Advances in the understanding of classical Hodgkin’s lymphoma (cHL) biology and immunology show that infiltrating immune cells and cytokines play different roles in relation to clinical outcomes. High levels of expression of the monocyte/macrophage lineage antigen CD163 were suggested to exert protumor effects. Lymphoid malignancies were found to express c-Met with a possible role in the pathogenesis of these diseases. Lymphoid malignancies often have a polyclonal B-cell infiltrate that can secrete immunoglobulins. This study aimed to evaluate the expressions of CD163 and c-Met and serum free light chain (sFLC) in relation to the clinicopathological features in patients with advanced cHL.
Thirty-four patients with cHL were enrolled. CD163 and c-Met expressions were assessed immunohistochemically on lymph node biopsy sections together with a pretreatment estimation of sFLC using Enzyme Linked Immunosorbent Assay (ELISA).
The median age of the patients was 30 years, with a 1 : 1 male to female ratio. High CD163 expression correlated with increased age, B symptoms, International Prognostic Score of at least 3, mixed cellularity subtype, and low response to treatment. Also, high c-Met expression was correlated with increased age at diagnosis, leukocytosis, B symptoms, and lower complete remission rates. Elevated sFLC correlated with increased age at diagnosis, lymphopenia, International Prognostic Score of at least 3, B symptoms, and lower complete remission rates.
In cHL, high expression of CD163 and c-Met and elevated sFLC correlates with adverse outcome.
The bone marrow niches are proposed to be the supportive microenvironment that offers cytoprotection from chemotherapy and confers a survival advantage to leukemic cells that could be responsible for relapses in patients with acute myeloid leukemia (AML). Osteopontin (OPN) and its receptor CD44v6 play a crucial role in leukemia cell homing to the bone marrow.
This study aimed at investigating the pattern of expression and prognostic impact of OPN and CD44v6 in AML patients and their correlation with each other.
The study was carried out on 70 patients with de-novo AML and 20 age-matched and sex-matched controls. Patients were diagnosed and classified according to the French American British classification/WHO (FAB/WHO) criteria by cytomorphology, immunophenotyping, and cytogenetic analysis. Cellular OPN and surface CD44v6 expression by blast cells was assessed by flow cytometry.
OPN was overexpressed by AML blasts (8.2–75.8%; median 25%) compared with the controls (<5%), with 32/70 (45.7%) showing higher levels than the median (>25%). CD44v6 was detected in 56/70 (80%) patients, with 30/70 (42.9%) showing high expression (≥20%). OPN expression was correlated positively with that of CD44v6, its overexpression being paralleled by an increase in that of CD44v6. Higher levels of OPN and CD44v6 were not related to patients’ clinical or laboratory data, FAB subtype, cytogenetic risk group, and initial response to primary induction chemotherapy. A shorter event-free survival was observed in patients with higher OPN and CD44v6 expression (4 months) compared with those with lower levels (16 months), and elevated OPN and CD44v6 at diagnosis were each identified as a negative independent prognostic marker.
OPN and its receptor CD44v6 levels of expression are increased in AML, correlate with each other, and their higher levels at diagnosis can be used as early prognostic markers to predict poor disease progression.
Human parvovirus B19 is a global and common infectious pathogen in humans, particularly in children.
The aim of the study was to compare the prevalence of human parvovirus B19 in children with a variety of hematological disorders with that in normal controls and to highlight the relationship between humoral immune response and the presence of viremia.
This study included 80 children with different hematological disorders. Ten healthy children matched for age and sex were also included as controls. The patients were classified into four groups: group I included 25 patients with chronic hemolytic anemia not in aplastic crisis; group II included 15 patients with hemolytic anemia in aplastic crisis; group III included 20 acute leukemia patients under chemotherapy; and group IV included 20 patients with newly diagnosed acute leukemia. B19-specific IgM and IgG antibodies were detected in patient sera by enzyme-linked immunosorbent assay, whereas B19 DNA was detected by nested PCR analysis.
A higher prevalence of B19-specific markers was found in patients compared with controls. In groups I and III, IgG positivity was the highest (52 and 50%, respectively). In group II, the rate of IgM positivity and viremia was the same (46%), followed by IgG positivity (33.3%). However, in group IV IgM positivity was the highest (35%), followed by IgG positivity (30%) and viremia (15%). Groups II, III, and IV showed a higher prevalence of recent B19 infection (53.3, 40, and 45%, respectively) compared with prior and absent infections, whereas in group I prior infection was the most prevalent (40%). None of the groups showed a significant relationship between B19 DNA and immunoglobulin detection, except group II, in which a significant association between the detection of B19 DNA and IgM existed. All groups of patients with positive markers for recent B19 infection had lower hemoglobin levels and RBC counts compared with controls; they also had reticulocytopenia and lymphocytosis.
B19 infection is highly prevalent among children with hematological disorders. B19 must be suspected and screened for in the presence of anemia in those patients with neutropenia and lymphocytosis. The direct detection of DNA by PCR needs to be coupled with serological testing for a more reliable diagnosis of B19 infections.
Janus kinases are cytoplasmic tyrosine kinases that mediate signaling from the cytokine receptors to the cell nucleus. Janus kinase 2 mutation (JAK2 V617F) analysis has been endorsed by the WHO for diagnosing polycythemia vera, essential thrombocythemia, and primary myelofibrosis. The aim of this study was to assess JAK2 V617F point mutation in healthy cigarette smokers compared with healthy nonsmokers and to correlate the presence of this mutation with some clinical and laboratory variables.
Group I comprised 34 cigarette smokers who have been smoking 10 or more cigarettes per day, every day of the week, for at least 10 consecutive years. Group II comprised 42 men who were nonsmokers with no history of drug abuse. In addition to routine laboratory investigations, detection of JAK2 V617F point mutation in peripheral blood neutrophils was assessed for all participants.
In this study, we found an increased percentage of JAK2 V617F mutation in cigarette smokers compared with nonsmokers. Further, we found a significant positive correlation between the percentage of JAK2 V617F mutation and age in both groups.
JAK2 V617F mutation has been detected in the healthy population; however, its incidence significantly increases in cigarette smokers. The mechanisms leading to excess JAK2 mutation and the importance of this mutation in smokers are yet to be elucidated and an adequate follow-up of healthy individuals who carry the mutation is recommended.