Chromosome 11 rearrangements in the different haematological neoplasias

The cases of chromosome 11 abnormalities in leukemic bone marrow cells have constituted 14.0% in acute lymphoblastic leukemia (ALL), 18.7% in acute myeloid leukemia (AML), and 16.7% in refractory anemia (RA). The bands of the short arms 11p13, 11p14, llp15 and the long arms 11q14, 11q21, 11q23 were involved in chromosome rearrangements. The rearrangements of the band 11q23 were detected more often. Reciprocal translocations were found with the highest frequency, while para- and pericentic invertions, terminal and intestitial deletions occured with the lower incidence. Deletions were found in RA cases only. Comparison with the clinical features showed no correlation with the age and the main haematological indexes including the amount of blast cells in the initial period. The results have showed the poor prognosis of the abnormalities not only of 11q21, 11q23 in acute leukemia (AL), but of 11p13, 11p15 in AML as well, while not enough data on this subject is availalbe in the literature.     

Cytogenetic and molecular cytogenetic investigations in relapse of B-cell chronic lymphocytic leukemia

Сhromosomal abnormalities have been analyzed in bone marrow cells of 61 patients with relapse of B-cell chronic lymphocytic leukemia. The cytogenetic results have allowed the structural stratification of the obtained karyotypes into ten groups of clones: normal, normal/near tetraploid, abnormal/normal, abnormal/ near tetraploid/normal, evolution of clonal chromosome abnormalities; evolution of clonal chromosome abnormalities/normal, evolution of clonal chromosome abnormalities/near tetraploid/normal, independent clones, independent/normal clones; and independent/near tetraploid/normal clones. The identified structural rearrangements included translocations, deletions, insertions, and duplications; however, deletions with the involvement of bands 17p12, 13q12–q14, 11q14, and 11q23 dominated (63.8%). The application of i-FISH helped to show the presence of one to four abnormalities per karyotype. The identified cytogenetic and molecular cytogenetic rearrangements may signify a multilevel nature of the process underlying the development of resistant karyotypes. The results obtained under both methods have revealed the presence of a heterogenic cell population with possibly different levels of chemotherapy resistance.     

Chromosome 11 rearrangements in various hematological neoplasias

Chromosome 11 abnormalities in leukemic bone marrow cells were observed in 14.0% of the cases of acute lymphoblastic leukemia (ALL), in 18.7% of acute myeloid leukemia (AML) cases, and in 16.7% of refractory anemia (RA) cases. Bands 11pl3, 11pl4, 11pl5 on the short arm and 11ql4, 11q21, 11q23 on the long arm of chromosome 11 were involved in these rearrangements. Rearrangements of band 11q23 were detected most often. Reciprocal translocations were found with the highest frequency, while para-and pericentic inversions and deletions, both terminal and interstitial, occurred less often. In RA cases only deletions were observed. Comparison of clinical features showed no correlation with age and major hematological indexes such as the number of blast cells in the initial period. These results show that the prognosis is poor in cases of abnormalities at both 11q21 and 11q23 in acute leukemia (AL) as well as in 11pl3 and 11pl5 in AML. This is the first observation of these phenomena.     

The occurrence of a ring 18, an accessory bisatellited fragment,and trisomy 21 within one sibship

Summary A family is presented in which there were three different chromosome abnormalities in the children although the parents were cytogenetically normal. The proband had the karyotype 46,XX,r(18)(p11q23), a phenotypically normal brother was 47,XY,+mar, and another brother was a typical case of Down's syndrome, karyotype 47,XY,+21. There is nothing in the parents' history that provides grounds for a hypothesis to explain the coincidence of the abnormalities.     

Chromosome duplications and deletions and their mechanisms of origin.

Duplications and deletions of the same gene loci or chromosome regions are known to produce different clinical manifestations and are significant factors in human morbidity and mortality. Extensive cytogenetic and molecular cytogenetic studies with cosmid and YAC probes in two patients with unique mosaicism for reciprocal duplication-deletion allowed us to further understand the origin of these abnormalities. The first patient's mosaic karyotype was 46,XX, inv dup(11) (q23q13)/46,XX,del(11)(q13q23). The second patient had a 46,XY,dup(7)(p11.2p13)/46,XY,del(7)(p11.2p13)/46,XY karyotype. Fluorescence in situ hybridization studies on the first patient placed the two breakpoints near the folate-sensitive fragile sites FRA11A and FRA11B. The presence of repeated sequences responsible for these fragile sites may have been involved in the patient's duplication-deletion. Our investigation leads us to conclude that, in addition to known mechanisms (such as unequal crossovers between homologs, unequal sister chromatid exchanges, excision of intrachromatid loops, and meiotic recombination within a single chromatid), duplication-deletion can also arise by the formation of an overlying loop followed by an uneven crossover at the level of the DNA strand.     

Fine mapping of the constitutional translocation t(11;22)(q23;q11)

Translocation t(11;22)(q23;q11) is the most common constitutional reciprocal translocation in man. Balanced carriers are phenotypically normal, except for decreased fertility, an increased spontaneous abortion rate and a possible predisposition to breast cancer in some families. Here, we report the high resolution mapping of the t(11;22)(q23;q11) breakpoint. We have localised the breakpoint, by using fluorescence in situ hybidisation (FISH) walking, to a region between D11S1340 and WI-8564 on chromosome 11, and D22S134 and D22S264 on chromosome 22. We report the isolation of a bacterial artificial chromosome (BAC) clone spanning the breakpoint in 11q23. We have narrowed down the breakpoint to an 80-kb sequenced region on chromosome 11 and FISH analysis has revealed a variation of the breakpoint position between patients. In 22q11, we have sequenced two BACs (BAC2280L11 and BAC41C4) apparently mapping to the region; these contain low copy repeats (LCRs). Southern blot analysis with probes from BAC2280L11 has revealed different patterns between normal controls and translocation carriers, indicating that sequences similar/identical to these probes flank the translocation breakpoint. The occurrence of LCRs has previously been associated with genomic instability and "unclonable" regions. Hence, the presence of such repeats renders standard translocation breakpoint cloning techniques ineffective. Thus, we have used high resolution fiber-FISH to study this region in normal and translocation cases by using probes from 22q11, LCRs and 11q23. We demonstrate that the LCR containing the gap in 22q11 is probably substantially larger than the previous estimates of 100 kb. Using fiber-FISH, we have localised the breakpoint in 22q11 to approximately 20-40 kb from the centromeric border of the LCR (i.e. the telomeric end of AC006547) and have confirmed the breakpoint position on 11q23.     

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome-specific probes

OBJECTIVE: Although information on the cytogenetic characteristics of meningioma tumors has accumulated progressively over the past few decades, information on the genetic heterogeneity of meningiomas is still scanty. The aim of the present study was to analyze by interphase fluorescence in situ hybridization (FISH) the incidence of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y in a group of 70 consecutive meningioma tumors. Another goal was to establish the potential associations among the altered chromosomes, as a way to assess both intertumoral and intratumoral heterogeneity. METHODS: For the purpose of the study, 70 patients diagnosed with meningioma were analyzed. Interphase FISH for the detection of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y was applied to fresh tumor samples from each of the patients studied. RESULTS: The overall incidence of numerical abnormalities was 76%. Chromosome Y in males and chromosome 22 in the whole series were the most common abnormalities (46% and 61%, respectively). Despite the finding that monosomy of chromosome 22/22q(-) deletions are the most frequent individual abnormality (53%), we have observed that chromosome gains are significantly more common than chromosome losses (60% versus 40%). Chromosome gains corresponded to abnormalities of chromosomes 1 (27%), 9 (25%), 10 (23%), 11 (22%), 14 (33%), 15 (22%), 17 (23%), and X in females (35%) and males (23%) whereas chromosome losses apart from chromosome 22 frequently involved chromosomes 14 (19%), X in males (23%), and Y in males (32%). Although an association was found among most gained chromosomes on one side and chromosome losses on the other side, different association patterns were observed. Furthermore, in the latter group, monosomy 22/22q(-) was associated with monosomy X in females and monosomy 14/14q(-) was associated with nulisomy Y in males. In addition, chromosome losses usually involved a large proportion of the tumor cells whereas chromosome gains were restricted to small tumor cell clones, including tetraploid cells. CONCLUSIONS: Our results show that meningiomas are genetically heterogeneous tumors that display different patterns of numerical chromosome changes, as assessed by interphase FISH.     

Emanuel syndrome due to unusual segregation of paternal origin

Emanuel syndrome is an inherited chromosomal abnormality resulting from 3:1 meiotic segregation from parental balanced translocation carrier t(11;22)(q23;q11), mostly of maternal origin. It is characterized by mental retardation, microcephaly, preauricular tag or sinus, ear anomalies, cleft or high arched palate, micrognathia, congenital heart diseases, kidney abnormalities, structural brain anomalies and genital anomalies in male. Here in, we describe a female patient with supernumerary der(22) syndrome (Emanuel syndrome) due to balanced translocation carrier father t(11;22) (q23;q11). She was mentally and physically disabled and had most of the craniofacial dysmorphism of this syndrome. Our patient had cleft palate, maldeveloped corpus callosum and hind brain with normal internal organs. Additionally, arachnodactyly, hyperextensibility of hand joints, abnormal deep palmar and finger creases, extra finger creases and bilateral talipus were evident and not previously described with this syndrome. Cytogenetic analysis and FISH documented that the patient had both translocation chromosomes plus an additional copy of der(22) with karyotyping: 47,XX,t(11; 22)(q23;q11),+der(22)t(11;22)(q23;q11). We postulated that this rare chromosomal complement can arise from; 2:2 segregation in the first meiotic division of the balanced translocation father followed by non-disjunction at meiosis II in the balanced spermatocyte.     

Genetic features of B-cell chronic lymphocytic leukemia

The genetic features of B-cell chronic lymphocytic leukemia (CLL) are currently being reassessed by molecular cytogenetic techniques such as fluorescence in situ hybridization (FISH). Conventional cytogenetic studies by chromosome banding are difficult in CLL mainly because of the low in vitro mitotic activity of the tumor cells, which leads to poor quantity and quality of metaphase spreads. Molecular genetic analyses are limited because candidate genes are known for only a few chromosomal aberrations that are observed in CLL. FISH was found to be a powerful tool for the genetic analysis of CLL as it overcomes both the low mitotic activity of the CLL cells and the lack of suitable candidate genes for analysis. Using FISH, the detection of chromosomal aberrations can be performed at the single cell level in both dividing and non-dividing cells, thus circumventing the need of metaphase preparations from tumor cells. Probes for the detection of trisomies, deletions and translocation breakpoints can be applied to the regions of interest with the growing number of clones available from genome-wide libraries. Using the interphase cytogenetic FISH approach with a disease specific set of probes, chromosome aberrations can be found in more than 80% of CLL cases. The most frequently observed abnormalities are losses of chromosomal material, with deletions in band 13q14 being the most common, followed by deletions in 11q22-q23, deletions in 17p13 and deletions in 6q21. The most common gains of chromosomal material are trisomies 12q, 8q and 3q. Translocation breakpoints, in particular involving the immunoglobulin heavy chain locus at 14q32, which are frequently observed in other types of non-Hodgkin's lymphoma, are rare events in CLL. Genes affected by common chromosome aberrations in CLL appear to be p53 in cases with 17p deletion and ataxia telangiectasia mutated (ATM), which is mutated in a subset of cases with 11q22-q23 aberrations. However, for the other frequently affected genomic regions, the search for candidate genes is ongoing. In parallel, the accurate evaluation of the incidence of chromosome aberrations in CLL by FISH allows the correlation of genetic abnormalities with clinical disease manifestations and outcome. In particular, 17p abnormalities and deletions in 11q22-q23 have already been shown to be among the most important independent prognostic factors identifying subgroups of patients with rapid disease progression and short survival. In addition, deletion 17p has been associated with resistance to treatment with purine analogs. Therefore, genetic abnormalities may allow a risk assessment for individual patients at the time of diagnosis, thus giving the opportunity for a risk-adapted management.     

Isolation of 1001 new markers from human chromosome 11, excluding the region of 11p13-p15.5, and their sublocalization by a new series of radiation-reduced somatic cell hybrids.

The determination of the physical map of human chromosome 11 will require more clones than are currently available. We have isolated an additional 1001 new markers in a bacteriophage vector from a somatic cell hybrid cell line that contains most of chromosome 11, except the middle of the short arm. These markers were localized to five different regions, 11p15-pter, 11p12-cen, 11q11-q14, 11q14-q23, and 11q23-qter, by a panel of previously characterized somatic cell hybrids. The region 11q11-14 harbors genes that have been shown to be important in breast cancer, B-cell lymphomas, centrocytic lymphomas, asthma, and multiple endocrine neoplasia, type 1 (MEN1). To determine the positions of the recombinant clones located there, we developed a new series of radiation-reduced somatic cell hybrids. These hybrids, together with those previously characterized, allowed us to map the 11q11-q14 markers into 11 separate segregation groups.     

Combined deletion 18q22.2 and duplication/triplication 18q22.1 causes microcephaly,mental retardation and leukencephalopathy

Chromosome 18 abnormalities rank among the most common autosomal anomalies with 18q being the most frequently affected. A deletion of 18q has been attributed to microcephaly, mental retardation, short stature, facial dysmorphism, myelination disorders, limb and genitourinary malformations and congenital aural atresia. On the other hand, duplications of 18q have been associated with the phenotype of Edwards syndrome. Critical chromosomal regions for both phenotypes are contentious. In this report, we describe the first case of an 11-year old male with a combined interstitial duplication 18q22.1, triplication 18q22.1q22.2 and terminal deletion 18q22.2q23 with phenotypic features of isolated 18q deletion syndrome and absence of phenotypic features characteristic of Edwards syndrome despite duplication of the suggested critical region. This report allows for reevaluation of proposed critical intervals for the phenotypes in deletion 18q syndrome and Edwards syndrome.     

Identification of DNA copy-number aberrations by array-comparative genomic hybridization in patients with schizophrenia

Chromosomal abnormalities are implicated as important markers for the pathogenesis in patients with schizophrenia. In this study, with using bacterial artificial chromosome (BAC) array-based comparative genomic hybridization (CGH), we analyzed DNA copy-number changes among 30 patients with schizophrenia. The most frequent changes were partial gain of Xq23 (52%) and loss of 3q13.12 (32%). Other frequent gains were found in: 1p, 6q, 10p, 11p, 11q, 14p, and 15q regions, and frequent losses were found in: 2p, 9q, 10q, 14q, 20q, and 22q regions. The set of abnormal regions was confirmed by real-time PCR (9q12, 9q34.2, 11p15.4, 14q32.33, 15q15.1, 22q11.21, and Xq23). All real-time PCR results were consistent with the array-CGH results. Therefore, it is suggested that array-CGH and real-time PCR analysis could be used as powerful tools in screening for schizophrenia-related genes. Our results might be useful for further exploration of candidate genomic regions in the pathogenesis of schizophrenia.     

Regional assignment of six polymorphic DNA sequences on chromosome 21 by in situ hybridization to normal and rearranged chromosomes.

We have assigned six polymorphic DNA segments to chromosomal subregions and have established the physical order of these sequences on the long arm of chromosome 21 by in situ hybridization of cloned probes to normal metaphase chromosomes and chromosomes 21 from individuals with three different structural rearrangements: an interstitial deletion, a ring chromosome, and a reciprocal translocation involving four different breakpoints in band 21q22. Segments D21S1 and D21S11 map to region 21q11.2----q21, D21S8 to 21q21.1----q22.11, and D21S54 to 21q21.3----q22.11; D21S23 and D21S25 are both in the terminal subband 21q22.3, but they are separated by a chromosomal breakpoint in a ring 21 chromosome, a finding that places D21S23 proximal to D21S25. The physical map order D21S1/D21S11-D21S8-D21S54-D21S23-D21S25 agrees with the linkage map, but genetic distances are disproportionately larger toward the distal end of 21q.     

人体乳腺癌细胞系Bcap－37和MCF－7的细胞遗传学研究

应用低温同步法与秋水酰胺处理,对人体乳腺癌细胞系Ｂｃａｐ－３７和ＭＣＦ－７的中期及早中期细胞进行Ｇ－显带分析。研究表明,Ｂｃａｐ－３７细胞染色体众数为６３,可识别其结构的标记染色体１７条;ＭＣＦ－７细胞染色体众数为５６,可识别其结构的标记染色体１３条。结合文献报道以及本研究结果显示,乳腺癌中最常涉及到第１、３、５、７、１１、１３和１７号染色体结构及数目的异常,染色体断裂点１ｐ１１（１ｑ１１）、１ｐ１３、３ｐ２１、３ｑ１１、５ｑ１１、６ｑ１３、６ｑ２３、７ｑ２２、１１ｐ１３和１１ｐ１５也经常涉及;它们可能与癌相关基因的激活和抗癌基因的丢失有关,从而在乳腺癌发生发展中起一定作用。     

11q- syndrome: three cases and a review of the literature.

We report on three children with de novo terminal deletions of the long arm of chromosome 11 (11q-) and breakpoints in 11q23-q24. Eighty-nine other patients with partial monosomy 11q have been reported and were reviewed by us. Salient features of 11q- syndrome are psychomotor retardation, trigonocephaly, telecanthus/hypertelorism, broad depressed nasal bridge, micrognathia, low set abnormal ears, cardiac anomalies and hand/foot anomalies. Renal agenesis and anal atresia are reported first here. Supratentorial white matter abnormality on CT and MRI present in our second patient was reported in three patients. Increased mortality is caused by cardiac anomalies. A third of all patients with partial monosomy 11q had thrombocytopenia or pancytopenia and this seems to be related to the absence of band 11q23-q24. Seventy-six percent of patients have de novo deletions with breakpoints in 11q21-q25. There is no obvious correlation between the length of the deleted segment and the severity of the symptoms. In unbalanced chromosomal patterns with deletions of 11q involving bands 11q23-q24 the typical phenotype of 11q- syndrome remains recognizable. Deletions distal to 11q24.1 do not produce the typical 11q- syndrome.     

Promiscuous genes and chromosomal rearrangements of hematopoietic malignancies

The nonrandomness of chromosomal abnormalities of hematopoietic malignancies, which has been established twenty years ago, has evidenced a more or less close relationship between some structural chromosomal abnormalities and leukemia subtypes. The same relation was, then, shown between gene and chromosome rearrangements. It becomes now obvious that genes involved in malignant proliferations may rearrange several different partner genes, as for instance the genes MLL, localised to chromosome band 11q23, and ETV6/TEL to 12p13. The study of these rearrangements is of particular importance in order to improve our knowledge of the functions of rearranged genes as well as their normal counterparts, and to analyse mechanisms favoring the occurrence of chromosomal rearrangements in malignancies.     

混合表型急性白血病的细胞及分子遗传学研究进展

混合表型急性白血病(mixed-phenotype acute leukemia, MPAL)是一类同时表达不止一个谱系特异性抗原的恶性克隆性疾病,发生率低,仅占急性白血病的2%~5%。多数MPAL患者可检测出克隆性染色体异常及分子遗传学改变,其中一些特异性异常如t(9;22)(q34;q11)及KMT2A重排在MPAL的诊断分型、靶向治疗及预后判断中具有重要的指导意义。近年来,随着全基因组测序、全外显子测序、靶向测序及单核苷酸多态性-微阵列比较基因组杂交等分子生物学技术的广泛应用,人们发现一些新的分子遗传学异常如ZNF384重排及WT1基因突变等也与疾病的发生发展及预后密切相关。这些发现进一步丰富了对MPAL发病机制的认识。现将有关MPAL细胞及分子遗传学的研究进展进行综述。     

复杂染色体重排的女性携带者与她健康的女儿

一例新生复杂染色体重排的女性携带者（complex chromosome rearrangement ,CCR）,易位涉及1号、5号和12号染色体。病人因2次自然流产而要求进行外周血淋巴细胞G显带核型分析。最初G显带核型疑为46,XX,t(1;5;12)(1pter→1q25::12q24→12qter;5qter→5p11::1q25→1qter;12pter→12q24::5p11→5pter).经荧光原位杂交（FISH）技术检测,证实患者的核型为46,XX,t(1;5;12)(1pter→1q23::12q22→12qter;5qter→5p11::1q25→1qter;12pter→12q22::1q23→1q25::5p11→5pter).7年后病人再次妊娠,并拒绝产前诊断。女婴足月分娩,生长发育正常。核型为46,XX。比较以前报告的女性复杂易位携带者与我们报告的病例可以认为,CCR并不总是表现为自然流产或分娩畸形儿,仍有机会生出正常的孩子。Abstract: We reported in the paper one case of a de novo complex chromosomal rearrangement (CCR) involving three different chromosomes,1, 5 and 12. Two pregnancies of the female carrier over three years resulted in two spontaneous abortions. Initial cytogenetic analysis of her peripheral lymphocyte by G banding suspected a karyotype 46,XX,t(1;5;12)(1pter →1q25::12q24→12qter;5qter→ 5p11::1q25→1qter;12pter →12q24::5p11→5pter). Fluorescense in -situ hybridization (FISH) was used to confirm the karyotype 46,XX,t(1;5;12)(1pter→1q23::12q22→12qter;5qter→5p11::1q25→1qter;12pter→12q22::1q23→1q25::5p11→5pter). Seven years later she was pregnant again and refused to have prenatal diagnosis. The fetus is normal both in phenotype and karyotype。Comparing previously reported female CCR carriers with the case, we conclude that female CCR carriers may not always present spontaneous abortion or have offspring with congenital malformation and can have chance to get a healthy child.     

Meiotic recombination and spatial proximity in the etiology of the recurrent t(11;22)

Although balanced translocations are among the most common human chromosomal aberrations, the constitutional t(11;22)(q23;q11) is the only known recurrent non-Robertsonian translocation. Evidence indicates that de novo formation of the t(11;22) occurs during meiosis. To test the hypothesis that spatial proximity of chromosomes 11 and 22 in meiotic prophase oocytes and spermatocytes plays a role in the rearrangement, the positions of the 11q23 and 22q11 translocation breakpoints were examined. Fluorescence in situ hybridization with use of DNA probes for these sites demonstrates that 11q23 is closer to 22q11 in meiosis than to a control at 6q26. Although chromosome 21p11, another control, often lies as close to 11q23 as does 22q11 during meiosis, chromosome 21 rarely rearranges with 11q23, and the DNA sequence of chromosome 21 appears to be less susceptible than 22q11 to double-strand breaks (DSBs). It has been suggested that the rearrangement recurs as a result of the palindromic AT-rich repeats at both 11q23 and 22q11, which extrude hairpin structures that are susceptible to DSBs. To determine whether the DSBs at these sites coincide with normal hotspots of meiotic recombination, immunocytochemical mapping of MLH1, a protein involved in crossing over, was employed. The results indicate that the translocation breakpoints do not coincide with recombination hotspots and therefore are unlikely to be the result of meiotic programmed DSBs, although MRE11 is likely to be involved. Previous analysis indicated that the DSBs appear to be repaired by a mechanism similar to nonhomologous end joining (NHEJ), although NHEJ is normally suppressed during meiosis. Taken together, these studies support the hypothesis that physical proximity between 11q23 and 22q11--but not typical meiotic recombinational activity in meiotic prophase--plays an important role in the generation of the constitutional t(11;22) rearrangement.     

CD11c在慢性淋巴细胞白血病诊断中的意义

目的:探讨CD11c抗原在慢性淋巴细胞白血病(chronic lymphocytic leukemia,CLL)中的表达及在临床诊断中的价值,以及CD11c抗原表达与患者的遗传学异常及预后参数的相关性。方法:采用多参数流式细胞术(flow cytometry,FCM)检测200例CLL患者、49例套细胞淋巴瘤(mantle cell lymphoma,MCL)患者CD11c的表达率和平均荧光强度(mean fluorescence intensity,MFI);并比较CLL患者CD11c的表达与预后参数ZAP-70和CD38表达的关系;同时采用荧光原位杂交(fluorescence in situ hybridization,FISH)技术检测CLL患者的P53缺失、13q14缺失、ATM缺失、6q23缺失、+12以及IGH重排,比较CD11c~+CLL患者与CD11c~-CLL患者遗传学特点。结果:CLL患者中CD11c阳性率为49.5%(99/200),MFI中位值为2.06(1.00～7.34);而MCL患者中CD11c阳性率为6.12%(3/49),MFI中位值为2.00(1.97～2.54)。CD11c在CLL中的表达率明显高于MCL,(x~2=30.62,P0.05)。CD11c~+CLL患者的ZAP-70和CD38阳性率均明显高于CD11c~-CLL患者(x~2=15.472,P0.05;x~2=11.556,P0.05),差异有统计学意义。而CLL患者的CD11c表达率与P53缺失、13q14缺失、ATM缺失、6q23缺失、+12、IGH重排的结果均无统计学差异。结论:CD11c对于辅助诊断CLL有重要价值,尤其有助于CLL和MCL的诊断和鉴别诊断。