Serpin A1 is overexpressed in ALK+ anaplastic large cell lymphoma and its expression correlates with extranodal dissemination

Duplantier, Marie-Michèle; Lamant, Laurence; Sabourdy, Frédérique; Reyniès, Aurélien de; Delsol, Georges; Espinos, Estelle

doi:10.1038/sj.leu.2404352

Cited by 16 publications

(10 citation statements)

References 26 publications

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“…The cell lines of Burkitt's lymphoma Daudi and the thymoma Ichikawa were cultured (0.5 × 10 6 ml −1 ) in complete RPMI 1640 medium supplemented with 10% heatinactivated FCS. Karpas-299 and COST ALCL cells were kept between 0.5 and 1 × 10 6 cells/ml in the same culture medium but supplemented with 15% FCS as previously described [37,38].…”

Section: Cell Culturementioning

confidence: 99%

“…COST is another CD30 + perforin + TCR − ALCL cell line that is also recognized and strongly stripped by the same ␥␦ T cells [32,37]. By contrast however, COST expresses high levels of serpin A1 [38], a potent inhibitor of granzyme/perforin-mediated lysis. Hence COST is much less efficiently killed by ␥␦ T lymphocytes (not shown), thereby providing an ideal model to answer the above question.…”

Section: Weak Stripping and Targeting Of Perforin Secretion In The Rementioning

confidence: 99%

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Human γδ T lymphocytes strip and kill tumor cells simultaneously

et al. 2007

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Section: Cell Culturementioning

confidence: 99%

Section: Weak Stripping and Targeting Of Perforin Secretion In The Rementioning

confidence: 99%

Human γδ T lymphocytes strip and kill tumor cells simultaneously

et al. 2007

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“…The hypothesis of a possible role of AAT in the development of lymphoprolipheration disorders was supported by an increased incidence of abnormal Pi phenotypes (Pi MZ, Pi SS) in malignant lymphomas [8]. Anaplastic large cell lymphoma is a subtype of non-Hodgkin's lymphoma, and some data suggest that serpin A1 has an invasion-promoting effect on its development [9].…”

Section: Discussionmentioning

confidence: 99%

Inherited Alpha-1 antitrypsin deficiency and chondrosarcoma: a possible causal relationship

Serapinas¹,

Strazdaite²,

Linauskienė³

et al. 2010

Biologija

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Alpha 1-antitrypsin deficiency is a genetic risk factor for manifestation of COPD and chronic liver diseases. There is an ongoing worldwide discussion concerning the role of serpins (serine protease inhibitors) in tumour genesis. Protease inhibitors such as alpha 1-antitrypsin have generally been considered to counteract tumour progression and metastases because of their ability to inhibit proteases. In this case report, we analyze relationship between inherited alpha-1 antitrypsin deficiency and chondrosarcoma. A 47-year-old woman was admitted to the hospital with relapse signs of humerus chondrosarcoma. The patient had also a history of COPD. After chest X-ray and CT, alpha 1-antitrypsin deficiency was suspected. Inherited alpha-1 antitrypsin deficiency (PiZZ homozygous genotype) was confirmed. Alpha 1-antitrypsin deficiency might have facilitated the development of chondrosarcoma. Because of low incidence rate of such diseases, we presume that there is a slight chance for such rare disorders to manifest concurrently in the same patient.

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“…46,47 SerpinA1 is also a plasma serine protease inhibitor regulated by ALK and may have an invasion-promoting effect in ALK + ALCL. 48…”

Section: Pathogenesis and Molecular Featuresmentioning

confidence: 99%

Pathobiology and Molecular Profiling of Peripheral T-Cell Lymphomas

Leval¹,

Gaulard²

2008

Hematology

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Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of rare diseases, usually manifesting clinical aggressiveness. Although important novel insights into the pathobiology of nodal PTCL have been gained recently from molecular profiling studies and clinico-pathological analyses, the pathogenetic molecular lesions remain to be deciphered for most entities. Angioimmunoblastic T-cell lymphoma (AITL) comprises CD4+ CXCL13+ neoplastic cells displaying overlapping immunophenotypical and molecular features with normal follicular helper T cells. This derivation might account for the presence of a prominent non-neoplastic component in AITL tissues and the clinical manifestations of the disease reflective of an immunological dysfunction. ALK+ anaplastic large cell lymphoma (ALCL), defined by ALK gene translocation with various gene partners, is composed of CD30+ ALK+ cells with a cytotoxic phenotype and usually carries a good prognosis. ALK– ALCL, now considered as a distinct disease entity, is morphologically and immunophenotypically similar to ALK+ ALCL, except for ALK expression, but has distinctive molecular features. PTCL, not otherwise specified (PTCL, NOS), the largest PTCL category, which is derived from activated CD4+ (or CD8+) T cells, is markedly heterogeneous, including at the molecular level. Gene expression profiling approaches have identified novel biomarkers of potential therapeutic interest, and suggest the existence of molecularly distinct PTCL, NOS subgroups.

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Serpin A1 is overexpressed in ALK+ anaplastic large cell lymphoma and its expression correlates with extranodal dissemination

Cited by 16 publications

References 26 publications

Human γδ T lymphocytes strip and kill tumor cells simultaneously

Human γδ T lymphocytes strip and kill tumor cells simultaneously

Inherited Alpha-1 antitrypsin deficiency and chondrosarcoma: a possible causal relationship

Pathobiology and Molecular Profiling of Peripheral T-Cell Lymphomas

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