Histologic progression in non-Hodgkin's lymphoma

Hubbard, SM; Ba, Chabner; DeVita, VT Jr; Simon, R; Berard, CW; Jones, R. B.; Garvin, A. Julian; Gp, Canellos; Osborne, C. Kent; Young, Richard L.

doi:10.1182/blood.v59.2.258.bloodjournal592258

Cited by 25 publications

(27 citation statements)

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“…The overall frequency and long‐term probability of transformation (27% at 15 years) in the present study are similar to other recently reported series (Table ) with some differences that are proabably due to variability of biopsy policies and follow‐up duration (Bastion et al , ; Giné et al , ; Montoto et al , ; Al‐Tourah et al , ). Our findings are also in keeping with other reports indicating a poorer clinical outcome after HT (Hubbard et al , ; Acker et al , ; Bastion et al , ; Giné et al , ; Montoto et al , ; Al‐Tourah et al , ; Yuen et al , ).…”

Section: Discussionsupporting

confidence: 93%

“…Nevertheless, histological transformation (HT) to a more aggressive DLBCL remains a critical event in the natural history of FL, usually associated with refractoriness to treatment, rapid clinical progression and dismal outcome (Giné et al , ; Montoto et al , ; Al‐Tourah et al , ; Montoto & Fitzgibbon, ) In most cases, it is clinically marked by rapidly growing adenopathy, B‐symptoms and rising lactate dehydrogenase (LDH) levels. Because of the different definition criteria, biopsy policies and length of follow‐up, the reported incidence of HT is widely variable, ranging from less than 15% to more than 60% in published series (Cullen et al , ; Hubbard et al , ; Acker et al , ; Horning & Rosenberg, ; Gallagher et al , ; Ersboll et al , ; Bastion et al , ; Giné et al , ; Montoto et al , ; Al‐Tourah et al , ; De Jong & de Boer, ; Yuen et al , ).…”

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confidence: 99%

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Incidence, risk factors and outcome of histological transformation in follicular lymphoma

et al. 2012

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SummaryHistological transformation (HT) into diffuse large B-cell lymphoma (DLBCL) was documented in 37 of the 281 (13%; 95% CI, 9-18) follicular lymphoma (FL) patients treated at our institute from 1979 to 2007. HT occurred at a median of 2·75 years from initial FL diagnosis and HT rate was 15% at 10 years and 26% at 14 years, with a plateau from that point onward. Patients with bulky or extranodal disease, or those diagnosed before 1990 had a significantly higher risk of HT. When initial treatment strategies were taken into account, a reduced HT risk was seen in the patients initially managed with a 'watch and wait' policy, while the risk appeared significantly increased in the small subset of 18 patients initially managed with rituximab plus chemotherapy (P = 0·0005). HT was associated with a significantly shorter cause-specific survival (P = 0·0002).

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

Incidence, risk factors and outcome of histological transformation in follicular lymphoma

et al. 2012

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“…For example, t(11;18) positive marginal zone B‐cell lymphomas (MZBL) of mucosa‐associated lymphoid tissue (MALT)‐type have not been reported so far to progress to DLBL 32–34 . Low risk variants of B‐CLL with mutated IgV genes rarely progress, 35,36 whereas FL implicate a high risk for progression to DLBL 11,12 , 37–46 …”

Section: Frequency Of Lymphoma Progressionmentioning

confidence: 99%

Pathology of lymphoma progression

Zettl

Pfeifer

et al. 2001

Histopathology

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Reflecting the stepwise process of oncogenesis, lymphomas may cumulatively develop a more aggressive phenotype during the course of disease, a process referred to as lymphoma progression. Although morphological, clinical and biological aspects of lymphoma progression do not always overlap, changes in lymphoma morphology frequently indicate alterations in the clinical and biological behaviour of the disease. Indolent and aggressive lymphomas in disease progression can either be clonally related or represent clonally unrelated neoplasms. We propose to use the term 'lymphoma progression' in a biological sense denoting only clonal development of and within a lymphoma entity. The term 'composite lymphoma' should be used as a merely descriptive morphological designation for different lymphoma entities in one individual irrespective of clonal relationship. Many types of aggressive B-cell non-Hodgkin's lymphomas and Hodgkin's lymphomas are reported to secondarily develop in lymphoma progression. Genetic changes associated with lymphoma progression frequently abrogate the differentiating effects of alterations occurring in indolent lymphomas, leading to increased cell proliferation. Within different lymphoma entities, high-risk disease variants mimicking lymphoma progression exist.

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“…Transformation of follicular lymphoma (FL) to diffuse large B‐cell lymphoma (DLBCL, t‐FL) occurs commonly (Cullen et al , 1979; Hubbard et al , 1982; Garvin et al , 1983; Horning & Rosenberg, 1984; Bastion et al , 1997), being generally associated with a poor prognosis (Armitage et al , 1981) despite the use of adjunctive high‐dose therapy in selected individuals (Bastion et al , 1997; Chen et al , 2001; Williams et al , 2001). Further biological insights and new therapeutic strategies are therefore urgently required if the outlook for these patients following transformation is to be improved.…”

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Transformation of follicular lymphoma to diffuse large B‐cell lymphoma proceeds by distinct oncogenic mechanisms

et al. 2006

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Summary This study was undertaken to further elucidate the biological mechanisms underlying the frequent event of transformation of follicular lymphoma (FL) to diffuse large B‐cell lymphoma (t‐FL). The gene expression profiles of 20 paired lymph node biopsies, derived from the same patient pre‐ and post‐transformation, were analysed using the Lymphochip cDNA microarray. TP53 mutation analysis was performed and copy number alterations at the c‐REL and CDNK2A examined. Immunohistochemistry was performed on an independent panel of paired transformation paraffin‐embedded samples. Transformed follicular lymphoma was predominantly of the germinal centre B‐like phenotype both at the mRNA and protein level. Despite this homogeneity, transformation proceeded by at least two pathways. One mechanism was characterised by high proliferation, as assessed by the co‐ordinately expressed genes of the proliferation signature. This group was associated with the presence of recurrent oncogenic abnormalities. In the remaining cases, proliferation was not increased and transformation proceeded by alternative routes as yet undetermined. Genes involved in cellular proliferation prevailed amongst those that were significantly increased upon transformation and T cell and follicular dendritic‐associated genes predominated amongst those that decreased. t‐FL is a germinal centre B (GCB)‐like malignancy that evolves by two pathways, one that is similar in proliferation rate to the antecedent FL and the other that has a higher proliferation rate and is characterised by the presence of recognised oncogenic abnormalities.

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Histologic progression in non-Hodgkin's lymphoma

Cited by 25 publications

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Incidence, risk factors and outcome of histological transformation in follicular lymphoma

Incidence, risk factors and outcome of histological transformation in follicular lymphoma

Pathology of lymphoma progression

Transformation of follicular lymphoma to diffuse large B‐cell lymphoma proceeds by distinct oncogenic mechanisms

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