Anomalous retinoblastoma protein expression in Sternberg-Reed cells in Hodgkin's disease: a comparative study with p53 and Ki67 expression

Sánchez‐Beato, Margarita; Martínez-Montero, J C; Doussis-Anagnostopoulou, T A; Gatter, Kevin C.; Garcia, Joseph F.; Lloret, E; Piris, Miguel Á.

doi:10.1038/bjc.1996.489

Cited by 14 publications

(13 citation statements)

References 33 publications

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“…[152][153][154] Levels of Rb are low in low-growth fraction BCLs, whereas they are higher in most high-growth fraction tumors. 151,155 NLP-HL also displays this direct correlation between Rb and proliferation, 156 and in blastoid MCL the expression and phosphorylation level of Rb are higher than in classical types. 152 A deviation from this pattern, consisting of partial or total loss of Rb expression in highly proliferative tumors, was detected in a group of high-growth fraction nonHodgkin lymphomas (NHLs) 151,157 and classical HL 156 ; this may be, at least in part, a consequence of genetic alterations, which have been found at low frequencies in different lymphoid malignancies.…”

Section: Alterations In the Rb Pathway In Lymphomasmentioning

confidence: 99%

“…151,155 NLP-HL also displays this direct correlation between Rb and proliferation, 156 and in blastoid MCL the expression and phosphorylation level of Rb are higher than in classical types. 152 A deviation from this pattern, consisting of partial or total loss of Rb expression in highly proliferative tumors, was detected in a group of high-growth fraction nonHodgkin lymphomas (NHLs) 151,157 and classical HL 156 ; this may be, at least in part, a consequence of genetic alterations, which have been found at low frequencies in different lymphoid malignancies. Loss of Rb was found to be an adverse prognostic factor in LBCL, in which there was a correspondence between high Rb protein levels and extended overall survival time, 158 and in HL, in which Rb loss was related to failure to achieve complete remission 159 ; monoallelic deletions of Rb predict poor outcome in MM.…”

Section: Alterations In the Rb Pathway In Lymphomasmentioning

confidence: 99%

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Cell cycle deregulation in B-cell lymphomas

Sánchez‐Beato

Sánchez-Aguilera

Piris

2003

Blood

324

274

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Disruption of the physiologic balance between cell proliferation and death is a universal feature of all cancers. In general terms, human B-cell lymphomas can be subdivided into 2 main groups, low-and high-growth fraction lymphomas, according to the mechanisms through which this imbalance is achieved. Most types of low-growth fraction lymphomas are initiated by molecular events resulting in the inhibition of apoptosis, such as translocations affecting BCL2, in follicular lymphoma, or BCL10 and API2/MLT1, in mucosa-associated lymphoid tissue (MALT) lymphomas. This results in cell accumulation as a consequence of prolonged cell survival. In contrast, high-growth fraction lymphomas are characterized by an enhanced proliferative activity, as a result of the deregulation of oncogenes with cell cycle regulatory functions, such as BCL6, in large B-cell lymphoma, or c-myc, in Burkitt lymphoma. Low-and high-growth fraction lymphomas are both able to accumulate other alterations in cell cycle regulation, most frequently involving tumor suppressor genes such as p16 INK4a , p53, and p27 KIP1 . As a consequence, these tumors behave as highly aggressive lymphomas. The simultaneous inactivation of several of these regulators confers increased aggressivity and proliferative advantage to tumoral cells. In this review we discuss our current knowledge of the alterations in each of these pathways, with special emphasis on the deregulation of cell cycle progression, in an attempt to integrate the available information within a global model that describes the contribution of these molecular changes to the genesis and progression of B-cell lymphomas. IntroductionAlthough studies in experimental models and analyses of virusinduced cell transformation have shown that cell cycle subversion is a key step in tumorigenesis, the available information on human tumors has only recently reached the critical threshold of knowledge that allows a reasonably clear understanding of the mechanisms of cell cycle inactivation and their contribution to the genesis and progression of human cancer. Here, we have chosen B-cell lymphoproliferative lesions on the understanding that the accumulation of data concerning alterations in specific key genes makes it possible to propose a general model that describes the role of these specific alterations in cell cycle regulators in the initiation and progression of these tumors.Lymphoma/leukemia is a group of different types of cancer of the lymphoid system, in which numerous entities feature distinctive molecular alterations (Table 1). The most frequent types of lymphoma are collectively denominated B-cell lymphomas (BCLs), a term that encompasses different entities with variable clinical behavior and diverse molecular features. Nevertheless, in general terms, it is possible to segregate BCLs into 2 main groups, defined as low-and high-growth fraction lymphomas that roughly overlap with previous definitions of low-and high-histologic grade.Low-growth fraction BCLs, including follicular lymphoma (FL), marginal zo...

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Section: Alterations In the Rb Pathway In Lymphomasmentioning

confidence: 99%

Section: Alterations In the Rb Pathway In Lymphomasmentioning

confidence: 99%

Cell cycle deregulation in B-cell lymphomas

Sánchez‐Beato

Sánchez-Aguilera

Piris

2003

Blood

324

274

View full text Add to dashboard Cite

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“…Third, by recruiting E2Fs, they prevent them from acting as transactivators on target genes (Arroyo and Raychaudhuri, 1992). Upon phosphoryla- (Hangaishi et al, 1996;Sauerbrey et al, 1998) MM 13/88* 15% (D) (Corradini et al, 1994;Dao et al, 1994; 12/68* 18% (E) Zandecki et al, 1995) HD 21/130 16% (E) (Sanchez-Beato et al, 1996) Numbers with an asterix (*) are composite results from two or more studies. Abbreviations are: Diagnoses: ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia; ATL, adult T-cell leukemia/lymphoma; CML BC, blast crisis of chronic myeloid leukemia; HD, Hodgkin's disease; MDS, myelodysplastic syndrome; NHL, non-Hodgkin lymphoma.…”

Section: Regulation Of the G1/s Checkpoint Of The Cell Cyclementioning

confidence: 99%

“…Genetic loss of the chromosome 13q14 region, the region where the Rb gene is located, is a common ®nding in Non-Hodgkin lymphomas (NHL) and B-cell chronic lymphocytic leukemia (B-CLL), but this deletion does not seem to involve the Rb gene (Brown et al, 1993;Hawthorn et al, 1993). In Hodgkin's lymphoma, 16% showed loss of the Rb protein (Sanchez-Beato et al, 1996) and individuals with high Rb protein expression (420% positive staining) had a better survival of 100 vs 70% after 100 months (Morente et al, 1997).…”

Section: Rbmentioning

confidence: 99%

Tumor suppressor genes in normal and malignant hematopoiesis

2002

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“…(2) Another group with an abnormally high pRb/p105/Ki67 ratio, which could be subject to conflicting interpretations: (i) excess pRb/p105 protein to control cell cycle progression; or (ii) adhesion of the pRb/p105 protein to other cellular or viral proteins, such as p53 and MDM2. This may suggest that there is an anomalous pattern of expression of pRb/p105 in some cases of classical forms of Hodgkin's disease (Sanchez-Beato et al, 1996).…”

Section: Retinoblastoma Gene Family In Tumours Of Lymphoid Tissuesmentioning

confidence: 99%

Retinoblastoma gene family expression in lymphoid tissues

2006

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It appears more and more clear that retinoblastoma (RB) family of proteins represents key molecules in tumour suppression. This family consists of pRb/p105, p107 and pRb2/p130, which participate in a gene regulatory network that governs the cellular response to antimitogenic signals, and whose deregulation constitutes one of the hallmarks of cancer. Irrespective of their structural and biochemical similarities, RB proteins carry out different functional tasks. The expression of RB gene family in the reactive lymphoid tissues again confirms the different role of each member in cell cycle control and differentiation of normal cells. These different functional properties appear to be maintained in tumours lymphoid tissues, where alterations of the RB/p105 gene appear to be relatively rare. In this review, we will summarize the current knowledge about the role of the RB proteins in reactive and neoplastic lymphoid tissue.

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Anomalous retinoblastoma protein expression in Sternberg-Reed cells in Hodgkin's disease: a comparative study with p53 and Ki67 expression

Cited by 14 publications

References 33 publications

Cell cycle deregulation in B-cell lymphomas

Cell cycle deregulation in B-cell lymphomas

Tumor suppressor genes in normal and malignant hematopoiesis

Retinoblastoma gene family expression in lymphoid tissues

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