A revised European-American classification of lymphoid neoplasms: a proposal from the International Lymphoma study group

The World Health Organization (WHO) classification of the lymphoid neoplasms updated in 2008 represents a worldwide consensus on lymphoma diagnosis and is based in two major principles: the stratification of neoplasms according to their cell lineage and their derivation of precursor or mature cells and the definition of non-overlapping distinct diseases that are clinically relevant. The identification of these diseases is based on a combination of morphology, immunophenotype, genetic, molecular, and clinical features. In addition to well-defined entities, the classification addresses open issues, such as provisional entities that correspond to categories for which there were insufficient evidence to support its recognition as distinct diseases at the time of publication and borderline categories with overlapping features between large B-cell lymphomas and Burkitt or Hodgkin lymphoma.

The World Health Organization Classification of Lymphoid Neoplasms

Chronic lymphocytic leukemia (CLL), the most frequent form of leukemia in Western countries, is characterized by the clonal proliferation and accumulation of neoplastic B lymphocytes in the blood, bone marrow, lymph nodes, and spleen. The median age of patients at diagnosis is 65 years, with only 10 to 15 percent under 50 years of age. In most series, more men than women are affected. The course of the disease is variable. Whereas some patients with CLL have a normal life span, others die within five years after diagnosis. During the past few years, important advances have been made in the . . .

Chronic lymphocytic leukemia.

Publisher Summary This chapter focuses on the genetic alterations of cyclins, cyclin dependent kinases (Cdk), and Cdk inhibitors in human cancer. Contemporary research into the molecular basis of cancer has two central tenets. The first is that cancer arises through alterations in the genetic make-up of the tumor cell. The second is that these changes are manifested in the breakdown of the processes that regulate cell growth and differentiation. In simplistic terms, cancer cells proliferate uncontrollably and fail to differentiate. The large numbers of tumors that show perturbations in the D cyclins themselves, their upstream regulators, or their downstream targets suggest that this pathway is extremely important in human cancer and holds great promise for therapeutic intervention. The conventional view of the cell division cycle is as a series of checkpoints or transitions at which certain criteria must be met before the cell proceeds to the next phase. The cyclin D1 gene, now given the locus designation CCNDI, maps to band q13 on the long arm of chromosome 11. The chapter also discusses the amplification of cyclin D1 in human tumors. When the gene for Cdk4 was located on chromosome 12q13, it was quickly realized that it too lies within a tumor-specific amplicon, which had been previously observed in human sarcomas of various types and in tumors of the central nervous system, particularly gliomas. There has been a great deal of interest in the cyclin-dependent kinase inhibitors that have been identified in mammalian cells. The chapter describes cyclin D1-p16-pRb pathway.

Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer.

BACKGROUND AND OBJECTIVES: Iron-induced cardiac disease remains the main cause of death in patients with thalassemia major, despite chelation therapy with deferoxamine. Deferiprone is an iron chelator that has the potential to be more effective than deferoxamine in removing intracellular iron from the heart. However, to date, no study has been designed to examine the frequency of cardiac complications and survival as the primary outcomes of a comparative study between these two chelators. This retrospective study assessed the survival and the occurrence of cardiac disease in all patients with thalassemia major treated for at least 4 years with deferiprone or deferoxamine at a single center. DESIGN AND METHODS: The patients were, on average, 18.4 years old at the start of the review period and were followed up, on average, for 6 years. At baseline there was no significant difference in the percentage of patients with cardiac disease in the two therapy groups. RESULTS:At the end of the study, cardiac dysfunction, expressed as worsening of pre-existing cardiac abnormality or development of new cardiac disease, was diagnosed in 2 (4%) of the 54 deferiprone-treated patients and in 15 (20%) of the 75 deferoxamine-treated patients, from the first to the last measurement (p = 0.007). The Kaplan Meier analysis of cardiac disease-free survival over the 5-year period was significantly more favorable in the deferiprone group (p = 0.003). INTERPRETATION AND CONCLUSIONS: None of the patients treated with deferiprone died, while 3 of the patients treated with deferoxamine died because of irreversible worsening of their cardiac condition during the study period. Findings from this study suggest that long-term therapy with deferiprone provides a greater cardio-protective effect against the toxicity of iron overload than does subcutaneous deferoxamine. Formal prospective studies are warranted to confirm this effect.

Rituximab-induced acute thrombocytopenia: a report of two cases.

Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia.

Trisomy 12 in chronic lymphocytic leukemia detected by fluorescence in situ hybridization: analysis by stage, immunophenotype, and morphology

The translocation t(11;14)(q13;q32) has been described in a spectrum of B-lymphoproliferative diseases and involves a putative oncogene, BCL1, which maps to chromosome band 11q13. Recent evidence indicates that this abnormality may delineate particular subtypes of lymphoma, such as intermediate lymphocytic and centrocytic lymphomas. Thus the possible significance of the t(11;14) within B-cell disorders should be reexamined in the light of a more objective approach to classifying these diseases by morphology, histology, and immunophenotype. We describe 16 patients with t(11;14)(q13;q32) from a series of 90 patients with chronic lymphoid disorders in whom clonal chromosome abnormalities were detected. All the cases were leukemic: prolymphocytic (B-PLL; 4/15 cases), chronic lymphocytic leukemia (CLL) with increase in prolymphocytes (2/9 cases), or non-Hodgkin lymphoma in leukemic phase, intermediate (3/4 cases), lymphoplasmacytic (2/2 cases), splenic lymphoma with villous lymphocytes (4/18 cases), and follicular (1 case). None of the CLL (25) or hairy cell leukemia cases (15) had t(11;14). Our findings showed that t(11;14) occurred in leukemias of mature B cells with lymphoplasmacytic features as judged by morphology and immunophenotype.

Translocation t(11;14)(q13;q32) in chronic lymphoid disorders.

Introduction: Concerns have been raised regarding the accuracy of diagnostic antigen testing for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. We compared the performance of the LumiraDx SARS-CoV-2 Antigen Test between symptomatic participants recruited prospectively during the Delta to Omicron variant transition in the USA. Methods: Two paired anterior nasal swabs were collected from each participant (adults and children) within 12 days of symptom onset between November 24th, 2021 and February 1st, 2022, during which time Omicron replaced Delta as the dominant variant in the sample population. Swabs were tested by the LumiraDx SARS-CoV-2 Antigen Test and compared using real-time polymerase chain reaction (RT-PCR) reference testing. Reference samples identified as positive were sequenced to identify the SARS-CoV-2 variant. Positive percent agreement (PPA) was calculated, with results stratified by RT-PCR cycle threshold (Ct). Results: Of the 38 participants for whom LumiraDx SARS-CoV-2 Antigen Test results were available, 36 were confirmed positive by RT-PCR. Overall, PPA of the LumiraDx SARS-CoV-2 Antigen Test was 94.7% (95% confidence interval: 82.3%, 99.4%) and PPA was 100% for samples with a Ct <33. Sufficient viral load for sequencing was present in nine samples (six Delta, three Omicron), all of which returned a positive result using the LumiraDx SARS-CoV-2 Antigen Test. There were no performance differences observed between participants with the Delta and Omicron variants. Conclusions: SARS-CoV-2 differences between Delta and Omicron variant mutations did not affect the performance of the LumiraDx SARS-CoV-2 Antigen Test which detects the nucleocapsid protein antigen. The LumiraDx SARS-CoV-2 Antigen Test can be a useful antigen test to diagnose emerging variants of coronavirus disease 2019.

Performance study of a point-of-care antigen test during the SARS-CoV-2 Delta to Omicron variant transition in the USA

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Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia.

Trisomy 12 in chronic lymphocytic leukemia detected by fluorescence in situ hybridization: analysis by stage, immunophenotype, and morphology

Translocation t(11;14)(q13;q32) in chronic lymphoid disorders.

Performance study of a point-of-care antigen test during the SARS-CoV-2 Delta to Omicron variant transition in the USA