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Myelocyte
Myelocyte
Myelocyte
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Myelocyte
Details
PrecursorPromyelocyte
Gives rise toMetamyelocyte
LocationBone marrow
Identifiers
THH2.00.04.3.04004
FMA83525
Anatomical terms of microanatomy
Basophilic[1]
Eosinophilic[2]
Neutrophilic[3]

A myelocyte is a young cell of the granulocytic series, occurring normally in bone marrow (can be found in circulating blood when caused by certain diseases).

Structure

[edit]

When stained with the usual dyes, the cytoplasm is distinctly basophilic and relatively more abundant than in myeloblasts or promyelocytes, even though myelocytes are smaller cells.

Numerous cytoplasmic granules are present in the more mature forms of myelocytes. Neutrophilic and eosinophilic granules are peroxidase-positive, while basophilic granules are not.

The nuclear chromatin is coarser than that observed in a promyelocyte, but it is relatively faintly stained and lacks a well-defined membrane.

The nucleus is fairly regular in contour (not indented), and seems to be 'buried' beneath the numerous cytoplasmic granules. (If the nucleus were indented, it would likely be a metamyelocyte.)

Measurement

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There is an internationally agreed method of counting blasts, with results from M1 upwards.

Development

[edit]

Promyelocyte → Myelocytes → metamyelocytes.

Additional images

[edit]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Myelocyte

View on Grokipedia
from Grokipedia
A myelocyte is a nucleated in the granulocytic lineage of hematopoiesis, representing an intermediate stage between the promyelocyte and , during which specific cytoplasmic granules first appear and the cell commits to differentiation into neutrophils, , or . These cells are primarily produced in the and are essential for generating mature granulocytes that contribute to innate immunity and inflammation responses. In morphology, myelocytes measure approximately 10-18 μm in diameter, featuring a round to oval nucleus with fine, dispersed and no visible nucleoli, surrounded by that transitions from basophilic to less intense blue as specific granules develop. The granules vary by subtype: neutrophilic myelocytes contain small, lilac or pinkish secondary granules; eosinophilic ones have larger, orange refractile granules; and basophilic myelocytes display prominent blue-black granules. This stage marks the final mitotic division in , during which the final mitotic divisions occur as part of the proliferative phase lasting approximately 4-6 days under normal conditions, after which the cells proceed to post-mitotic maturation without further division. Normally confined to the bone marrow's hematopoietic islands, myelocytes are not found in peripheral blood, but their presence there—known as a "left shift"—indicates accelerated due to , , administration, or pathological conditions like myeloid neoplasms. In clinical practice, myelocytes are identified via light microscopy of aspirates or blood smears stained with Wright-Giemsa, aiding in the of hematologic disorders such as leukemias or myelodysplastic syndromes.

Definition and Overview

Definition

A myelocyte is an immature granulocytic leukocyte primarily located in the , serving as a committed precursor in the myeloid differentiation pathway. It represents the stage immediately following the promyelocyte and preceding the in the development of granulocytes, during which the cell continues to proliferate as part of the mitotic pool in . At this juncture, myelocytes synthesize and accumulate specific cytoplasmic granules that define their future mature form, marking a transition from early proliferative phases to more specialized maturation. Myelocytes are classified into three principal subtypes based on the lineage they pursue and the characteristics of their granules: neutrophilic myelocytes, which are precursors to neutrophils and feature azurophilic primary granules alongside emerging secondary granules that stain neutrally; eosinophilic myelocytes, destined to become with granules that exhibit affinity for acidic dyes like ; and basophilic myelocytes, which develop into and contain granules staining with basic dyes. These distinctions arise during the promyelocyte-to-myelocyte transition, where lineage commitment directs granule composition and function. The nomenclature "myelocyte" originates from the Greek roots "myelo-" (referring to , the site of its production) and "-cyte" (denoting a cell), underscoring its role as a marrow-derived cellular intermediate. The term was coined by in 1887, in his seminal description of granulocyte granulation patterns using techniques.

Historical Context

The myelocyte was first observed by in 1879 during his pioneering staining experiments using dyes, which enabled the visualization and differentiation of granular cells in the myeloid lineage. Ehrlich's work, detailed in his publication Beiträge zur Kenntniss der granulirten Bindegewebszellen, introduced the term "myelocyte" to describe these immature precursors, revolutionizing the study of hematopoiesis by distinguishing them from other leukocytes based on granule affinity. By the early 1900s, hematologists such as Otto Naegeli had formalized within comprehensive cell lineage models, positioning them as key intermediates in development downstream from the , which Naegeli described in 1900 as the ancestral cell of the myeloid series. This framework advanced understanding of normal blood cell production and pathological deviations. A notable milestone came in 1910 with R. Dunger's method for counting circulating , which improved the enumeration of specific subtypes. In the , the detection of circulating myelocytes emerged as a critical diagnostic feature in early evaluations, particularly for distinguishing chronic myeloid leukemia from other disorders, as immature myeloid cells like myelocytes appeared in peripheral smears. This period marked a shift in terminology from ad hoc morphological descriptions tied to "myeloblast-derived" cells toward more systematic . The French-American-British (FAB) classification, proposed in 1976, standardized these terms, integrating myelocyte maturation stages into subtypes of for consistent global diagnostics.

Morphology

Cytoplasmic Features

The cytoplasm of myelocytes is abundant and exhibits basophilia due to its rich content of ribosomes and , reflecting active protein synthesis during this stage of granulocyte development. As these cells mature from promyelocyte precursors, the cytoplasm transitions from a relatively agranular state to one containing both azurophilic (primary) granules and lineage-specific (secondary) granules, which are visible under . In neutrophilic myelocytes, azurophilic granules are peroxidase-positive and contain lysosomal enzymes, including , which contribute to activity; these granules appear pink-purple when stained. The specific granules in neutrophilic myelocytes are fine, pale, and lightly acidophilic, distinguishing them from the coarser primary granules. myelocytes feature specific granules that show a strong affinity for stains, appearing orange-red and larger in size compared to those in neutrophilic counterparts. Basophilic myelocytes contain specific granules that stain deep blue and exhibit metachromatic properties, often appearing violet under certain dyes like toluidine blue. Biochemically, the cytoplasm of myelocytes includes enzymes such as , which is detectable in neutrophilic forms and supports cellular functions during . is also present as an energy reserve in the cytoplasm, particularly in maturing granulocytes. Mitochondria in myelocytes show no significant quantitative or structural changes compared to those in promyelocyte , maintaining a similar distribution within the cytoplasm.

Nuclear Characteristics

The nucleus of a myelocyte is typically or kidney-shaped, measuring approximately 7-10 μm in , and features a slightly indented contour without segmentation. This indentation marks an early stage in nuclear remodeling during maturation, distinguishing myelocytes from earlier precursors like promyelocytes, which have rounder nuclei. The pattern in the myelocyte nucleus is coarser and more condensed compared to that in promyelocytes, exhibiting clumped regions while retaining prominent areas that support ongoing transcriptional activity. This granular, reddish-blue appearance reflects progressive and differentiation, with the facilitating the synthesis of lineage-specific proteins. Nucleolar remnants in myelocytes are faint or absent, signaling a reduction in ribosomal RNA synthesis relative to earlier blast stages. While some myelocytes may retain a poorly defined nucleolus outlined by chromatin condensation, most lack visible nucleoli, correlating with decreased proliferative capacity. This nuclear feature complements the cytoplasmic basophilia observed in these cells, indicating active but maturing .

Development and Maturation

Origin from Precursor Cells

Myelocytes originate in the bone marrow as part of the granulocytic lineage during hematopoiesis, deriving directly from promyelocytes, which themselves develop from myeloblasts. Myeloblasts emerge from the granulocyte-macrophage progenitor (GMP), which arises from the common myeloid progenitor (CMP), an oligopotent progenitor committed to the myeloid pathway downstream of hematopoietic stem cells (HSCs). This sequential progression—HSCs to CMP to GMPs to myeloblasts to promyelocytes to myelocytes—represents the initial phases of myeloid commitment, where multipotent progenitors progressively restrict their potential to granulocyte fates. The development of myelocytes occurs within the specialized hematopoietic microenvironment of the bone marrow niche, which provides essential signals for progenitor survival and differentiation. HSCs and early myeloid precursors reside in endosteal and perivascular regions, interacting with stromal cells, endothelial cells, and to maintain quiescence or promote lineage specification. Cytokines, particularly (G-CSF), exert a pivotal influence on this process for the neutrophilic lineage, stimulating the proliferation of CMP-derived progenitors and driving their maturation toward myelocytes by activating downstream signaling pathways such as JAK-STAT. Key markers of commitment to the myelocyte stage include the final proliferative phase, where the last mitotic divisions occur following promyelocyte proliferation, after which cells lose the high proliferative capacity of earlier precursors like myeloblasts and promyelocytes, transitioning to post-mitotic maturation in metamyelocytes. This is accompanied by the initial synthesis of lineage-specific granules: azurophilic (primary) granules form in promyelocytes, while specific (secondary) granules first appear in , signifying irreversible differentiation. For eosinophilic subtypes, interleukin-5 (IL-5) signaling enhances the replication and differentiation of committed precursors into eosinophilic .

Differentiation Stages

The differentiation of myelocytes represents a critical phase in , progressing through a defined sequence of morphological and functional changes within the . From the myelocyte stage, cells advance to , characterized by an indented or kidney-shaped nucleus and reduced cell size, followed by band cells with a horseshoe-shaped nucleus, and finally segmented granulocytes featuring multi-lobed nuclei capable of release into circulation. This maturation sequence typically spans 5-7 days in the , during which cells undergo post-mitotic development without further division, ensuring the production of functional granulocytes. Regulatory mechanisms tightly control this progression, primarily through transcription factors that orchestrate for lineage commitment and survival. Key factors such as C/EBPε and PU.1 promote granulocytic differentiation by activating genes involved in granule formation and cytoskeletal remodeling, with C/EBPε particularly essential for terminal maturation beyond the promyelocyte stage. If maturation stalls, anti-apoptotic proteins like MCL-1 maintain viability, but failure in these pathways triggers via the mitochondrial route, preventing the accumulation of dysfunctional precursors. Subtype-specific pathways diverge during this phase to tailor granulocytes for distinct immune roles. In neutrophil lineage, myelocytes exhibit initial chromatin condensation that intensifies in metamyelocytes, resulting in a more compact, heterochromatic nucleus that supports the cell's high mobility and phagocytic capacity. For eosinophils, myelocytes accumulate Charcot-Leyden crystal protein within granules, a lysophospholipase that forms distinctive bipyramidal crystals and contributes to during parasitic defense. These adaptations ensure lineage fidelity, building on origins from promyelocyte precursors.

Function and Role

Involvement in Granulopoiesis

The myelocyte serves as a critical intermediate stage in the granulopoiesis pathway within steady-state hematopoiesis, bridging the proliferative promyelocyte phase and the post-mitotic maturation toward neutrophils. In healthy adults, this process generates approximately 10^{11} neutrophils daily to maintain immune , with myelocytes contributing by undergoing final rounds of division and initiating lineage-specific differentiation in the . Myelocytes represent the last proliferative compartment in granulopoiesis, where cells retain mitotic capacity before halting division upon transition to metamyelocytes, driven by transcription factors such as C/EBPε that promote differentiation over proliferation. Under steady-state conditions, this proliferation is tightly regulated to sustain baseline neutrophil output, but during emergency granulopoiesis—triggered by infections—myelocytes accelerate maturation and facilitate the accelerated release of immature granulocytes into circulation to bolster innate immunity. In the bone marrow microenvironment, myelocytes localize to endosteal and perivascular niches, responding to stromal cell-derived signals that support their and differentiation. Key interactions involve /CXCR4 signaling from osteoblasts and endothelial cells for cellular retention, alongside cytokines like G-CSF and IL-6 from stromal components that fine-tune proliferative and differentiative responses. At this stage, development of secondary specific granules commences, aligning with the cell's commitment to identity.

Granule Synthesis and Storage

In myelocytes, the formation and maturation of cytoplasmic granules represent a critical phase in , distinguishing primary (azurophilic) and secondary (specific) granules based on their synthesis timing and contents. Primary granules are initially assembled in the preceding promyelocyte stage through from the Golgi apparatus, incorporating components such as and cathepsins, which undergo posttranslational processing that continues into the early myelocyte phase to achieve functional maturity. These granules serve as the cell's first line of defense reservoirs, with defensin-rich variants emerging near the promyelocyte-myelocyte transition to enhance their bactericidal potential. Secondary granules, in contrast, are synthesized de novo during the myelocyte stage, originating from the trans-Golgi network on the distal face of the Golgi complex, where proteins like , collagenase, and gelatinase are packaged into less dense structures. In eosinophilic myelocytes, secondary granules incorporate major basic protein (MBP), initially produced as a precursor (pro-MBP) that is proteolytically matured within the granule matrix, contributing to the crystalloid core structure essential for antiparasitic activity. These granules function primarily as intracellular storage compartments for antimicrobial peptides and enzymes, maintaining them in an inactive or precursor form until required for release during the final maturation to granulocytes or upon activation. Primary granules store potent microbicidal agents like defensins and cathepsins, while secondary granules hold peptides such as cathelicidins (e.g., hCAP-18), which are synthesized in myelocytes and targeted to these vesicles for regulated deployment. This compartmentalization allows myelocytes to build a graded arsenal, with granule contents mobilized sequentially in mature cells to combat infection without premature cytotoxicity.

Clinical Significance

Normal Distribution and Counts

In healthy adults, myelocytes constitute approximately 5-20% of the nucleated cells in aspirates, reflecting their role as intermediate precursors in . This proportion aligns with the typical myeloid-to-erythroid ratio of 2:1 to 4:1 in normal adult marrow cellularity. In neonates, myelocyte percentages are higher, often exceeding those in adults due to elevated cellularity (typically 80% or more) and enhanced granulopoietic activity to support early immune demands. Myelocytes are absent from the peripheral blood of healthy individuals, as they do not typically exit the until further maturation. They appear rarely in blood, comprising less than 0.5% of leukocytes on average. During , shows changes in myelocyte populations, with early myelocytes increased in the first and second trimesters and a decrease in late myelocytes in the third trimester, reflecting a left shift in driven by increased granulopoietic activity to meet heightened physiological demands, including expanded and potential risks.

Pathological Appearances

In leukemias, myelocytes exhibit pathological appearances characterized by increased numbers of immature forms in the peripheral blood and bone marrow. In chronic myeloid leukemia (CML), particularly during the chronic phase, there is a proliferation of granulocytic precursors, leading to a prominent peak in myelocytes alongside neutrophils, often with and all stages of myeloid differentiation visible. In (AML) subtypes M1 and M2, immature myelocytes are elevated in M2 cases, where maturation proceeds beyond blasts to include more than 10% promyelocytes and myelocytes, contrasting with the minimal maturation in M1. These deviations reflect dysregulated driven by genetic abnormalities like the BCR-ABL1 fusion in CML or various translocations in AML. Reactive conditions also feature altered myelocyte appearances, notably a left shift indicating accelerated release of immature cells from the . In severe bacterial , this manifests as increased circulating myelocytes, metamyelocytes, and band forms, often appearing 1-2 days after infection onset due to cytokine-mediated demargination and production. Similarly, in myelodysplastic syndromes (MDS), hypogranular variants of myelocytes are common, showing reduced cytoplasmic granules and nuclear hyposegmentation as part of dysmyelopoiesis, contributing to ineffective hematopoiesis. These changes signify a compensatory response to stress or clonal defects, respectively. Morphological anomalies in myelocytes further highlight disease-specific alterations. In megaloblastic anemia, precursors like myelocytes may display hypersegmented nuclei with more than five lobes, alongside giant metamyelocytes, due to impaired from or , though this is more pronounced in mature neutrophils. In sepsis, toxic granulation appears in myelocyte cytoplasm as coarse, dark azurophilic granules, reflecting accelerated granule production and release in response to inflammatory stimuli. These features aid in distinguishing reactive from neoplastic processes but require correlation with clinical context.

Diagnostic and Research Aspects

Identification Techniques

Myelocytes are primarily identified in clinical laboratories through light microscopy of stained blood or smears, where Wright-Giemsa highlights their characteristic morphology, including a round to oval nucleus with fine, dispersed and pale blue containing azurophilic and specific granules. This technique differentiates myelocytes from more mature granulocytes by visualizing the granules' color and distribution, with primary (azurophilic) granules appearing reddish-purple and secondary granules developing as the cell matures. In routine practice, a manual differential count is performed by examining at least 100 to 200 cells under to quantify the proportion of myelocytes relative to other leukocytes, ensuring accurate identification based on size (12-18 μm) and nuclear features. Flow cytometry provides an immunophenotypic approach to detect and characterize myelocytes by targeting surface markers indicative of myeloid lineage commitment. Key markers include CD13 (aminopeptidase N), CD15 (Lewis X antigen), and CD33 (Siglec-3), which are expressed on immature myeloid cells like myelocytes, allowing distinction from lymphoid cells and more primitive blasts. Additionally, high side scatter (SSC) properties in flow cytometry reflect the increased cytoplasmic granularity due to granule accumulation, further confirming myelocyte identity when combined with forward scatter for cell size assessment. This multiparametric analysis is particularly useful in bone marrow aspirates, where gating strategies isolate the myeloid compartment for precise enumeration. For detailed ultrastructural examination, electron microscopy reveals the fine morphology of myelocyte granules, enabling of their formation, composition, and maturation stages not visible by light microscopy. Transmission electron microscopy shows primary granules as dense, membrane-bound structures containing enzymes like , while secondary granules appear less electron-dense with crystalline lattices in neutrophilic myelocytes. This technique has been instrumental in studying granule biogenesis, demonstrating sequential incorporation of proteins via the Golgi apparatus in and myelocytes. In pathological contexts, such as , electron microscopy can highlight aberrant granule structures, though primary identification relies on the aforementioned light-based methods.

Recent Advances

Recent advances in myelocyte research have leveraged single-cell RNA sequencing (scRNA-seq) to uncover transcriptional heterogeneity within myeloid progenitors, including myelocytes, during emergency . Studies have identified distinct subpopulations of granulocyte-monocyte progenitors (GMPs) that exhibit varied gene expression profiles, revealing dedicated trajectories toward differentiation under inflammatory stress. For instance, scRNA-seq analyses have shown that emergency conditions, such as , induce a rapid shift in hematopoietic stem cells toward myeloid-biased output, with myelocyte-stage cells displaying upregulated genes for granule formation and migration. Therapeutic strategies targeting myelocyte differentiation have advanced significantly in (AML), where , a inhibitor, received full FDA approval in 2020 for in older or unfit patients. promotes in immature leukemic blasts, including those blocked at the myelocyte stage, by disrupting anti-apoptotic signaling and enhancing the efficacy of hypomethylating agents like . has demonstrated that venetoclax sensitivity correlates with lower differentiation states, such as primitive myeloblasts, while monocytic-differentiated cells show resistance, guiding personalized treatment approaches. Research from 2020 to 2023 has highlighted the role of myelocytes in COVID-19-associated hyperinflammation, with expanded immature granulocytes, including myelocytes, contributing to storms and tissue damage. scRNA-seq of peripheral from severe cases revealed dysregulated myeloid expansion, where myelocyte-like cells overexpressed pro-inflammatory genes such as S100A8/A9, exacerbating . These findings suggest that immature myeloid responses drive the hyperinflammatory , informing potential interventions to modulate in viral . Emerging CRISPR-edited mouse models have elucidated the impact of GFI1 mutations on myelocyte maturation, linking them to congenital and predisposition. In Gfi1-mutant mice, /Cas9 knock-in of patient-derived variants disrupts transcriptional repression, leading to arrested at the myelocyte-to-metamyelocyte transition and increased susceptibility to . These models, developed around 2020 and refined in subsequent studies, demonstrate how GFI1 dosage affects accessibility in progenitors, providing platforms for testing maturation-promoting therapies. As of 2025, ongoing research continues to explore targeted therapies in AML that influence myelocyte differentiation, though no major new breakthroughs specific to myelocyte biology have been reported beyond refinements in single-cell and genomic approaches.

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