Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma of Natural Killer (NK) Lineage: Quest for Another NK-Lineage Neoplasm

Nakamura, Fumihiko; Tatsumi, E; Tani, Akemi; Kumagai, Shunichi; Nishikori, M; Nagai, Tomoko

doi:10.1182/blood.v89.12.4665

Cited by 15 publications

(7 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In their quest for another NK-lineage neoplasm, Nakamura et al [14] emphasized the importance of the CD7 + , CD5 − , CD2 + , CD56 + phenotype in the definition of what they called ALL/lymphoblastic lymphoma of NK lineage. CD56 + leukemia/blastic lymphoma cases described in the literature, however, demonstrate remarkable heterogeneity in terms of T-antigen expression.…”

Section: Fig 3 (A) Tcrbv Gene Segment Usage In Blast Cells From Patmentioning

confidence: 99%

“…These lymphomas are frequently localized in the nasopharyngeal region, are often seen in patients of Asian origin, associated with EBV infection, and demonstrate aggressive clinical behavior [3][4][5][6][7]. While acute leukemias with both myeloid and NK antigenic properties have been well established [8,9], the definition of acute NK-cell leukemia/blastic NKlymphoma as a distinct clinicopathologic entity among the lymphoid leukemias has been plagued by a broad spectrum of morphologic, immunophenotypic, and clinical features [8,[10][11][12][13][14][15]. As expected from the proven reported to date demonstrate antigenic characteristics typical of early T-lymphocytes, such as selected cytoplasmic CD3 proteins, concomitantly with the NK-cell marker CD56 but not CD16 or CD57.…”

Section: Introductionmentioning

confidence: 99%

“…As expected from the proven reported to date demonstrate antigenic characteristics typical of early T-lymphocytes, such as selected cytoplasmic CD3 proteins, concomitantly with the NK-cell marker CD56 but not CD16 or CD57. While in true NK cells, T-cell receptor (TCR) genes remain in germline configuration during development [16], data on clonal TCR gene rearrangements in lymphoid NK-cell leukemias are inconsistent [10][11][12][13][14][15]17,18]. To date, there have been no reports on CD56 + B-lineage ALL.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Rare adult acute lymphocytic leukemia with CD56 expression in the ECOG experience shows unexpected phenotypic and genotypic heterogeneity

et al. 2001

View full text Add to dashboard Cite

Expression of CD56, a marker of natural killer (NK) cells, in acute lymphocytic leukemia (ALL) is rare and, to date, has been described only in non-B lineage ALL. Among 194 patients with CD56 analysis on the ongoing Eastern Cooperative Oncology Group (ECOG) ALL trial, E2993, 6 cases of CD56+ ALL were found (3.1%) with a median of 95% of blast cells expressing CD56, compared with a median of 1% of blast cells in CD56- ALL (P = 0.0001). FAB-L2 characteristics dominated, without granulation. Blast cells from four CD56+ patients expressed T-cell antigens at variable levels of maturation. A clonal rearrangement of the T-cell receptor beta (TCRbeta) gene was detected only in one patient. TCRbeta variable gene usage studies in this and one other CD56+ ALL patient demonstrated a significantly perturbed usage pattern in both patients when compared with control lymphocytes. The two remaining cases typed as early pre-B ALL (CD19+, CD10+), with one case co-expressing CD7. Cytogenetically, 4 patients were normal, 1 complex abnormal, and 1 Philadelphia chromosome positive. Epstein-Barr virus (EBV) sequences were detected in one T- and both B-lymphoid cases. Our data suggest that CD56 is expressed at a precursor stage common to the T- and the B-cell lineage.

show abstract

Section: Fig 3 (A) Tcrbv Gene Segment Usage In Blast Cells From Patmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Rare adult acute lymphocytic leukemia with CD56 expression in the ECOG experience shows unexpected phenotypic and genotypic heterogeneity

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Myeloid/NK cell precursor acute leukemia is a myeloperoxidase negative and Sudan black staining negative acute leukemia, and shows sCD3 − CD56 + and myeloid antigens (CD13 and/or CD33) (2, 5). Precursor NK cell ALL is a leukemia with phenotype of sCD3 − CD56 + , and negative for B‐cell (CD19, CD20) and myeloid (CD13, CD33) antigens (2, 6). This disease shows germinal configuration of T‐cell receptor and immunoglobulin genes (2, 6).…”

mentioning

confidence: 99%

“…Precursor NK cell ALL is a leukemia with phenotype of sCD3 − CD56 + , and negative for B‐cell (CD19, CD20) and myeloid (CD13, CD33) antigens (2, 6). This disease shows germinal configuration of T‐cell receptor and immunoglobulin genes (2, 6). Chronic NK lymphocytosis is characterized by chronic expansion of NK cells (more than 600 NK cells/ μ L for more than 6 month) without clinical lymphomas (2, 7, 8).…”

mentioning

confidence: 99%

Methylation status analysis of cell cycle regulatory genes (p16INK4A, p15INK4B, p21Waf1/Cip1, p27Kip1 and p73) in natural killer cell disorders

Kawamata¹,

Inagaki²,

Mizumura³

et al. 2005

European J of Haematology

View full text Add to dashboard Cite

Natural killer (NK) cell disorders are rare diseases. Genetic abnormalities of the several tumor suppressor genes, including p15INK4B, p16INK4A/p14ARF, p53, p73, and Rb genes have been reported. Deletions and point mutations of these genes are frequently detected in these diseases. It has been reported that tumor suppressor genes are inactivated by DNA methylation of the promoter region and/or first exon of the genes in a variety of human cancers. In this study we analyze the methylation status of the genes associated with cell cycle regulation, including p16INK4A, p15INK4B, p21/Waf1/Cip1, p27/Kip1, p73, and p14ARF, by methylation specific (MS) PCR and/or bisulfite sequencing. We examined 29 cases of NK cell disorders (five aggressive NK cell leukemia/lymphoma, three blastic NK cell lymphoma/leukemia, five nasal NK cell lymphoma, three myeloid/NK cell precursor acute leukemia, 13 chronic NK lymphocytosis). We found methylation of the first exon of the p16INK4A gene in two cases (one aggressive, one blastic), and methylation of the p14ARF gene in one aggressive NK cell leukemia. Bisulfite sequencing revealed that methylation of the p15 and p27 genes was rare in these disorders. MS-PCR suggested that the p73 and p21 genes were methylated in seven cases, respectively (p73: one blastic, one nasal, five chronic; p21: one myeloid/NK, one aggressive, one nasal, and four chronic); bisulfite sequencing confirmed that methylated alleles of these genes were dominant in the samples except three cases (one myeloid/NK, one aggressive, and one chronic) in which methylated alleles of the p21 genes were less than 34% of all alleles. These results suggested that inactivation of the cell cycle regulatory genes by DNA methylation could be associated with tumorigenesis in NK cell disorders, not only aggressive subtypes but also chronic subtype.

show abstract

Blastic natural killer cell lymphoma/leukemia (CD56‐positive blastic tumor)

Suzuki

Nakamura

Suzumiya

et al. 2005

Cancer

View full text Add to dashboard Cite

We performed cytological examination of urethral brushing to study aberrant E‐Cadherin expression as a possible marker for papillomavirus in cytological samples. A total of 30 cytobrush male urethral smears were examined E‐cadherin expression and human papillomavirus (hpv) was confirmed using PCR‐DNA. The age range was 19–36 years (mean: 27 years), 17 (56.7%) cases corresponded to low‐risk HPV and 13 (43.3%) cases were high‐risk HPV. The mean age ranges were 25.77 ± 5.90 years for high‐risk HPV and 26.77 ± 4.31years for low‐risk HPV. Pap smears showed dyskeratosis in 23 (76.7%) cases, koilocytes in 13 (43.3%) cases, infection or bacterial background in 14 (43.7%) cases, suggestive changes of Gardnerella infection in 7 (23.3%) cases, and Chlamydia in 3 (10%) cases. Immunohistochemistry was positive for membrane E‐Cadherin; there was weak expression in 13 (43.3%) cases, moderate expression in 11 (36.7%) cases (P = 0.109) (Figs. 3a and b), and strong expression in 6 (20%) cases. There were a statistically significant correlations between E‐Cadherin expression and koilocytes (P = 0.007), individual cell dyskeratosis (P = 0.041), and HPV risk (P = 0.000). We concluded that the loss of E‐Cadherin membrane expression was greater in high‐risk HPV cases and was associated with individual cell dyskeratosis features and koilocytes. There were statistically significant correlations between E‐Cadherin expression and dyskeratosis (P = 0.043), koilocytes (P = 0.007), and type of HPV (P = 0.000). Using male urethral smears to test for the loss of E‐Cadherin membrane expression is simple, rapid, specific and more sensitive than conventional morphologic observations. We concluded that E‐Cadherin can be used to discriminate between high‐ and low‐risk papillomavirus in urethral cytologic specimens. Diagn. Cytopathol. 2010;38:583–589. 2009 Wiley‐Liss, Inc.

show abstract

Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma of Natural Killer (NK) Lineage: Quest for Another NK-Lineage Neoplasm

Cited by 15 publications

References 12 publications

Rare adult acute lymphocytic leukemia with CD56 expression in the ECOG experience shows unexpected phenotypic and genotypic heterogeneity

Rare adult acute lymphocytic leukemia with CD56 expression in the ECOG experience shows unexpected phenotypic and genotypic heterogeneity

Methylation status analysis of cell cycle regulatory genes (p16INK4A, p15INK4B, p21Waf1/Cip1, p27Kip1 and p73) in natural killer cell disorders

Blastic natural killer cell lymphoma/leukemia (CD56‐positive blastic tumor)

Contact Info

Product

Resources

About