Rearrangements of bcl-6, bcl-2, c-myc and 6q deletion in B-diffuse large-cell lymphoma: Clinical relevance in 71 patients

Vitolo, Umberto; Gaïdano, Gianluca; Botto, Barbara; Volpe, Gisella; Audisio, Ernesta; Bertini, M; Calvi, R; Freilone, Roberto; Novero, Domenico; Orsucci, Lorella; Pastore, Cristina; Capello, Daniela; Parvis, Guido; Sacco, Cosimo; Zagonel, Vittorina; Carbone, Antonino; Mazza, U; Palestro, Giorgio; Saglio, Giuseppe; Resegotti, L

doi:10.1023/a:1008201729596

Cited by 81 publications

(68 citation statements)

References 39 publications

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“…28 Patients with BCL6 genetic alterations were subsequently described to have a better clinical outcome, 19 but this has been contradicted by other studies. 20,29 All clinical characteristics were also evenly distributed between patients with rearranged and those with germ-line BCL6 in such studies. 20,29 Thus, it is still controversial whether the BCL6 gene can be a useful marker for defining a subset of DLBLs.…”

Section: Figurementioning

confidence: 84%

“…20,29 All clinical characteristics were also evenly distributed between patients with rearranged and those with germ-line BCL6 in such studies. 20,29 Thus, it is still controversial whether the BCL6 gene can be a useful marker for defining a subset of DLBLs. In an attempt to establish definite dividing lines among DLBL cases, three groups have been identified in the present study on the basis of their surface markers: group I (CD5 + CD10 − CD20 + type), group II (CD5 − CD10 + CD20 + type), and group III (CD5 − CD10 − CD20 + type).…”

Section: Figurementioning

confidence: 84%

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Molecular and immunological dissection of diffuse large B cell lymphoma: CD5+, and CD5− with CD10+ groups may constitute clinically relevant subtypes

et al. 1999

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Diffuse large B cell lymphoma (DLBL) constitutes the greatest percentage of adult non-Hodgkin's lymphomas and represents a diverse spectrum of lymphoid neoplasms. Clinicopathologic, phenotypic and genotypic findings were correlated and compared for 63 DLBL cases to investigate whether they represent clinically relevant subtypes. They were all cyclin D1 negative and were phenotypically divided into three groups, ie group I (CD5 + type, n = 11), group II (CD5 − CD10 + type, n = 19), and group III (CD5 − CD10 − type, n = 33). Data were correlated by observing the respective gene rearrangement and expression of BCL2 and BCL6. In clinical aspects, the group I cases demonstrated a significantly inferior survival than those of the other two groups (log-rank test, P = 0.016). Although rearrangement of BCL2 and BCL6 did not show any inclination to a specific subgroup, the immunohistochemical detection of BCL2 was less frequent, at a statistically significant level (P = 0.011), in group II (50%) than in group I (82%) and III (82%) cases. This appears to confirm the unique aspect of the CD5 − CD10 + type DLBL, indicating a certain relationship with the normal germinal center cells which usually lack BCL2 expression. The BCL6 protein expression was detected in most of the present DLBL cases (92%) irrespective of this grouping. These data suggest that the phenotypic delineation by the detection of CD5 and CD10 will improve our understanding of DLBL and be helpful in a future subgrouping of DLBL.

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Section: Figurementioning

confidence: 84%

Section: Figurementioning

confidence: 84%

Molecular and immunological dissection of diffuse large B cell lymphoma: CD5+, and CD5− with CD10+ groups may constitute clinically relevant subtypes

et al. 1999

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“…Such alterations, most commonly 6q deletions, represent one of the most frequent karyotypic abnormalities encountered in the B-lymphoid neoplasms (10%-40%). 18,41,42,[51][52][53][54][55] While possibly correlating with an inferior outcome in follicular lymphoma, 42 they have no prognostic significance in most other neoplasms. In BL, 6q deletions have been found in 10% to 20% of cases in previously reported series 4,6 and in cell lines.…”

Section: Discussionmentioning

confidence: 99%

Secondary chromosomal abnormalities predict outcome in pediatric and adult high‐stage Burkitt lymphoma

Onciu

Schlette

Zhou

et al. 2006

Cancer

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Recent studies suggest that the hypodigms representing the two earliest Australopithecus (Au. anamensis and Au. afarensis) form an ancestor‐descendant lineage. Understanding the details of this possible transition is important comparative evidence for assessing the likelihood of other examples of ancestor‐descendant lineages within the hominin clade. To this end we have analyzed crown and cusp base areas of high resolution replicas of the mandibular molars of Au. anamensis (Allia Bay and Kanapoi sites) and those of Au. afarensis (Hadar, Laetoli, and Maka). We found no statistically significant differences in crown areas between these hypodigms although the mean of M1 crowns was smaller in Au. anamensis, being the smallest of any Australopithecus species sampled to date. Intraspecies comparison of the areas of mesial cusps for each molar type using Wilcoxon signed rank test showed no differences for Au. anamensis. Significant differences were found between the protoconid and metaconid of Au. afarensis M2s and M3s. Furthermore, the area formed by the posterior cusps as a whole relative to the anterior cusps showed significant differences in Au. afarensis M1s and in Au. anamensis M2s but no differences were noted for M3s of either taxon. Developmental information derived from microstructural details in enamel shows that M1 crown formation in Au. anamensis is similar to Pan and shorter than in H. sapiens. Taken together, these data suggests that the overall trend in the Au. anamensis‐Au. afarensis transition may have involved a moderate increase in M1 crown areas with relative expansion of distal cusps. Am J Phys Anthropol , 2012. © 2012 Wiley Periodicals, Inc.

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“…Approximately 50% of these tumors involve Ig gene rearrangements into BCL2, BCL6 or C-MYC chromosomal loci Vitolo et al, 1998 and references therein). Interestingly, the incidence of C-MYC gene rearrangements in tumors from HIV seropositive individuals is considerably higher than in those with no prior HIV exposure (Ladanyi et al, 1991).…”

Section: Non-burkitt's Lymphomamentioning

confidence: 99%

MYC oncogenes and human neoplastic disease

1999

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c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, we ®rst summarize data, derived mainly from non-clinical studies, indicating that these oncoproteins actually serve quite di erent roles in vivo. This concept necessarily lies at the heart of the basis for the observation that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences. We also review evidence implicating each of the above MYC genes in speci®c neoplastic diseases and have attempted to identify unresolved questions which deserve further basic or clinical investigation. We have made every attempt to review those diseases for which signi®cant and con®rmatory evidence, based on studies with primary tumor material, exists to implicate MYC members in their causation and/or progression.

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Rearrangements of bcl-6, bcl-2, c-myc and 6q deletion in B-diffuse large-cell lymphoma: Clinical relevance in 71 patients

Abstract: The analysis of molecular lesions in B-DLCL may be useful for a better diagnostic definition; however, in this study we were unable to show that the evaluated genetic lesions had a significant impact on clinical outcome.

Cited by 81 publications

References 39 publications

Molecular and immunological dissection of diffuse large B cell lymphoma: CD5+, and CD5− with CD10+ groups may constitute clinically relevant subtypes

Molecular and immunological dissection of diffuse large B cell lymphoma: CD5+, and CD5− with CD10+ groups may constitute clinically relevant subtypes

Secondary chromosomal abnormalities predict outcome in pediatric and adult high‐stage Burkitt lymphoma

MYC oncogenes and human neoplastic disease

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