Yi Zhou

University of Texas MD Anderson Cancer Center, Houston, Texas, United States

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Publications (9)24.24 Total impact

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    ABSTRACT: Allogeneic hematopoietic stem cell transplantation (HSCT) is highly effective for treating acute lymphoblastic leukemia (ALL). However, many ALL patients relapse after HSCT. There has been a continuing effort to improve identification of patients at high risk of relapse, with the goal of early intervention to improve outcome. In this retrospective analysis, we examined the impact of minimal residual disease (MRD) on the risk of hematologic relapse in 149 adult patients with ALL undergoing allogeneic HSCT in morphologic remission. MRD was assessed at time of HSCT and following HSCT. Patients with pre-transplant MRD had a trend for shorter progression-free survival (PFS) at 2 years compared with patients without MRD, nearing statistical significance, 28% vs. 47%, p=0.08, on univariate analysis. This trend remained on multivariate analysis with better PFS in patients without MRD at time of HSCT, hazard ratio (HR) 0.62 (95% CI 0.37, 1.04), p=0.07. Additionally, emergence of MRD post-HSCT was a strong predictor for overt hematologic relapse (HR 4, p<0.001) with a median latency interval of 3.8 months. These findings demonstrate the predictive value of monitoring for MRD peri-transplant in adult patients with ALL.
    Clinical lymphoma, myeloma & leukemia 08/2014;
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    ABSTRACT: Chronic myelogenous leukemia (CML) in blast phase (BP) is frequently accompanied by cytogenetic abnormalities in addition to t(9;22)(q34;q11.2). We describe a 72-year-old woman with a history of CML, treated with imatinib, and in complete remission for 23 months when she developed sudden coagulopathy as a manifestation of BP. Bone marrow (BM) aspiration and biopsy revealed hypercellular BM with numerous promyelocytes with cytochemical analysis of a BM aspirate smear showing strong myelokperoxidase positivity. Auer rods were also identified. Conventional cytogenetic analysis showed 46,XX,der(3)t(3;15)(q21;q15)t(15;17)(q24.1;q21.2),t(9;22)(q34;q11.2),der(15)t(3;15),del(17)(q21)[20]. The presence of BCR-ABL1 and PML-RARA were confirmed by fluorescence in situ hybridization (FISH) and reverse transcription-polymerase chain reaction (RT-PCR). Molecular studies showed no mutations in ABL1, FLT3, NPM1, RAS, KIT, IDH1, IDH2, and JAK2 genes. The patient was treated with all-trans retinoic acid and arsenic trioxide and achieved complete cytogenetic remission with no evidence of PML-RARA detected by FISH and RT-PCR and low level of BCR-ABL1 fusion transcripts detected by RT-PCR. The patient expired as a result of multiorgan system failure 2 months later. Based on our review of the literature, this is the second confirmed case of CML developing t(15;17)(q24.1;q21.2)/PML-RARA at time of BP. Although the BP resembled de novo acute promyelocytic leukemia (APL) morphologically, this patient had a more aggressive clinical course (compared with de novo APL) and died of complications of therapy.
    Journal of Hematopathology. 12/2013;
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    ABSTRACT: Terminal deoxynucleotidyl transferase (TdT) can be downregulated in minimal residual disease of T-acute lymphoblastic leukemia/lymphoma (T-ALL/LBL) after chemotherapy. TdT-negative T-ALL/LBL cases are rare and have not been well characterized. We studied the clinicopathologic features of de novo T-ALL/LBL patients treated at our institution during 2003-2011, with an emphasis on immunophenotype and survival of TdT-negative versus TdT-positive cases. Absence of TdT expression was defined as <10% lymphoblasts positive. Seven (12%) TdT-negative cases were identified from a cohort of 59 de novo T-ALL/LBL. The TdT-negative and TdT-positive cases were similar with regard to gender, percentage of patients with a high leukocyte count (>100 × 10(9)/l), central nervous system involvement, and an abnormal karyotype. However, patients with TdT-negative T-ALL/LBL had a significantly higher rate of disease progression and shorter overall survival. Although not statistically significant, TdT-negative T-ALL/LBL cases were associated with an older median age and higher percentage of 'early T precursor' (ETP) immunophenotype than TdT-positive cases. Absence of TdT expression identifies a subset of high-risk T-ALL/LBL that overlaps with, but is not identical to, the ETP leukemia, providing additional prognostic value.Modern Pathology advance online publication, 24 May 2013; doi:10.1038/modpathol.2013.78.
    Modern Pathology 05/2013; · 5.25 Impact Factor
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    ABSTRACT: Acute promyelocytic leukemia (APL) is an aggressive disease that requires prompt diagnosis and therapy. Flow cytometry immunophenotyping can serve as a screening test for APL before the results of cytogenetic or molecular testing for t(15;17)(q22;q21)/PML-RARα are often dimly expressed or absent in APL. We used flow cytometry immunophenotyping with an antibody panel including CD11a and CD18 to assess 36 APL and 33 other AML cases. HLA-DR, CD11a, and CD18 were absent in 81% of APL and 12% of other AML cases (specificity, 88%). By further including combinations of HLA-DR-, CD2+, and either CD11a- or CD18-, we identified 92% of APL cases with 85% specificity. These data compare favorably with the combination of HLA-DR-, CD34-, and CD117+ for APL diagnosis, which had a sensitivity of 64% in this study.
    American Journal of Clinical Pathology 11/2012; 138(5):744-50. · 2.88 Impact Factor
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    ABSTRACT: Mantle cell lymphoma (MCL) and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) share many features and both arise from CD5+ B-cells; their distinction is critical as MCL is a more aggressive neoplasm. Rarely, cases of composite MCL and CLL/SLL have been reported. Little is known about the nature of these cases and, in particular, the clonal relationship of the 2 lymphomas. Eleven composite MCL and CLL/SLL cases were identified. The clinical, morphologic and immunophenotypic features of the MCL and CLL/SLL were characterized. IGH (immunoglobulin heavy chain) gene analysis was performed on microdissected MCL and CLL/SLL components to assess their clonal relationship. Ten patients had lymphadenopathy, and 7 patients had bone marrow involvement. The MCL component had the following growth patterns: in situ (n = 1), mantle zone (n = 3), nodular and diffuse (n = 3), diffuse (n = 3), and interstitial in the bone marrow (the only patient without lymphadenopathy) (n = 1); 6 MCLs had blastoid or pleomorphic and 5 small lymphocytic features. The CLL/SLL component was nodular (n = 9) or diffuse (n = 2). All MCL were CD5(+) and cyclin D1(+) with t(11;14) translocation. All CLL/SLL were CD5(+), CD23(+) and negative for cyclin D1 or t(11;14). IGH gene analysis showed that the MCL and CLL/SLL components displayed different sized fragments, indicating that the MCL and CLL/SLL are likely derived from different neoplastic B-cell clones. The lack of a clonal relationship between the MCL and CLL/SLL components suggests that MCL and CLL/SLL components represent distinct disease processes and do not share a common progenitor B-cell.
    Human pathology 08/2012; · 3.03 Impact Factor
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    ABSTRACT: Plasma cell myeloma (PCM) exhibits immunophenotypic aberrancies that can be used for minimal residual disease (MRD) detection after therapy. The authors sought to determine whether non-neoplastic plasma cells, especially in the bone marrow (BM) post various therapies, would exhibit immunophenotypic variations interfering PCM MRD detection. The authors studied the flow cytometric immunophenotypes of non-neoplastic plasma cells from 50 BM specimens, including 12 untreated BM and 38 BM specimens from patients with non-plasmacytic haematological malignancies undergoing various therapies, and compared with 59 BM specimens positive for PCM MRD. Non-neoplastic plasma cells showed heterogeneous expressions of CD45 (78% (41-100)) and CD19 (80% (52-97)), and were negative for CD20 and CD117. CD56 was observed in a small subset (6% (0-37)) and CD28 in a larger subset (15% (0-59)) of non-neoplastic plasma cells, with the latter more frequently expressed in post-treatment BMs (p=0.01). However, despite a partial immunophenotypic overlap, PCM cells could be reliably discriminated from non-neoplastic plasma cells by the presence of a higher number of aberrancies (3 (1-6) vs 0 (0-2)) and stronger intensity and uniformity of aberrant expression (p<0.001 in each marker using a cut-off value). In addition, simultaneous assessment of cytoplasmic κ/λ with surface markers detected light chain restriction in all 59 PCM cases. In conclusion, non-neoplastic plasma cells in BM are more immunophenotypically heterogeneous than previously understood; however, these immunophenotypic variations differ from those of PCM. With advances in multicolour flow cytometry and application of recently validated markers, PCM MRD may still be reliably distinguished from non-neoplastic plasma cells.
    Journal of clinical pathology 06/2012; 65(9):823-9. · 2.43 Impact Factor
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    ABSTRACT: Bone marrow assessment for myelodysplastic syndrome (MDS) in a patient who develops cytopenia(s) following cancer therapy is challenging. With recent advances in multi-color flow cytometry immunophenotypic analysis, a CD34(+) progenitor-focused 7-color assay was developed and tested in this clinical setting. This assay was first performed in 73 MDS patients and 53 non-MDS patients (developmental set). A number of immunophenotypic changes were differentially observed in these two groups. Based on the sensitivity, specificity and reproducibility, a core panel of markers was selected for final assessment that included increased total CD34(+) myeloblasts; decreased stage I hematogones; altered CD45/side scatter; altered expression of CD13, CD33, CD34, CD38, CD117, and CD123; aberrant expression of lymphoid or mature myelomonocytic antigens on CD34(+) myeloblasts; and several marked alterations in maturing myelomonocytic cells. The data were translated into a simplified scoring system which was then used in 120 patients with cytopenia(s) secondary to cancer therapy over a 2-year period (validation set). With a median follow-up of 11 months, this assay demonstrated 89% sensitivity, 94% specificity, and 92% accuracy in establishing or excluding a diagnosis of MDS.
    Leukemia research 05/2012; 36(8):974-81. · 2.36 Impact Factor
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    ABSTRACT: B-lymphoblastic leukemia/lymphoma, also known as B-acute lymphoblastic leukemia, is derived from B-cell progenitors. B-acute lymphoblastic leukemia occurs predominantly in children, but can occur at any age. Risk-adapted intensive chemotherapy is effective in treating most children with B-acute lymphoblastic leukemia, but this approach is less successful in adults. Recent developments in genome-wide genetic analysis in B-acute lymphoblastic leukemia have provided insights into disease pathogenesis and prognosis. B-acute lymphoblastic leukemia cases usually carry a primary genetic event, often a chromosome translocation, and a constellation of secondary genetic alterations that are acquired and selected dynamically in a nonlinear fashion. These genetic changes commonly affect cellular mechanisms that control B-cell differentiation and proliferation. The cooperative interaction between inactivation of hematopoietic transcription factors involved in differentiation (class II mutation) and activating mutations involved in cell proliferation (class I mutation) is reminiscent of the pathogenic model of acute myeloid leukemia. The resulting improved molecular understanding of B-acute lymphoblastic leukemia is helping to refine disease risk stratification and discover new therapeutic approaches for patients with refractory disease. In this review, we first summarize the clinicopathologic and immunophenotypic features of B-acute lymphoblastic leukemia and introduce current understanding of B-cell development and B-acute lymphoblastic leukemia leukemogenesis. We then focus on recent advances in genetic analysis and gene expression profiling of B-acute lymphoblastic leukemia and discuss the implications of these findings for disease evolution, risk prediction, and possible novel therapeutic approaches.
    Human pathology 05/2012; 43(9):1347-62. · 3.03 Impact Factor
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    ABSTRACT: This study is focused on therapy-related myeloid neoplasms after the most promising frontline FCR (fludarabine, cyclophosphamide, and rituximab) therapy in previously untreated chronic lymphocytic leukemia patients. A total of 28 therapy-related myeloid neoplasm patients were identified, including 19 patients from 3 well-controlled FCR frontline trials (n=426 patients), giving an estimated frequency of 4.5% (1.9-8.3%) in a follow-up period of 44 months (range 5-122 months). Clinically, therapy-related myeloid neoplasms could emerge directly from 'prolonged myelosuppression' after FCR (10 patients), or after achieving complete hematological recovery (n=18). The overall latency was 35 months (range 3-118 months), with the former group of 23 months and the latter 42 months (P<0.001). In all, 10 cases presented as therapy-related acute myeloid leukemia and 18 as therapy-related myelodysplastic syndromes. Abnormal cytogenetics was present in 26 of 27 (96%) patients, with frequent chromosomes 5 and 7 abnormalities. The median survival was 7 months after therapy-related myeloid neoplasms. Our results indicate that the risk of therapy-related myeloid neoplasms secondary to frontline FCR therapy may not be as high as previously reported after removing the confounding factor of previous cytotoxic exposure, but this risk increased with older age and likely growth factor co-administration. Therapy-related myeloid neoplasms after FCR therapy shares clinicopathological features with therapy-related myeloid neoplasms secondary to other alkylating agents, but has a shorter latency interval indicating possible synergetic effects of the nucleotide analog fludarabine. The fact that therapy-related myeloid neoplasms can directly emerge from 'prolonged myelosuppression' warrants a bone marrow examination to rule out therapy-related myeloid neoplasms in this clinical setting.
    Modern Pathology 11/2011; 25(2):237-45. · 5.25 Impact Factor