Breast

Noninvasive lobular neoplasia

LCIS florid


Editorial Board Member: Julie M. Jorns, M.D.
Deputy Editor-in-Chief: Gary Tozbikian, M.D.
Victoria M. Jones, M.D.
Kristen E. Muller, D.O.

Last author update: 14 May 2024
Last staff update: 14 May 2024

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PubMed Search: LCIS florid

Victoria M. Jones, M.D.
Kristen E. Muller, D.O.
Page views in 2024 to date: 956
Cite this page: Jones VM, Muller KE. LCIS florid. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/breastLCISflorid.html. Accessed May 19th, 2024.
Definition / general
  • Nonclassical or variant form of lobular carcinoma in situ (LCIS) where acini and ducts are markedly distended with little to no intervening stroma, sometimes imparting a mass-like architecture and comprising cells with cytologic features of classical LCIS (type A or type B cells) with or without comedonecrosis and calcifications
Essential features
  • Nonclassical or variant form of lobular carcinoma in situ (LCIS) defined by markedly distended acini / ducts of involved terminal duct lobular units (TDLUs) with scanty to no intervening stroma or an expanded acinus / duct filling at least 1 high power field (~40 - 50 cells in diameter)
  • Cells share cytologic features of classic LCIS (type A or type B cells) and lack significant cytologic atypia and pleomorphism
  • Commonly unifocal and shows a continuous distribution compared to classic LCIS
  • Shows features of a high risk precursor lesion of invasive carcinoma with a higher upgrade rate, increased association with invasive carcinoma and more genetic complexity compared to classic LCIS
Terminology
  • Florid LCIS or LCIS, florid type (F-LCIS)
  • LCIS with necrosis / comedonecrosis
  • Lobular neoplasia (can include atypical lobular hyperplasia and LCIS)
  • LCIS, variant type (not recommended)
  • The term florid is not synonymous with extensive or diffuse
ICD coding
  • ICD-10
    • D05 - carcinoma in situ of breast
    • D05.0 - lobular carcinoma in situ of breast
    • D05.00 - lobular carcinoma in situ of unspecified breast
    • D05.01 - lobular carcinoma in situ of right breast
    • D05.02 - lobular carcinoma in situ of left breast
  • ICD-11: 2E65.0 - lobular carcinoma in situ of breast
Epidemiology
Sites
Pathophysiology
  • First described in 2006 as a form of LCIS with central necrosis (Am J Surg Pathol 2006;30:1445)
  • Early tumorigenesis of LCIS is marked by loss of heterozygosity of the wild type allele and inactivating mutations of E-cadherin (Br J Cancer 1997;76:1131)
  • E-cadherin, encoded by the CDH1 gene on chromosome 16q22.1, is a cell - cell adhesion molecule that helps maintains lobular architecture
  • Clonal relationship to classic LCIS: harbors characteristic signature of LCIS showing 16q loss and 1q gain (Hum Pathol 2013;44:1998)
  • Florid LCIS is proposed to progress from classic LCIS by acquiring additional genetic (i.e., frequent ERBB2 or ERBB3 alterations, CCND1 amplifications) and chromosomal alterations (Mod Pathol 2020;33:1287, Mod Pathol 2020;33:1078, Hum Pathol 2013;44:1998)
  • Significantly more genome alterations and amplifications compared to classic LCIS (Hum Pathol 2013;44:1998)
  • Similar genetic complexity as apocrine pleomorphic LCIS (Hum Pathol 2013;44:1998)
Etiology
Diagnosis
  • Diagnostic core or excisional biopsy, surgical excision
Radiology description
Radiology images

Contributed by Kristen E. Muller, D.O. and Victoria M. Jones, M.D.
Mammographic calcifications

Mammographic calcifications

Prognostic factors
Treatment
Microscopic (histologic) description
  • Diagnosis requires the presence of at least 1 of 2 architectural features (Mod Pathol 2020;33:1287, Am J Surg Pathol 2019;43:399, Ann Diagn Pathol 2020;45:151481)
    • Markedly distended acini / ducts of involved TDLUs with little to no intervening stroma or
    • Expanded acinus / duct filling at least 1 high power field (~40 - 50 cells in diameter)
  • Marked distention of acini and ducts with little intervening stroma may impart a confluent, mass-like architecture
  • Solid, dyshesive, monomorphic proliferation of classic LCIS type A cells (scant cytoplasm, small uniform nuclei, inconspicuous nucleoli) or type B cells (increased cytoplasm, larger nuclei, more prominent nucleoli) (Am J Surg Pathol 2019;43:399, Ann Diagn Pathol 2020;45:151481)
  • Absence of marked nuclear pleomorphism and atypia, distinguishes from pleomorphic LCIS
  • Comedo or single cell necrosis is common, up to 71% of cases (Mod Pathol 2020;33:1287, Mod Pathol 2021;34:1495)
  • Comedo type necrosis, mitosis and apoptosis are more frequent in florid LCIS than in pleomorphic LCIS (Hum Pathol 2018;78:163)
  • May observe apocrine features (rounded, enlarged nuclei with prominent nucleoli and abundant eosinophilic and granular cytoplasm), more commonly in ER negative cases (Mod Pathol 2021;34:1495)
  • Rarely composed entirely of signet ring cells, which has a high frequency of associated invasive lobular carcinoma (80% of 10 cases in small series) (Arch Med Res 2010;41:436)
  • Often coexists with classic or pleomorphic LCIS
Microscopic (histologic) images

Contributed by Kristen E. Muller, D.O. and Victoria M. Jones, M.D.
Florid LCIS with mass-like architecture Florid LCIS with mass-like architecture

Florid LCIS with mass-like architecture

Single acinus

Single acinus

Little intervening stroma

Little intervening stroma

Necrosis

Necrosis


Calcifications

Calcifications

Type B cells Type B cells

Type B cells

Type A cells

Type A cells

Mitoses

Mitoses


Apocrine features Apocrine features

Apocrine features

Invasive lobular carcinoma

Invasive lobular carcinoma

E-cadherin

E-cadherin

Positive stains
Negative stains
Molecular / cytogenetics description
  • Florid LCIS shares the LCIS molecular hallmarks of 16q loss and 1q gain (Mod Pathol 2020;33:1287, Mod Pathol 2020;33:1078)
    • CDH1 gene encoding for E-cadherin on chromosome 16
  • Pathogenic alterations in CDH1, ERRB2, PIK3CA, ERRB3, RUNX1, FOXA1, CCND1 and CBFB (Mod Pathol 2020;33:1287, Mod Pathol 2020;33:1078)
  • Frequent ERBB2 / ERBB3 alterations (HER2 / HER3) are associated with more aggressive potential and invasive lobular carcinoma (Mod Pathol 2020;33:1078)
  • Additional, complex genomic alterations including (Mod Pathol 2020;33:1078)
    • Gain of interstitial or whole arm 17q, loss of distal or whole arm 8p, 11q and 17p, loss of distal or whole arm 18q or whole chromosome 18, loss of 13q or whole chromosome 13, gain of distal or whole arm 16p, gain of 8q or whole chromosome 8
  • Significantly more fraction genome alteration and loss, number of breakpoints and chromosomes with breakpoints and amplifications than classic LCIS (Hum Pathol 2013;44:1998)
  • Similar genetic complexity to apocrine pleomorphic LCIS (Hum Pathol 2013;44:1998)
Videos

Lobular carcinoma in situ and high risk breast lesions

Sample pathology report
  • Breast, right, core needle biopsy:
    • Lobular carcinoma in situ (LCIS), florid type (see comment)
    • Comment: The biopsy shows ducts and lobules that are markedly distended by a proliferation of classic LCIS cells (small, round, discohesive, uniform cells) with comedo type necrosis and calcifications. An E-cadherin immunostain is negative in lesional cells supporting interpretation as florid LCIS.
Differential diagnosis
Board review style question #1

The photomicrographs above are from a 63 year old woman who underwent core needle biopsy for screen detected calcifications. An E-cadherin immunostain is negative in lesional cells. What is the most appropriate diagnosis?

  1. Atypical lobular hyperplasia
  2. Ductal carcinoma in situ
  3. Lobular carcinoma in situ, classic type
  4. Lobular carcinoma in situ, florid type
  5. Lobular carcinoma in situ, pleomorphic type
Board review style answer #1
D. Lobular carcinoma in situ, florid type. The images show markedly expanded acini with central necrosis and calcification and little intervening stroma. The cells are uniform, small and round without marked pleomorphism. The differential usually includes ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS). A negative E-cadherin immunostain supports interpretation as LCIS and given the marked distention with scanty stroma, florid LCIS is the best diagnosis. Answer B is incorrect because this lesion is negative for E-cadherin and DCIS would have it retained. Answer C is incorrect because this meets diagnostic criteria for florid LCIS given the marked acinar distention. Answer E is incorrect because the lesional cells lack cytologic features of pleomorphic LCIS. Answer A is incorrect because atypical lobular hyperplasia (ALH) shows similar cytologic features to florid LCIS; however, criteria for ALH include either type A or type B cells that distend 50% or more acini within a lobule but not uniformly present throughout the entire terminal duct lobular unit (TDLU) or involves all acini in a TDLU but does not distend the acini. In contrast, florid LCIS shows markedly distended acini in a TDLU.

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Reference: LCIS florid
Board review style question #2

Which of the following is a true statement regarding florid lobular carcinoma in situ (LCIS)?

  1. Florid LCIS is always HER2 negative
  2. Florid LCIS is not typically detected by mammography
  3. Florid LCIS is rarely upgraded to invasive carcinoma; thus, surgical excision is not recommended
  4. Florid LCIS shares the classic LCIS molecular hallmarks of 16q loss and 1q gain
Board review style answer #2
D. Florid LCIS shares the classic LCIS molecular hallmarks of 16q loss and 1q gain. In addition, florid LCIS has significantly more genomic alterations and amplifications compared to classic LCIS and in some studies, shows a similar genetic complexity to apocrine pleomorphic LCIS. Answer B is incorrect because florid LCIS is frequently detected by imaging and presents with calcifications (most commonly) or a mass / density. Answer C is incorrect because the upgrade rate to invasive carcinoma or DCIS is between 17 and 39%. Although consensus guidelines are not yet available, most experts agree that surgical excision should be recommended. Answer A is incorrect because florid LCIS is reported to be HER2 positive 13 - 18% of the time and shows frequent ERBB2 / ERBB3 alterations in molecular studies.

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Reference: LCIS florid
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