Definitions and Classifications

Slide 1 · Definitions and Classifications

Lymphoid neoplasms

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Distinguish leukemia and lymphoma as patterns of presentation, not mutually exclusive tumor classes.

Organize lymphoid neoplasms by lineage and differentiation stage.

Relate anatomic distribution, secretory effects, and basic laboratory studies to classification.

Apply the morphology–immunophenotype–genotype–clinical framework.

Slide 3 · Names describe where disease is found

Leukemia and lymphoma originally denoted apparently distinct disorders.

Overlap in marrow, blood, and tissue involvement blurs that distinction.

The terminology mainly reflects the usual distribution at presentation.

Leukemia

Marrow ± blood

Lymphoma

Tissue mass

Slide 4 · Leukemia: Marrow-centered presentation

Widespread marrow involvement defines the traditional leukemic pattern.

Peripheral blood involvement is usual but not obligatory.

The classification does not require a discrete tissue mass.

Neoplastic lymphoid cells

Diffuse marrow involvement

± circulating blood cells

Slide 5 · Lymphoma: Tissue-mass presentation

A lymphoma commonly forms a discrete mass of lymphoid cells.

Lymph nodes are frequent sites, but extranodal organs are also involved.

The word lymphoma does not exclude simultaneous marrow or blood disease.

Neoplastic lymphoid cells

Discrete nodal / tissue mass

Possible systemic spread

Slide 6 · Leukemia and lymphoma can be one entity

Certain named lymphomas acquire substantial circulating tumor cells.

Tumors identical to leukemias can arise as masses without detectable marrow disease.

Site of first detection alone cannot establish biologic lineage.

Lymphomatous phase

Mass-dominant

Leukemic phase

Marrow / blood-dominant

Slide 7 · Changing distribution changes the clinical label

An initially mass-forming lymphoma can later produce a leukemic presentation.

This progression is not unusual in incurable lymphomas.

Reassessment of the same entity must consider all involved compartments.

Tissue-dominant disease

Marrow involvement

Circulating cells

Slide 8 · B-ALL and T-ALL illustrate naming overlap

B-ALL and T-ALL are precursor-cell neoplasms in the same broad diagnostic family.

Their names deliberately combine leukemia and lymphoma.

Distribution and lineage are separate dimensions of classification.

Immature B lineage

B-ALL / lymphoma

Immature T lineage

T-ALL / lymphoma

Slide 9 · Hodgkin and non-Hodgkin lymphomas

Hodgkin lymphoma is separated because of distinctive pathologic characteristics.

The other lymphoma groups are conventionally termed non-Hodgkin lymphomas (NHLs).

The distinction also has clinical and treatment implications.

Lymphomas

Hodgkin lymphoma

Non-Hodgkin lymphomas

Slide 10 · Non-Hodgkin lymphoma is an umbrella term

NHL encompasses multiple B-, T-, and NK-lineage neoplasms.

Individual entities differ in differentiation stage and anatomic behavior.

An NHL label is not a sufficient final disease classification.

B-cell neoplasms

T-cell neoplasms

NK-cell neoplasms

Slide 11 · Hodgkin lymphoma is a special family

The category is organized around Reed–Sternberg cells and their variants.

Classic subtypes and a nodular lymphocyte-predominant form.

Its spread pattern differs from many NHLs.

Reed–Sternberg cells / variants

Hodgkin lymphoma

Distinctive spread / clinical behavior

Slide 12 · Plasma cell neoplasms form a special group

Plasma cell tumors most often originate in bone marrow.

Peripheral blood and lymph nodes are less frequently involved.

Their clinical consequences often derive from skeletal disease or secreted immunoglobulin.

Plasma cell neoplasm

Bone marrow / skeleton

Protein-related effects

Slide 13 · Three dimensions must be kept separate

Distribution: Leukemic, nodal, or extranodal.

Biology: B-, T-, NK-, or Hodgkin-associated tumor lineage.

Differentiation: Precursor (immature) or peripheral (mature).

Distribution

Lineage

Maturation

Slide 14 · Anatomy often predicts first symptoms

The dominant organ compartment largely determines presentation.

Nodal enlargement, extranodal dysfunction, marrow failure, or bone destruction are different patterns.

Secreted proteins and cytokines can generate additional systemic symptoms.

Lymph nodes

Extranodal organs

Marrow

Skeleton

Slide 15 · Nodal lymphoma: Painless enlargement

About two-thirds of NHLs present with enlarged lymph nodes account.

Virtually all Hodgkin lymphomas present with nodal enlargement.

The nodes are often nontender; Palpation alone is not a tissue diagnosis.

Non-Hodgkin lymphoma

Often nodal

Hodgkin lymphoma

Typically nodal

Slide 16 · Extranodal NHL affects many organs

The remaining NHLs may present through extranodal involvement.

Skin, stomach, and brain as examples.

Organ-specific symptoms may precede recognition of a lymphoid mass.

Skin

Stomach

Brain

Slide 17 · Extranodal location changes the clinical question

A skin lesion directs attention to cutaneous lymphoid neoplasia.

A gastric lesion raises the possibility of a primary or secondary lymphoid tumor.

An intracranial lesion may require evaluation for a lymphoid process.

Site of lesion

Tissue sampling

Lineage-aware diagnosis

Slide 18 · Leukemia often suppresses hematopoiesis

Tumor cells occupying marrow compromise normal blood-cell production.

Clinical manifestations therefore often reflect marrow failure.

Peripheral blood may show tumor cells but their presence is not obligatory.

Tumor cells in marrow

Normal hematopoiesis suppressed

Cytopenia-related symptoms

Slide 19 · Marrow failure produces three clinical signals

Reduced erythropoiesis can contribute to anemia-related symptoms.

Reduced normal leukocyte output can predispose to infection.

Reduced platelet production can increase bleeding risk.

Erythroid cells → anemia

Normal leukocytes → infection

Platelets → bleeding

Slide 20 · Myeloma damages the skeleton

Multiple myeloma is the most common plasma cell neoplasm described in this passage.

Skeletal destruction creates mechanically weakened bone.

Pain can result from pathologic fractures.

Marrow plasma cell tumor

Bone destruction

Fracture-related pain

Slide 21 · Bone disease and protein disease differ

Skeletal lesions account for one major group of myeloma-related manifestations.

Secreted whole immunoglobulins or fragments account for another.

A single plasma cell neoplasm can cause both.

Plasma cell tumor

Skeletal effects

Secretory effects

Slide 22 · Secreted products can dominate disease effects

Not every lymphoma symptom is caused by direct tissue replacement.

Products made by tumor cells may alter distant organ function.

Host immune cells responding to tumor can also release clinically important mediators.

Lymphoid tumor

Tumor-derived proteins

Host-derived mediators

Slide 23 · Plasma cells may secrete intact or partial Ig

Plasma cell neoplasms can release whole immunoglobulin molecules.

Some release immunoglobulin fragments.

Consequences of the secreted proteins may be central to clinical presentation.

Whole immunoglobulin

Intact antibody

Ig fragments

Partial protein products

Slide 24 · Hodgkin lymphoma: Host-cell cytokines

Fever can occur in Hodgkin lymphoma.

The textbook links this systemic symptom to cytokines released by nonneoplastic inflammatory cells.

The reactive tumor microenvironment can therefore shape the phenotype.

Hodgkin tumor

Reactive inflammatory cells

Cytokine-associated fever

Slide 25 · Peripheral T-cell tumors: Tumor cytokines

Some peripheral T-cell lymphomas retain functional T-cell properties.

Neoplastic T cells can release proinflammatory cytokines and chemokines.

This mechanism differs from the reactive-cell cytokines emphasized in Hodgkin lymphoma.

Neoplastic functional T cell

Cytokines / chemokines

Inflammatory symptoms

Slide 26 · Distinguish mass effect from soluble effects

Direct effects arise from nodal, organ, marrow, or bone infiltration.

Indirect effects arise from immunoglobulin or cytokine secretion.

Both mechanisms may contribute to the same patient's symptoms.

Direct tumor burden

Anatomic effects

Secreted mediators

Systemic effects

Slide 27 · Why classification needs a shared system

Lymphoid neoplasms contain numerous biologically distinct entities.

Historical classification systems provoked major disagreements.

Formal classification integrates morphology, differentiation, genetics, and clinical behavior.

Heterogeneous tumors

Shared diagnostic criteria

Reproducible taxonomy

Slide 28 · WHO and ICC are distinct modern frameworks

Competing WHO and International Consensus Classification (ICC) systems.

The chapter teaches the WHO-based framework.

Differences between classifications should not be silently blended.

WHO

Textbook framework

ICC

Separate consensus system

Slide 29 · Four pillars support classification

Morphology: Observable architecture and cytology.

Immunophenotype: Proteins indicating lineage or maturation.

Genotype and clinical findings: Molecular alterations and disease context.

Morphology

Immunophenotype

Genotype

Clinical context

Slide 30 · Morphology localizes the diagnostic problem

Histology reveals tissue infiltration and patterns of architecture.

Cytologic features help identify the proliferating cell population.

Morphology is necessary but often not sufficient for final classification.

Tissue section

Architecture + cytology

Initial category

Slide 31 · Immunophenotype defines differentiation

Lineage-associated antigens characterize the neoplastic population.

Patterns of marker expression are interpreted as a panel.

The same antigen may occur on more than one normal lineage or maturation stage.

Marker panel

Lineage / stage assignment

Refined differential

Slide 32 · Genotype adds a clonal molecular dimension

Lymphoid tumors may contain characteristic genetic changes.

Antigen-receptor rearrangements can serve as clonal signatures.

Molecular information complements, rather than replaces, tissue diagnosis.

Tumor genetic features

Clonality / subtype evidence

Integrated classification

Slide 33 · Clinical findings are part of classification

Presentation as a mass or marrow-centered disease conveys distribution.

Site of disease provides differential-diagnostic context.

Clinical information is integrated with laboratory and pathologic findings.

Patient distribution

Clinical presentation

Pathology integration

Slide 34 · Five broad groups organize lymphoid tumors

The textbook WHO summary groups tumors by lineage and stage of differentiation.

Immature and mature B-cell, and immature and mature T/NK-cell, categories are separated.

Hodgkin lymphoma is retained as a fifth category.

Precursor B-cell

Peripheral B-cell

Precursor T-cell

Peripheral T- / NK-cell

Hodgkin lymphoma

Slide 35 · Precursor versus peripheral means immature versus mature

“Precursor” designates immature lymphoid-cell neoplasms.

“Peripheral” designates mature B-, T-, or NK-cell neoplasms.

Stage of normal differentiation is used as an organizing principle.

Precursor

Immature lymphoid cell

Peripheral

Mature lymphoid cell

Slide 36 · Precursor B-cell category

The Robbins table lists B-cell acute lymphoblastic leukemia/lymphoma (B-ALL).

This is a neoplasm of immature B-lineage cells.

Leukemia and lymphoma presentations belong to the same umbrella entity.

Immature B cell

B-ALL / lymphoma

Slide 37 · Precursor T-cell category

The Robbins table lists T-cell acute lymphoblastic leukemia/lymphoma (T-ALL).

The neoplastic cells are immature T-lineage lymphoblasts.

This category is distinct from mature peripheral T-cell lymphoma.

Immature T cell

T-ALL / lymphoma

Slide 38 · The two precursor categories are parallel

Both are defined by immature lymphoid differentiation.

B versus T identity establishes the branch.

A leukemia/lymphoma presentation does not substitute for lineage determination.

B precursor

B-ALL / lymphoma

T precursor

T-ALL / lymphoma

Slide 39 · Peripheral B-cell neoplasms: Overview

This broad family comprises mature B-cell tumors.

Nodal, splenic, leukemic, and plasma-cell-associated disease names.

The enumerated examples are not exhaustive.

Small / leukemic names

Nodal lymphoma names

Splenic names

Plasma cell-related

Slide 40 · Mature B-cell entities: CLL/SLL and splenic

Chronic lymphocytic leukemia / small lymphocytic lymphoma is one named entity.

Splenic B-cell lymphomas and leukemias form a listed group.

Both illustrate why anatomic presentations coexist within mature B classification.

CLL / SLL

Paired leukemia–lymphoma name

Splenic B neoplasms

Splenic-associated grouping

Slide 41 · Mature B-cell entities: Marginal and mantle

Marginal zone lymphoma is a listed peripheral B-cell neoplasm.

Mantle cell lymphoma is another distinct listed neoplasm.

The normal counterpart and distinctive features require entity-specific evaluation.

Marginal zone lymphoma

Mantle cell lymphoma

Slide 42 · Mature B-cell entities: Follicular and diffuse

Follicular lymphoma and diffuse large B-cell lymphoma appear as separate named entities.

Their names reflect different histologic concepts.

Classification should not rely on a label fragment in isolation.

Follicular lymphoma

Named entity

Diffuse large B-cell lymphoma

Named entity

Slide 43 · Mature B-cell entities: Burkitt and related

Burkitt lymphoma is a distinct named peripheral B-cell neoplasm.

Lymphoplasmacytic lymphoma is separately listed.

The table enumerates entities without supplying complete diagnostic criteria.

Burkitt lymphoma

Lymphoplasmacytic lymphoma

Slide 44 · Plasma cell tumors belong in the B-cell spectrum

The textbook places plasma cell neoplasms within the peripheral B-cell grouping.

Plasma cells are terminally differentiated antibody-producing cells.

Marrow-predominant involvement distinguishes their usual distribution.

Mature B-cell lineage

Plasma-cell differentiation

Plasma cell neoplasm

Slide 45 · Peripheral B-cell family at a glance

The textbook table names CLL/SLL, splenic groups, marginal zone, and mantle cell lymphoma.

It also names follicular, diffuse large B-cell, Burkitt, and lymphoplasmacytic lymphoma.

Plasma cell neoplasms complete this summary list.

CLL / SLL

Splenic B-cell lymphomas

Marginal zone

Mantle cell

Follicular

Diffuse large B-cell

Burkitt

Lymphoplasmacytic

Plasma cell neoplasms

Slide 46 · Peripheral T-cell and NK-cell family

The broad group includes tumors of mature T cells and NK cells.

The Robbins examples span blood, skin, nodes, and extranodal sites.

A site-based label is helpful but does not replace cellular classification.

Leukemic

Cutaneous

Nodal

Extranodal

Slide 47 · Mature T-cell leukemic names

T-cell prolymphocytic leukemia is listed.

T-large granular lymphocytic leukemia is listed.

Adult T-cell leukemia/lymphoma is a third named member of this family.

T-prolymphocytic leukemia

T-large granular lymphocytic leukemia

Adult T-cell leukemia/lymphoma

Slide 48 · Cutaneous T-cell names

Mycosis fungoides and Sézary syndrome are each named in the peripheral T/NK grouping.

These illustrate the importance of skin-related presentation.

A cutaneous location still requires clinicopathologic evaluation.

Mycosis fungoides

Named cutaneous T-cell tumor

Sézary syndrome

Named cutaneous T-cell tumor

Slide 49 · Nodal T-cell lymphoma names

Peripheral T-cell lymphoma, not otherwise specified (NOS), is listed.

Anaplastic large-cell lymphoma is separately listed.

Nodal T-follicular helper cell lymphoma is separately listed.

Peripheral T-cell lymphoma, NOS

Anaplastic large-cell lymphoma

Nodal T-follicular helper lymphoma

Slide 50 · Extranodal T-cell lymphoma names

The table includes enteropathy-associated T-cell lymphoma.

Subcutaneous panniculitis-like T-cell and hepatosplenic T-cell lymphomas are listed.

The names signal sites or patterns but are not themselves diagnostic criteria.

Enteropathy-associated

Subcutaneous panniculitis-like

Hepatosplenic T-cell

Slide 51 · Mature NK-cell-associated names

Extranodal NK/T-cell lymphoma is included in this category.

NK-cell leukemia is separately listed.

These reflect an NK-associated branch, not a precursor B or T entity.

Extranodal NK/T-cell lymphoma

Named entity

NK-cell leukemia

Named entity

Slide 52 · Hodgkin lymphoma: Two table branches

The textbook groups classic Hodgkin lymphoma subtypes together.

It also lists nodular lymphocyte-predominant disease.

Terminology can vary among classification frameworks; Retain the source edition when quoting its taxonomy.

Hodgkin lymphoma

Classic HL subtypes

Nodular lymphocyte-predominant

Slide 53 · Classic Hodgkin lymphoma subtypes

Nodular sclerosis and mixed cellularity are listed classic subtypes.

Lymphocyte-rich and lymphocyte-depleted are also listed.

These are named histopathologic subtypes; Criteria are detailed in the later Hodgkin section.

Nodular sclerosis

Mixed cellularity

Lymphocyte-rich

Lymphocyte-depleted

Slide 54 · This table is a teaching summary, not a full atlas

Robbins Table 13.4 explicitly omits some rare entities.

Each named subtype demands more detail than a family-level classification slide provides.

Use one specified classification version for a diagnostic report.

Textbook summary

Broad teaching structure

Definitive classification

Entity-specific criteria

Slide 55 · Clinical suspicion requires tissue confirmation

Clinical findings can raise suspicion for a lymphoid neoplasm.

The chapter states that histologic examination of involved tissue is required for diagnosis.

Lineage marker and genetic studies are important complementary tests.

Clinical / radiologic suspicion

Histologic tissue study

Ancillary studies

Slide 56 · Morphology and markers answer different questions

Histology determines tissue pattern and the nature of the cell proliferation.

Protein markers support lineage, activation, and differentiation stage.

Concordant findings yield a more defensible classification than either alone.

Morphology

Architecture + cytology

Immunophenotype

Protein expression

Slide 57 · T-cell-associated markers are contextual

CD3 is associated with thymocytes and mature T cells.

CD4 marks helper T cells and a subset of thymocytes.

CD8 marks cytotoxic T cells, some thymocytes, and some NK cells.

CD3

CD4

CD8

Slide 58 · CD5 is not absolutely T-cell specific

CD5 is expressed by T cells.

A small subset of normal B cells also expresses CD5.

It must be interpreted alongside a broader panel of markers.

T cells

Common CD5 expression

Subset of B cells

Also CD5 positive

Slide 59 · B-cell-associated markers differ by stage

CD19 marks pre-B cells and mature B cells, but not plasma cells table.

CD20 appears after CD19 during pre-B development and in mature B cells.

CD79a marks marrow pre-B cells and mature B cells.

CD19

CD20

CD79a

Slide 60 · CD10 is present in distinct B-cell stages

The source lists CD10 on pre-B cells.

CD10 is also present on germinal center B cells.

This dual distribution limits interpretation of CD10 as a standalone stage marker.

Pre-B cells

CD10 can be expressed

Germinal center B cells

CD10 can be expressed

Slide 61 · CD21 and CD23 add B-cell context

CD21 is listed on mature B cells and follicular dendritic cells and acts as an EBV receptor.

CD23 is associated with activated mature B cells.

Neither should be interpreted without lineage, morphology, and other markers.

CD21

CD23

Slide 62 · NK-associated markers have overlap

CD16 is associated with NK cells and granulocytes.

CD56 is associated with NK cells and a subset of T cells.

Coexpression and clinical setting are more informative than a single positive stain.

CD16

CD56

Slide 63 · CD34 indicates a progenitor compartment

CD34 on hematopoietic stem cells and many progenitors.

Its expression informs immaturity but does not, alone, determine lineage.

The full classification still integrates morphology and other markers.

CD34

Stem / progenitor context

Slide 64 · Reed–Sternberg-associated antigens

CD15 is associated with granulocytes and Reed–Sternberg cells or variants.

CD30 is an activation marker expressed by activated B cells, T cells, and monocytes.

The textbook also lists CD30 on Reed–Sternberg cells and variants.

CD15

CD30

Slide 65 · CD45 is a broad leukocyte marker

CD45 is also called leukocyte common antigen (LCA).

The table describes it as present on leukocytes.

As with all markers, tumor context and staining patterns matter.

CD45

Leukocyte common antigen

Slide 66 · Some markers overlap the myeloid lineage

CD11c occurs on granulocytes, monocytes, macrophages, and hairy-cell leukemias.

CD13, CD14, CD33, and CD64 occur on differing myeloid or monocytic compartments.

Lineage assignment requires interpretation of a coordinated panel.

CD11c

CD13 / CD14

CD33 / CD64

Slide 67 · A malignant lymphoid clone has a shared receptor

Antigen receptor gene rearrangement usually precedes malignant transformation.

Descendant tumor cells therefore inherit the same rearranged receptor sequence.

This molecular identity provides evidence of clonality.

One rearranged lymphoid progenitor

Malignant expansion

Shared receptor sequence

Slide 68 · Polyclonal and monoclonal are different patterns

Reactive lymphoid responses contain many antigen-receptor rearrangements.

A malignant clone generally carries one characteristic rearrangement.

Testing can help distinguish reactive from clonal lymphoid proliferations.

Polyclonal response

Diverse receptor sequences

Monoclonal tumor

Shared receptor sequence

Slide 69 · Clonal sequences permit sensitive follow-up

Each receptor gene rearrangement generates a distinctive DNA sequence.

That sequence can be used to search for residual malignant lymphocytes.

Clinical interpretation must link the molecular signal to the original tumor.

Tumor receptor sequence

Molecular assay

Residual clone detection

Slide 70 · Lymphoid tumors resemble stages of development

Most lymphoid neoplasms resemble recognizable stages of B- or T-cell differentiation.

This resemblance is central to the classification framework.

Immature versus mature status is therefore a biologic distinction.

Differentiation stage

Immature precursor

Mature peripheral

Slide 71 · B-cell lineage is most common

That 85%–90% of lymphoid neoplasms are of B-cell origin.

Most remaining lymphoid neoplasms arise from T cells.

NK-cell-origin tumors are rare.

B-cell origin

Majority (85%–90%)

T- / NK-cell origin

Smaller fractions

Slide 72 · Lymphoid tumors can impair immunity

Neoplasms may reduce protective immune function, increasing infection susceptibility.

Some are associated with breakdown of immune tolerance and autoimmunity.

Both abnormalities may coexist in the same patient.

Lymphoid neoplasm

Reduced protective immunity

Autoimmune phenomena

Slide 73 · Immunodeficiency also increases lymphoma risk

Inherited or acquired immunodeficiency increases risk for some lymphoid neoplasms.

Neoplasms linked to oncogenic viruses such as EBV.

Immunodeficiency is thus both a possible consequence and a predisposing context.

Immune surveillance impairment

Risk of virus-associated neoplasia

Lymphoid tumor

Slide 74 · Neoplastic lymphocytes retain homing programs

Normal lymphocytes express adhesion molecules and chemokine receptors.

Neoplastic cells may preserve these trafficking features.

The retained programs help explain characteristic tissue locations.

Adhesion + chemokine receptors

Tissue homing

Characteristic distribution

Slide 75 · Site-specific homing: Two examples

Follicular lymphoma cells tend to home to lymph-node germinal centers.

Cutaneous T-cell lymphomas preferentially involve the skin.

The cell's differentiation program helps explain site predilection.

Follicular lymphoma

Germinal centers

Cutaneous T-cell lymphoma

Skin

Slide 76 · Recirculation explains early dissemination

Normal lymphocytes circulate between blood and lymphoid tissues.

Neoplastic B and T cells may recirculate similarly.

Many lymphoid tumors are already distributed across sites at diagnosis.

Lymphoid tissue

Blood / lymphatics

Additional tissues

Slide 77 · Some lymphoid tumors remain localized

Hodgkin lymphoma may be limited to one nodal group.

Marginal zone lymphoma may be restricted to a chronically inflamed site.

These exceptions qualify the general observation of dissemination.

Hodgkin lymphoma

Sometimes one nodal group

Marginal zone lymphoma

Sometimes one inflamed site

Slide 78 · Hodgkin and NHL differ in spread pattern

Hodgkin lymphoma often spreads in a relatively orderly, stepwise pattern.

Many NHLs disseminate widely and less predictably.

Patterns overlap; Spread alone does not establish the diagnosis.

Hodgkin lymphoma

Often orderly / stepwise

Non-Hodgkin lymphoma

Often early / noncontiguous

Slide 79 · Staging has different decision utility

Staging conveys prognostic information in lymphoid tumors.

Its particular therapeutic relevance in Hodgkin lymphoma.

Tumor identity remains essential when interpreting disease stage.

Entity identification

Extent of spread

Prognostic / therapeutic context

Slide 80 · Integrative approach to a lymphoid neoplasm

Establish the dominant presenting compartment.

Examine the involved tissue and identify the tumor-cell population.

Integrate lineage / differentiation markers, molecular findings, and clinical distribution.

Report a defined entity using one named classification framework.

Distribution + morphology

Lineage / molecular evidence

Integrated entity

Slide 81 · Case: Painless cervical lymphadenopathy

A persistent, nontender enlarged lymph node suggests, but does not prove, lymphoma.

Histologic evaluation establishes the presence and pattern of an abnormal infiltrate.

Immunophenotypic and genetic findings distinguish Hodgkin or specific NHL entities.

Painless nodal mass

Tissue histology

Integrated subtype

Slide 82 · Case: Cytopenias with marrow lymphoid cells

A marrow-dominant lymphoid neoplasm may present as leukemia.

Suppression of normal hematopoiesis explains accompanying cytopenic symptoms.

A circulating tumor-cell count alone does not define the neoplasm’s lineage.

Marrow involvement

Reduced normal hematopoiesis

Lineage characterization

Slide 83 · Case: Bone pain and monoclonal protein

Skeletal destruction and pathologic fractures suggest a plasma cell process.

Secreted immunoglobulin or fragments may also drive organ dysfunction.

The combination of anatomic and protein effects focuses classification.

Bone destruction + pain

Secreted Ig / fragments

Plasma cell assessment

Slide 84 · Case: Lesion at an extranodal site

An extranodal mass must be evaluated according to its involved organ.

A tissue-defined lymphoma cannot be typed from location alone.

Morphology, lineage-associated proteins, genetics, and clinical findings are combined.

Extranodal tissue lesion

Histology + marker panel

Defined lymphoid entity

Slide 85 · Diagnostic pitfalls to avoid

Do not equate “leukemia” with a lineage and “lymphoma” with another lineage.

Do not diagnose a subtype from one surface antigen or one presenting site.

Do not treat a summary taxonomy as a complete list of diagnostic criteria.

Do not combine terminology from WHO and ICC without identifying the chosen edition.

Slide 86 · Synthesis: Biology, site, and evidence

Leukemia and lymphoma describe distribution; The definitive entity captures tumor biology.

The WHO summary groups lymphoid neoplasms by lineage and differentiation stage.

Clinical effects arise from distribution, marrow replacement, bone injury, and secreted products.

Morphology with immunophenotypic, genetic, and clinical context supports classification.

Slide 87 · Selected reference

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th edition (2026).

Section: Lymphoid Neoplasms — Definitions and Classifications.

WHO-oriented classification overview and immune-cell antigen distributions.

The complete entity definitions and diagnostic criteria require dedicated classification references.