Although T-cell/histiocyte rich large B-cell lymphoma (THRLBCL) is an aggressive diffuse large B-cell lymphoma (DLBCL), its morphology can resemble nodular lymphocyte predominant Hodgkin lymphoma (NLPHL). These two entities are closely related: both diseases contain neoplastic cells with similar morphologic and immunophenotypic features but differ with respect to their architecture and the nature of the reactive background. Due to the overlapping features between THRLBCL and NLPHL, it is sometimes impossible to distinguish these two entities; thus, ""grey zone"" lymphoma is used to define some of those cases. Because of the morphologic and immunophenotypic similarities between THRLBCL and NLPHL, it is possible that these two entities may represent different stages of the same disease. A possible biological relation of THRLBCL with NLPHL has been suggested. Overlapping recurrent genetic abnormalities (gain of 4q and loss of 19p) might be the genetic link between THRLBCL and NLPHL....

Forty five cases carrying the t(2;11)(p21;q23) have been reported in the literature, mostly in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Some of these cases involve rearrangements of the the MLL gene (also known as KMT2A), on 11q23, which confers a more aggressive behavior in myeloid neoplasms. Several individual case reports, as well as series such as 19 cases reported by Bousquet et al., 2008 and 7 cases by Dvorak et al., 2014, describe myeloid neoplasms carrying the t(2;11)(p21;q23) without an MLL gene rearrangement, with possible prognostic implications. The authors of this paper describe two additional cases from their institution....

This CARD addresses the following questions: 1) how should in situ follicular neoplasia be defined and diagnosed? and 2) how should people/patients with in situ follicular neoplasia be managed?...

Review on t(7;12)(q36;p13), with data on clinics, and the genes involved....

Fanconi anemia (FA) is a rare human recessive syndrome featuring bone marrow failure, myelodysplasia, and predisposition to cancer as well as chromosome fragility and hypersensitivity to DNA interstrands crosslinking agents. FA was described in 1927 by the Swiss pediatrician Giuseppe Fanconi, which reported a first family with three affected sibling presenting developmental defects and anemia. FA cells are hypersensitive, at both cellular and chromosomal levels, to the exposure to DNA interstrands crosslinking agents, like mitomycin C, diepoxybutane, cis-platinum or photoactivated psoralen. The chromosomal response to DNA interstrands crosslinks (ICLs)-inducing agents is so typical that the observation of both the induced frequency of chromosome aberrations and their type, i.e. tri- and quadri-radials, is considered the best diagnostic criteria for FA. Indeed, looking simply at the clinical hallmarks of the patients, it is difficult to distinguish FA patients from several other bone marrow failure syndromes. Alternatively, since the FA cells need more time to pass through both G2 and S phases than normal cell, the analysis by flow cytometry of the over accumulation of the FA cells in G2 following exposure to ICL-inducing agents could be a useful approach for diagnosis. More recently, molecular and biochemical approaches looking at gene mutations, proteins expression and/or post-translational modifications are used to validate cytogenetics conclusions. To date 19 different genes (FANC) have been associated to FA. The FANC proteins constitute a pathway which essential function is to deal with replication stress assuring the transmission of a stable genome from one cell to the daughters and acting both during replication, to cope with stalled replication forks, but also in G2 and M phases, to resolve un-replicated or not fully replicated regions before telophase. For review: Duxin and Walter, 2015; Bogliolo and Surralles, 2015; Walden and Deans, 2014; Soulier 2011; Lobitz and Velleuer, 2006....