphoblastic, one was T-lymphoblastic, but expressed myeloid-related antigens, and two were predominantly myeloid. t(8;14)(q24;q11) leukemia/lymphoma and other ALLs involving 13(q11) have in common a high tumor burden, early spread to extramedullary sites, a propensity to form T-lymphoblastic or T-myeloid cell lines and, usually, an aggressive clinical course.     

Plasmacytoid monocyte proliferation associated with myeloproliferative disorders.

Plasmacytoid T-cell (PTC) lymphoma is a rare clinicopathologic entity characterized by generalized lymphadenopathy in association with a myeloproliferative disorder. Hepatosplenomegaly and weight loss frequently are present. Nodal T-zone expansion by mononuclear cells with ultrastructural and immunohistochemical features typical of PTC is diagnostic. All of the five previously reported cases of PTC lymphoma coincided with or heralded the onset of a clinically aggressive myeloid leukemia. This strong association and recent immunohistochemical findings in reactive or neoplastic PTC favored a monocyte/macrophage derivation of these cells, and it has been suggested that they be renamed plasmacytoid monocytes (PM). Two additional cases of PTC lymphoma were studied at the institutions of the authors, and the findings supported the concept that PTC belong to the monocytic lineage. The disease presentation was generalized lymphadenopathy with constitutional symptoms. One patient also had hepatosplenomegaly and bilateral renal enlargement concomitantly with myelofibrosis with myeloid metaplasia that progressed within months to acute myelogenous leukemia. Similar rapid evolution of acute monoblastic leukemia occurred in the other patient. Tumor cells within subtotally effaced lymph nodes had positive findings for CD45, CD4, CD7, and LN2 and negative findings for CD3, CD8, and beta F1. Occasional cells had positive findings for CD2. One case demonstrated CD5, HLA-DR, CD71, and CD43 (Leu-22)-positive cells. The myeloid/monocyte-associated antigens CD14 and CD68 were identified in both. The tumor cells lacked the B-cell markers LN1, CD20 (L26), CD19, and CD22 and did not rearrange immunoglobulin heavy chain genes and T-cell receptor beta, gamma, and delta chain genes. The term plasmacytoid T-zone lymphoma or PM proliferation is more appropriate for this rare disease. The close association of the PM proliferation with a myeloproliferative disorder indicates that the two entities are related.