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Prussian blue reacts with ferric iron in hemosiderin and ferritin, producing blue granules that allow storage iron to be graded. It is the standard stain for evaluating marrow iron on aspirate particles.
CD45 is the leukocyte common antigen, and its expression varies by lineage and maturity. Plotting CD45 against side scatter separates lymphocytes, monocytes, granulocytes, and blasts into characteristic regions.
G-banding uses trypsin to partially digest chromatin, followed by Giemsa staining, creating alternating light and dark bands used to identify chromosomes and abnormalities. Quinacrine produces Q-bands, silver stains nucleolar organizer regions, and heat-plus-Giemsa produces R-bands.
Myeloperoxidase is present in the primary granules of granulocytic and monocytic cells, so positivity supports myeloid lineage. Lymphoid, erythroid, and megakaryocytic cells are generally myeloperoxidase negative.
EDTA preserves cell morphology and prevents clotting for aspirate smears and cell counts. Heparin can produce background staining and platelet clumping, citrate dilutes the sample, and oxalate can alter cell morphology.
New methylene blue precipitates residual ribosomal RNA in reticulocytes, producing a blue network that allows them to be counted. Wright-Giemsa can show polychromasia but is less reliable for reticulocyte counting.
Fluorescence in situ hybridization uses fluorescent probes that hybridize to the BCR and ABL1 loci and can detect the fusion in interphase nuclei without metaphases. G-banded karyotype requires dividing cells, while Southern blot and Sanger sequencing are not routine fusion screens.
CD61 is an integrin expressed on megakaryocytes and platelets and is a standard marker for megakaryocytic lineage. Erythroid, plasmacytic, and myeloid cells are generally CD61 negative.
Silver impregnation stains reticulin fibers black and is used to assess marrow fibrosis. Masson trichrome highlights collagen, Periodic acid-Schiff stains glycogen, and Congo red stains amyloid.
JAK2 V617F is a somatic mutation in myeloid cells, so peripheral blood leukocytes are the usual and adequate sample. Bone marrow is not required for this mutation, buccal swabs test germline DNA, and plasma lacks cellular DNA.
The dilute Russell viper venom time is sensitive to lupus anticoagulants and is commonly used with a mixing or confirmatory step. Prothrombin time, thrombin time, and fibrinogen assays assess different pathways or fibrinogen and are not confirmatory for lupus anticoagulant.
High-performance liquid chromatography separates and quantifies hemoglobin fractions, including HbA2, which is typically elevated in beta-thalassemia trait. Osmotic fragility, direct antiglobulin testing, and G6PD testing evaluate different red cell disorders.
Quantitative reverse-transcription PCR measures BCR-ABL1 transcript levels and is the standard method for monitoring tyrosine kinase inhibitor response and measurable residual disease in CML. It does not determine lineage, iron status, or platelet function.
Hairy cell leukemia cells classically show tartrate-resistant acid phosphatase positivity that resists tartrate inhibition. Chronic lymphocytic leukemia, acute promyelocytic leukemia, and multiple myeloma are not defined by this staining pattern.
Congo red binds amyloid fibrils and produces apple-green birefringence under polarized light. Hemosiderin is highlighted by Prussian blue, fibrin by trichrome or related stains, and lipofuscin is a wear-and-tear pigment.
FISH with PML and RARA probes detects the fusion even when metaphases are normal or unavailable. Serum protein electrophoresis, reticulin staining, and CD45 gating do not detect this specific gene fusion.
The core biopsy preserves marrow architecture and allows overall cellularity, topography, and fibrosis to be assessed. Neutrophil segmentation, platelet morphology, and rouleaux are better evaluated on aspirate or peripheral blood smears.
Allele-specific real-time PCR uses primers designed for the exact variant and can detect low-level mutant alleles. Sanger sequencing has lower sensitivity, karyotype detects chromosomal changes, and reticulin staining is histologic.
Paroxysmal nocturnal hemoglobinuria results from loss of glycosylphosphatidylinositol-anchored proteins, including CD55 and CD59, on red cells and granulocytes. CD34 marks immaturity, CD19 with CD5 is a T-cell lymphoma pattern, and CD45 is not increased on erythrocytes.
Hemodilution from peripheral blood falsely lowers aspirate cellularity, so the core biopsy is preferred for assessing overall cellularity and architecture. The biopsy remains interpretable and is not invalidated by a diluted aspirate.
Immediate and sustained correction indicates a factor deficiency, because normal plasma supplies the missing factor. Inhibitors and lupus anticoagulants typically fail to correct or show time-dependent behavior, and heparin may prolong the mixing study.
Minimal residual disease flow cytometry uses leukemia-associated immunophenotypic aberrations and multiple B-cell markers to identify rare residual blasts against normal hematogones. CD45/SSC gating alone or morphology lacks the needed sensitivity and specificity.
Droplet digital PCR partitions DNA into many reactions and can detect very low BCR-ABL1 levels with high precision, exceeding standard RQ-PCR in deep response. Karyotype and FISH are less sensitive for minimal residual disease.
In a normal cell, the BCR and ABL1 probes remain on separate chromosomes, producing separate red and green signals without fusion. A t(9;22) cell typically shows two fusion signals with this probe design.
CD34 is expressed on hematopoietic stem cells and early progenitors and is lost as cells commit to mature lineages. It is therefore the standard marker for progenitor enumeration and selection. The other markers are lineage-restricted to T cells, B cells, or granulocytes.
The proerythroblast is the first erythroid precursor that can be recognized by light microscopy. It is large with a prominent nucleolus and basophilic cytoplasm. Subsequent maturation proceeds through basophilic, polychromatophilic, and orthochromic normoblasts.
Primary granules appear during the promyelocyte stage, when the cell is still relatively large and basophilic. Secondary granules begin to accumulate at the myelocyte stage. Later forms such as metamyelocytes and band neutrophils contain both granule types but are not the first to show primary granules.
Adult hemoglobin A, composed of two alpha and two beta chains, makes up the vast majority of hemoglobin after infancy. HbF is the major fetal hemoglobin, and HbA2 is a minor adult fraction. HbH is an abnormal beta-chain tetramer seen in alpha-thalassemia.
Reticulocytes retain residual ribosomal RNA and organelles for a short period after enucleation, which is why they stain with supravital dyes such as new methylene blue. Mature erythrocytes have lost this RNA. Neither mature erythrocytes nor reticulocytes normally contain a nucleus.
Bone marrow cellularity declines with age and is often estimated as roughly 100 minus age, so a 40-year-old would be expected to have cellularity near 50% to 60%. Among the choices, 50% is the appropriate approximate value. Marked deviations suggest hypocellular or hypercellular marrow disorders.
Ferrochelatase inserts ferrous iron into protoporphyrin IX to form heme, completing the pathway. ALA synthase catalyzes the committed first step, while the other enzymes act at earlier intermediate steps. Deficiency of ferrochelatase causes erythropoietic protoporphyria.
Erythropoietin is synthesized predominantly by peritubular interstitial fibroblast-like cells in the kidney, which sense hypoxia through the HIF pathway. The liver contributes a smaller amount in adults. Renal tubular cells and marrow macrophages do not produce most circulating erythropoietin.
Granulocyte colony-stimulating factor stimulates proliferation and maturation of neutrophil precursors and promotes their release from the marrow. IL-5 mainly affects eosinophils, thrombopoietin drives platelet production, and erythropoietin supports erythroid cells.
Thrombopoietin is produced mainly by hepatocytes in the liver, with smaller contributions from the kidney and marrow stroma. It stimulates megakaryocyte maturation and platelet production. Bone marrow and spleen are important sites of platelet production and pooling but are not the predominant source of thrombopoietin.
GATA1 is required for erythroid and megakaryocytic differentiation and activates lineage-specific genes such as globins and platelet factors. PU.1 and CEBPA promote myeloid programs, while PAX5 is a B-cell commitment factor. These factors help establish lineage identity from multipotent progenitors.
Impaired DNA synthesis delays nuclear maturation while cytoplasmic hemoglobinization proceeds, producing nuclear-cytoplasmic asynchrony. This is accompanied by megaloblastic erythroid precursors and hypersegmented neutrophils. Ring sideroblasts and basophilic stippling point to different disorders.
Surface IgM first appears on the immature B cell after successful heavy- and light-chain rearrangement. Pro-B cells are rearranging heavy-chain genes, and pre-B cells express cytoplasmic mu chain but not surface IgM. Mature naive B cells express both IgM and IgD.
Cortical thymocytes are predominantly CD4 and CD8 double-positive and undergo positive selection there. Single-positive CD4 or CD8 cells are more mature and are found mainly in the medulla. Double-negative cells are early precursors before CD4 and CD8 expression.
Specific granules contain lactoferrin, gelatinase, and other antimicrobial proteins. Myeloperoxidase, elastase, and azurocidin are concentrated in azurophilic primary granules. Granule content helps identify neutrophil maturation and function.
Macrophage colony-stimulating factor binds CSF1R and promotes monocyte survival and macrophage differentiation. IL-5 supports eosinophils, thrombopoietin supports megakaryocytes, and erythropoietin supports erythroid cells.
IL-5 is the key cytokine for eosinophil lineage commitment, proliferation, and survival. IL-4 promotes Th2 responses, IL-7 supports lymphocyte development, and IL-12 drives Th1 and NK-cell responses.
Definitive hematopoietic stem cells first emerge in the aorta-gonad-mesonephros region and later seed the fetal liver for expansion. The yolk sac produces primitive erythroid and macrophage progenitors but not the first long-term repopulating stem cells. The fetal liver and umbilical cord are later sites.
The spleen can resume erythropoiesis in response to severe stress, producing extramedullary erythroid islands. The liver may also contribute but is less important in adults. The thymus and lymph nodes are primarily lymphoid organs.
CXCL12 produced by marrow stromal cells binds CXCR4 on hematopoietic stem cells and promotes their retention in the niche. Disruption of this axis mobilizes stem cells into peripheral blood. SCF, angiopoietin, and Notch signals support stem-cell maintenance but are not the main retention mechanism.
The erythropoietin receptor lacks intrinsic kinase activity and signals through the associated tyrosine kinase JAK2. JAK2 activation leads to STAT5 phosphorylation and promotes erythroid survival and proliferation. JAK3, BTK, and SYK mediate other cytokine or antigen-receptor pathways.
PAX5 maintains B-cell identity and represses plasma-cell genes; its silencing is required for terminal plasma-cell differentiation. BLIMP1 then drives the secretory program, with support from IRF4 and XBP1. Loss of PAX5 allows the cell to exit the mature B-cell state.
Iron deficiency depletes storage iron, so serum ferritin falls and total iron-binding capacity rises as transferrin increases. Transferrin saturation is low because circulating iron is insufficient to fill available binding sites.
Inflammatory cytokines increase hepcidin, which blocks iron release from macrophages and reduces intestinal iron absorption. The resulting iron-restricted erythropoiesis and blunted erythropoietin response produce a normocytic or microcytic anemia.
Ring sideroblasts form when iron accumulates in mitochondria around the nucleus of erythroid precursors, usually because heme synthesis is defective. This produces a ring of Prussian blue-positive granules on iron staining.
Beta-thalassemia trait reduces beta-globin output, so compensatory delta-globin production raises hemoglobin A2. Hemoglobin A2 elevation on electrophoresis or chromatography is a key diagnostic clue.