Types of Invasive Breast Carcinoma

Slide 1 · Types of Invasive Breast Carcinoma

Histologic patterns, biologic associations, and diagnostic distinctions

Invasive carcinoma of no special type • Special histologic subtypes • Clinicopathologic correlations

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Distinguish invasive carcinoma of no special type from special histologic subtypes.

Explain the three morphologic variables used in Nottingham histologic grading.

Recognize characteristic invasive architectures and their diagnostic mimics.

Relate selected subtypes to receptor groups, dissemination, and clinical presentation.

Separate inflammatory carcinoma as a presentation from histologic classification.

Slide 3 · The organizing principle: Architecture before label

Identify invasion

Recognize malignant epithelial cells infiltrating breast stroma.

Classify pattern

No special type, or a definable special morphology.

Characterize biology

Assess grade and relevant receptor phenotype.

Slide 4 · Most invasive breast malignancies are adenocarcinomas

Approximately 20 morphologically defined subtypes of invasive carcinoma.

Histologic type reflects tumor architecture, growth pattern, and cellular morphology.

Special types have distinctive morphologic phenotypes; Not every pattern is a separate type.

Type, grade, and receptor expression describe different dimensions of a carcinoma.

Slide 5 · No special type dominates the classification

Invasive breast carcinoma of no special type (NST) accounts for approximately 75% of invasive cases.

A heterogeneous category • Not one uniform microscopic architecture

Slide 6 · A special type must have distinctive morphology

Special types are separated from NST by characteristic tumor architecture or cytomorphology.

Some have recognizable genomic or receptor associations.

A specific pattern should not be equated automatically with a single molecular profile.

The source emphasizes selected informative subtypes rather than all named rare entities.

Slide 7 · NST: An irregular infiltrative architecture

Tumor cells infiltrate fibrofatty tissue in haphazard glands, nests, cords, or single cells.

The extent of associated stromal reaction is highly variable.

Irregular invasion can produce an ill-defined gross and radiologic margin.

Architectural variability helps explain the breadth of NST appearances.

Schematic architecture — not a tissue specimen

Slide 8 · Desmoplasia drives the classic hard mass

An exuberant fibrous stromal reaction commonly surrounds infiltrating NST glands or nests.

Stromal fibrosis contributes to firmness and irregular radiodense margins.

Cut sections may be chalky-white; Focal calcifications can produce a grating sensation.

This classical appearance is common, not universal.

Schematic architecture — not a tissue specimen

Slide 9 · NST can be deceptively well circumscribed

If tumor grows as sheets with little stromal reaction, the mass may appear circumscribed.

Circumscription does not demonstrate benignity or exclude invasive carcinoma.

Architectural assessment must consider the lesional periphery and surrounding tissue.

The source contrasts this pattern with strongly desmoplastic NST.

Slide 10 · NST may be almost invisible macroscopically

Scattered neoplastic glands or single cells can infiltrate otherwise unremarkable fat.

Weak desmoplastic response may make a primary tumor hard to palpate or image.

This mechanism helps explain some clinically occult invasive carcinomas.

An inconspicuous mass does not imply an in situ process.

Schematic architecture — not a tissue specimen

Slide 11 · Medullary pattern belongs within NST

Some high-grade NSTs form relatively cohesive sheets with prominent tumor-infiltrating lymphocytes.

These were previously designated “medullary carcinoma.”

The separate entity proved insufficiently reproducible diagnostically.

Robbins calls this NST with medullary pattern.

Schematic architecture — not a tissue specimen

Slide 12 · Tumor-infiltrating lymphocytes: Contextual feature

Prominent lymphocytes may accompany high-grade tumors showing a medullary pattern.

The inflammatory infiltrate is a tumor-associated microscopic observation.

It does not, by itself, establish a special histologic type.

Do not confuse this finding with the clinical entity inflammatory breast carcinoma.

Slide 13 · Nottingham grade measures differentiation

Tubule formation

How much of the tumor develops recognizable glandular lumina?

Nuclear pleomorphism

How variable and atypical are tumor nuclei?

Mitotic activity

How actively are cells dividing on histologic assessment?

Slide 14 · Grading and typing answer different questions

Descriptor

What it measures

Examples

Histologic type

Predominant architectural / cellular pattern

NST, lobular, tubular

Histologic grade

Differentiation and proliferation

Nottingham grades 1–3

Receptor phenotype

ER, PR, HER2 expression

Luminal-associated, HER2-positive, TNBC

Slide 15 · Tubule formation indicates glandular differentiation

Well-formed lumina reflect retention of glandular epithelial architecture.

Grade 1 carcinomas frequently grow in tubules or cribriform formations.

Poorly differentiated tumors tend to form solid nests or sheets.

Tubule formation is one component of the composite Nottingham assessment.

Schematic architecture — not a tissue specimen

Slide 16 · Nuclear pleomorphism indicates cytologic atypia

Grade 1 cells show relatively small, uniform nuclei.

With loss of differentiation, nuclei become enlarged and irregular.

Grade 3 carcinomas typically show striking nuclear atypia.

Nuclear morphology is interpreted together with architecture and mitoses.

Slide 17 · Mitotic activity estimates proliferative behavior

Grade 1 tumors show a low proliferative rate and scarce mitoses.

Grade 2 tumors have more mitotic figures than well-differentiated examples.

High mitotic activity commonly accompanies grade 3 morphology.

Counts require a standardized laboratory method; No unsupported numeric thresholds are given here.

Slide 18 · Grade 1: Structured glands and uniform nuclei

Tubular or cribriform glandular architecture predominates.

Nuclei are small and relatively monomorphic.

Mitotic figures are uncommon examples.

This combination represents well-differentiated morphology.

Schematic architecture — not a tissue specimen

Slide 19 · Grade 2: Mixed glandular and solid growth

Tumor may show glandular structures beside solid cell clusters.

Single infiltrating cells can be present.

Nuclear atypia and mitoses are intermediate relative to grades 1 and 3.

This represents moderately differentiated morphology.

Schematic architecture — not a tissue specimen

Slide 20 · Grade 3: Ragged nests and sheets

Infiltrating irregular sheets or nests replace organized gland formation.

Nuclei are enlarged and pleomorphic.

Proliferation is high and tumor necrosis may be present.

This combination signifies poorly differentiated morphology.

Schematic architecture — not a tissue specimen

Slide 21 · Morphologic differences across grades

Feature

Grade 1

Grade 2

Grade 3

Architecture

Tubular / cribriform

Mixed glands and solid clusters

Ragged nests / solid sheets

Nuclei

Small, uniform

More atypical

Large, irregular

Mitoses

Few

Intermediate

Many

Necrosis

Not characteristic

Variable

May be prominent

Slide 22 · Histologic grade is relevant across invasive types

All invasive carcinomas are graded using the Nottingham system.

The composite score incorporates tubule formation, pleomorphism, and mitotic rate.

Grade is not synonymous with invasive tumor size or anatomical stage.

Specific histologic types may differ substantially in their usual differentiation.

Slide 23 · Special histologic types form biologic clusters

Usually luminal

Lobular, mucinous, tubular, cribriform, papillary.

Often HER2-positive

Apocrine and invasive micropapillary.

Often triple-negative

Metaplastic and certain salivary gland–like types.

Slide 24 · “Usually” is not “always” for receptor groups

The subtype-to-receptor associations are probabilistic.

Histomorphology does not replace ER, PR, or HER2 testing.

Exceptions must remain possible even when a pattern is classical.

Receptor and histologic classifications supply complementary information.

Slide 25 · Invasive lobular carcinoma is the main special type

Invasive lobular carcinoma is second most common and accounts for up to 15% of invasive cases.

Defining feature: Loss of cellular cohesion • Often luminal ER-positive/HER2-negative

Slide 26 · Lobular carcinoma: A single-file invasion pattern

Dyscohesive neoplastic cells infiltrate as linear cords or individual cells.

The single-file architecture is a diagnostic morphologic hallmark.

Minimal mass-forming stromal reaction may conceal disease on imaging.

Assessment requires inspection of tumor distribution in the stroma.

Schematic architecture — not a tissue specimen

Slide 27 · Signet-ring change in lobular carcinoma

Intracytoplasmic mucin can displace the nucleus to the cellular periphery.

Signet-ring cells may be found amid dyscohesive tumor cells.

Distinguish intracellular mucin from large extracellular mucin lakes.

A signet-ring phenotype alone is not equivalent to mucinous carcinoma.

Schematic architecture — not a tissue specimen

Slide 28 · Lobular carcinoma often causes little desmoplasia

Rather than a conspicuous firm nodule, the lesion may diffusely infiltrate breast tissue.

Minimal stromal response contributes to subtle imaging findings.

Detection difficulties derive partly from how cells occupy the existing tissue.

Clinical and radiologic findings must be integrated with histology.

Slide 29 · E-cadherin links genotype to cell cohesion

CDH1 / E-cadherin

E-cadherin participates in epithelial cell-cell adhesion.

Loss of expression

Most invasive lobular carcinomas lose E-cadherin expression.

Dyscohesive growth

Cells separate and infiltrate as single files or small groups.

Slide 30 · The CDH1 germline association

Heterozygous germline CDH1 mutations in affected families.

Such carriers have increased risk for lobular breast carcinoma.

The same association encompasses gastric signet-ring carcinoma.

This is a susceptibility association, not evidence that every lobular carcinoma is hereditary.

Slide 31 · Lobular carcinoma has distinctive metastatic sites

Peritoneum and retroperitoneum are recognized sites.

Gastrointestinal tract, ovaries, and uterus can be involved.

Leptomeningeal spread may produce carcinomatous meningitis.

The unusual distribution broadens the differential diagnosis of secondary lesions.

Slide 32 · Lobular carcinoma versus NST

Feature

Invasive lobular

Invasive NST

Invasion

Dyscohesive, single-file cords

Variable glands, nests, sheets

Stromal reaction

Often scant

Often desmoplastic

E-cadherin

Usually lost

Not defined by loss

Detection

May be subtle / diffuse

Often irregular mass

Distinctive spread

Peritoneal and GI sites

No subtype-specific pattern stated here

Slide 33 · Mucinous carcinoma: Gelatinous gross appearance

The mass may be soft, rubbery, and gelatinous.

Gross borders can be pushing or relatively circumscribed.

Extracellular mucin accounts for its characteristic consistency.

Mucinous carcinoma belongs among the subtypes usually in the luminal group.

Schematic architecture — not a tissue specimen

Slide 34 · Mucinous carcinoma: Tumor islands in mucin

Neoplastic epithelial clusters float in abundant extracellular mucin lakes.

Cell clusters vary in size and arrangement.

The extracellular location of mucin is diagnostically essential.

This architecture explains the gelatinous cut-surface appearance.

Schematic architecture — not a tissue specimen

Slide 35 · Extracellular versus intracellular mucin

Feature

Mucinous carcinoma

Lobular carcinoma with signet-ring cells

Mucin location

Extensive extracellular mucin pools

Inside individual tumor cells

Tumor architecture

Clusters floating in mucin

Dyscohesive single files

Diagnostic emphasis

Mucin lakes and cell groups

Discohesion and epithelial phenotype

Slide 36 · Tubular carcinoma: Infiltrating well-formed glands

Invasive architecture consists of well-formed tubular structures.

The cells show a striking degree of glandular differentiation.

Tubular carcinoma is usually within the luminal receptor group.

Architecture can appear bland despite genuine stromal invasion.

Schematic architecture — not a tissue specimen

Slide 37 · Tubular carcinoma may mimic a benign lesion

Small, well-organized glands may be mistaken for a sclerosing benign process.

The central diagnostic question is the invasive arrangement of atypical tubules.

Apparent blandness does not eliminate the need to establish invasion.

This sclerosing-lesion diagnostic pitfall.

Slide 38 · Cribriform carcinoma: Perforated tumor nests

Invasive tumor nests contain multiple rounded punched-out spaces.

This creates a sieve-like or cribriform architecture.

Cribriform carcinoma usually belongs to the luminal group.

The key recognition feature is invasive cribriform growth.

Schematic architecture — not a tissue specimen

Slide 39 · Tubular versus cribriform architecture

Feature

Tubular carcinoma

Cribriform carcinoma

Principal structure

Separate small glandular tubules

Invasive nests with multiple lumina

Visual impression

Discrete open-lumen glands

Sieve-like nests

Shared association

Often ER-positive/HER2-negative

Often ER-positive/HER2-negative

Teaching pitfall

Can resemble sclerosing lesions

Do not identify type from a single lumen

Slide 40 · Papillary carcinoma contains true fibrovascular cores

The papillae are real fronds lined by neoplastic epithelial cells.

Each true papilla has a fibrovascular central axis.

Papillary carcinoma is included among usually luminal special types.

The presence of true cores distinguishes it from micropapillary pattern.

Schematic architecture — not a tissue specimen

Slide 41 · Papillary is an architectural, not receptor-only diagnosis

Observe cellular lining and supporting fibrovascular fronds.

Papillary histology must be assessed in the context of invasion.

An ER-positive result cannot independently identify papillary carcinoma.

Micropapillary carcinoma uses the name “papillary” despite lacking these cores.

Slide 42 · Luminal-associated special types: Comparison

Subtype

Signature morphology

Selected clinical/biologic note

Lobular

Single-file, dyscohesive cells

E-cadherin loss; unusual metastases

Mucinous

Clusters in mucin lakes

Soft gelatinous gross lesion

Tubular

Well-formed small glands

Can mimic benign sclerosis

Cribriform

Perforated invasive nests

Sieve-like architectural growth

Papillary

True epithelial-lined fibrovascular cores

Distinguish from micropapillary

Slide 43 · Apocrine carcinoma: Eosinophilic cytoplasm

Tumor cells resemble glandular cells lining sweat glands.

Cytoplasm is abundant, eosinophilic, and may be granular.

Nuclei are enlarged with conspicuous nucleoli.

Apocrine carcinoma among types more likely to overexpress HER2.

Schematic architecture — not a tissue specimen

Slide 44 · Apocrine morphology is not a HER2 test

The apparent apocrine phenotype is cytologic: Large nuclei, nucleoli, abundant cytoplasm.

HER2 overexpression is an association rather than a defining histologic criterion.

Direct receptor assessment remains necessary.

The source does not assert uniform HER2 positivity in apocrine carcinoma.

Slide 45 · Invasive micropapillary carcinoma forms hollow balls

Aggregates of neoplastic cells form hollow ball-like structures.

They lie in intercellular fluid spaces, giving an illusion of papillary formations.

The apparent papillae lack genuine fibrovascular cores.

Robbins groups this type among carcinomas more likely to overexpress HER2.

Schematic architecture — not a tissue specimen

Slide 46 · Micropapillary is a morphologic misnomer

Feature

True papillary carcinoma

Invasive micropapillary carcinoma

Core

Fibrovascular core present

No true fibrovascular core

Growth

Epithelial-lined fronds

Hollow balls in fluid spaces

Receptor association

Usually luminal

More likely HER2-overexpressing

Classification lesson

True papillary architecture

Papillary-like illusion

Slide 47 · HER2-associated morphologies are not interchangeable

Apocrine and micropapillary carcinomas are architecturally dissimilar.

Apocrine refers mainly to eosinophilic granular cytoplasm and nucleoli.

Micropapillary refers to hollow cell clusters lacking true vascular cores.

Their shared HER2 association must not obscure these structural differences.

Slide 48 · Metaplastic carcinoma shows divergent differentiation

Carcinoma develops overt squamous or mesenchymal-like differentiation.

Mesenchymal-like elements may be spindle-shaped, cartilaginous, or osseous.

Many metaplastic tumors are triple-negative.

The category is biologically and prognostically heterogeneous.

Schematic architecture — not a tissue specimen

Slide 49 · Squamous differentiation in metaplastic carcinoma

Neoplastic epithelium acquires a squamous phenotype.

This is evidence of divergent tumor differentiation.

The epithelial lineage must be reconciled with the unusual histology.

Not all metaplastic carcinomas are predominantly squamous.

Schematic architecture — not a tissue specimen

Slide 50 · Spindle and mesenchymal morphology

Spindle-cell architecture can resemble a primary stromal lesion.

Other metaplastic forms may display chondroid or osseous differentiation.

The broad phenotype explains important morphologic differential diagnoses.

The subtype is not defined by a single uniform cell shape.

Schematic architecture — not a tissue specimen

Slide 51 · Metaplastic tumors may express myoepithelial-like profiles

Many metaplastic carcinomas with myoepithelial-like gene expression.

These tumors are frequently triple-negative by ER, PR, and HER2 criteria.

The molecular resemblance is a group-level observation.

Do not infer a specific marker positivity rate or diagnostic panel from this excerpt.

Slide 52 · Metaplastic carcinoma: Prognosis is not uniform

Metaplastic breast carcinoma is often associated with poor clinical outcome.

Robbins recognizes unusual indolent metaplastic subtypes.

Low-grade adenosquamous carcinoma is one example.

Fibromatosis-like metaplastic carcinoma is another exception.

Broad categorization must preserve these prognostic distinctions.

Slide 53 · Low-grade adenosquamous carcinoma

An uncommon, relatively indolent metaplastic subtype.

The name reflects the combination of glandular and squamous differentiation.

It should not be presumed to share the outcome of aggressive metaplastic forms.

Exact diagnostic criteria are not detailed in the supplied section.

Slide 54 · Fibromatosis-like metaplastic carcinoma

An uncommon, relatively indolent metaplastic subtype.

Its fibromatosis-like growth broadens the differential of spindle-cell breast lesions.

Its clinical behavior differs from the generally aggressive metaplastic group.

Detailed immunohistochemical criteria are beyond the provided Robbins excerpt.

Slide 55 · Triple-negative carcinomas are histologically diverse

TNBC means absence of ER, PR, and HER2 expression, not one morphology.

Metaplastic carcinomas are commonly triple-negative and often aggressive.

Some triple-negative salivary gland–like carcinomas have a comparatively favorable course.

Receptor status alone cannot determine prognosis without tumor type and extent.

Slide 56 · Salivary gland–like breast carcinomas

Adenoid cystic

Rare breast counterpart of salivary gland morphology.

Mucoepidermoid

Rare tumor with the salivary-type designation.

Secretory

Rare subtype with distinctive histologic morphology.

Slide 57 · Salivary gland–like types: A prognostic exception

Robbins groups adenoid cystic, mucoepidermoid, and secretory breast carcinomas.

They closely resemble corresponding salivary gland tumors.

These rare forms are usually triple-negative yet are relatively favorable compared with usual aggressive TNBC patterns.

This demonstrates why histologic type can qualify receptor-based expectations.

Slide 58 · Adenoid cystic carcinoma

An uncommon salivary gland–like subtype of invasive breast carcinoma.

It among rare triple-negative tumors with relatively favorable prognosis.

Its designation reflects similarity to its salivary gland counterpart.

The supplied section does not provide detailed architecture or molecular criteria.

Slide 59 · Mucoepidermoid carcinoma

An uncommon breast carcinoma analogous to the salivary gland entity.

It belongs to a small favorable-outcome group of triple-negative special types.

The given textbook excerpt lists the type without detailed morphology.

Avoid adding unverified diagnostic thresholds or translocation claims.

Slide 60 · Secretory carcinoma: A distinct special type

Secretory carcinoma is a rare salivary gland–like breast carcinoma.

It among special types and groups it with relatively favorable TNBC subtypes.

The label denotes a distinct histologic type, not nonspecific glandular secretion.

Exact molecular alterations are not provided in the supplied source excerpt.

Slide 61 · Subtype, receptor phenotype, and outcome

Group

Selected types

Robbins emphasis

Usually luminal

Lobular, mucinous, tubular, cribriform, papillary

Distinct architectures; usually ER+/HER2−

More likely HER2+

Apocrine, micropapillary

Distinct cytology vs structure

Often TNBC, aggressive

Many metaplastic forms

Squamous / mesenchymal differentiation

Rare TNBC, favorable

Adenoid cystic, mucoepidermoid, secretory

Salivary gland–like counterparts

Slide 62 · Inflammatory breast carcinoma is not a histologic type

“Inflammatory” breast carcinoma describes a clinical presentation caused by dermal lymphovascular tumor emboli.

Clinical syndrome, not a distinctive epithelial architecture • The term does not imply primary infection

Slide 63 · Dermal lymphovascular obstruction causes edema

Extensive carcinoma cell plugs occupy dermal lymphovascular spaces.

Lymphatic outflow obstruction produces diffuse swelling and skin thickening.

Clinical erythema accompanies the edematous presentation.

The defining mechanism is tumor embolization, not inflammatory-cell infiltrates.

Schematic architecture — not a tissue specimen

Slide 64 · Peau d’orange is a mechanical consequence

Edematous skin remains tethered to deep breast structures by Cooper ligaments.

Localized tethering against diffuse swelling produces an orange-peel texture.

The skin changes reflect dermal lymphatic blockage and fixation.

This finding can occur without a palpable discrete mass.

Carcinoma embolus

Schematic architecture — not a tissue specimen

Slide 65 · Inflammatory carcinoma: Why clinical confusion occurs

Erythema and swelling may resemble an infectious process.

The designation is a misnomer because inflammatory infiltrates are typically not the explanation.

Delay can occur if the appearance is attributed solely to infection.

Underlying carcinoma is commonly high grade and diffusely infiltrative.

Slide 66 · Most invasive cancers present as a palpable or screened mass

Primary cancers are identified by palpation or imaging-based screening.

Screen-detected cancers are often smaller luminal tumors confined to the breast.

Clinically apparent masses are more common with aggressive HER2-positive and triple-negative disease.

The detection pattern is an association, not a substitute for receptor testing.

Slide 67 · Advanced local growth alters the breast examination

Pectoralis invasion can produce fixation to the chest wall.

Dermal involvement can result in retraction or dimpling.

Central tumors may retract the nipple.

These clinical findings reflect anatomic extent rather than a specific histologic subtype.

Slide 68 · Occult primary carcinoma may first appear as metastasis

An axillary node or distant metastasis may occasionally precede identification of the breast primary.

The primary can be small, obscured by dense tissue, or minimally desmoplastic.

Ultrasound or MRI may reveal lesions missed by examination or mammography.

Insidious invasive patterns should remain in the differential.

Slide 69 · Illustrative case: Subtle invasive lobular carcinoma

Illustrative teaching vignette

Breast imaging shows only ill-defined subtle distortion. Histology reveals individual tumor cells aligned in linear cords with limited stromal response.

Interpretation

Pattern favors invasive lobular carcinoma rather than a desmoplastic NST mass.

E-cadherin loss is an expected biologic association, not a replacement for morphology.

A weakly palpable lesion is consistent with insidious infiltration.

Slide 70 · Illustrative case: Grading a high-grade NST

Illustrative teaching vignette

An invasive lesion grows as irregular sheets. Tumor cells have enlarged pleomorphic nuclei, conspicuous mitotic activity, and a focus of necrosis.

Interpretation

Morphology is compatible with poorly differentiated (grade 3) carcinoma.

Grading rests on gland formation, nuclear atypia, and mitotic rate together.

The histologic grade alone does not establish HER2 or triple-negative status.

Slide 71 · Illustrative case: Papillary or micropapillary?

Illustrative teaching vignette

An invasive tumor forms round cellular aggregates apparently floating in tissue spaces. No central fibrovascular core is seen in the aggregates.

Interpretation

The absence of true cores favors invasive micropapillary architecture.

True papillary carcinoma instead contains epithelial-lined fibrovascular fronds.

Assess HER2 directly; A receptor association is not proof of type.

Slide 72 · Illustrative case: A triple-negative spindle lesion

Illustrative teaching vignette

An invasive breast malignancy shows a substantial spindle-cell component. ER, PR, and HER2 are negative.

Interpretation

Metaplastic carcinoma belongs in the differential because mesenchymal-like growth is recognized.

Triple-negative status supports a group association but does not independently establish type.

Clinical behavior differs among metaplastic subtypes.

Slide 73 · Pattern-based differential: Five recognition pivots

Look for

Consider

Exclude confusion with

Single-file discohesive cells

Invasive lobular

NST with scattered glands

Large extracellular mucin lakes

Mucinous

Signet-ring intracellular mucin

Infiltrating well-formed small glands

Tubular

Benign sclerosis

True fibrovascular cores

Papillary

Micropapillary

Hollow clusters without true cores

Micropapillary

Papillary

Spindle / squamous elements

Metaplastic

Purely stromal lesion

Slide 74 · Histologic pattern is a map, not the whole diagnosis

Histologic type captures reproducible growth pattern and tumor cytology.

Nottingham grade captures degree of differentiation and cell division.

ER, PR, and HER2 provide biologic and therapeutic context.

Clinical extent and metastatic spread remain separate dimensions.

Subtype assessment should preserve uncertainty when architecture is incomplete.

Slide 75 · Five distinctions that prevent classification errors

NST with medullary pattern is not a separate medullary histologic type.

Papillary carcinoma has real fibrovascular cores; Micropapillary carcinoma does not.

Lobular signet-ring change is not equivalent to extracellular mucinous growth.

Triple-negative receptor status does not imply a single prognosis.

Inflammatory carcinoma is a clinical syndrome, not a special microscopic carcinoma subtype.

Slide 76 · Primary reference and source limits

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th edition (2026), Chapter 23, The Breast.

Core source: “Types of Invasive Breast Carcinoma,” printed pp. 961–964.

Adjacent source context: “Clinical Presentation” (p. 964) and prognostic factors (p. 964).

Figures 23.20–23.22 were described in source text but not reproduced; native figures here are explanatory schematics.

Original chapter PDF was not available for direct page/figure verification.