Breast lumps pathophysiology

Jump to navigation Jump to search

Breast lumps Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Breast lumps from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Breast lumps pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Breast lumps pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Breast lumps pathophysiology

on Breast lumps pathophysiology

Breast lumps pathophysiology in the news

Blogs on Breast lumps pathophysiology

Directions to Hospitals Treating Breast lumps

Risk calculators and risk factors for Breast lumps pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shadan Mehraban, M.D.[2]

Overview

Breast development is influenced by different hormones such as estrogen, progesterone, prolactin, and estradiol. The pathophysiology of breast lumps depends on the histological subtypes. Histological findings of breast lumps are different from each other which lead to diagnosis. It is thought that breast lumps are the result of hormonal events and genetic mutations. Estrogen and progesterone may increase risk of benign proliferative disease to 74% and benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Gene mutations are classified into 3 categories based on cancer risk such as BRCA1, BRCA2, TP53 considered as high risk mutations, Homozygous ataxia-telangiectasia, somatic mutation in CHEK2, BRIP1, PALB2 moderate risk mutations, and low risk genes mutation are not determined yet.

Pathophysiology

Physiology

Histological changes of breast

Histological changes of breast undergo continuous changes throughout the life:[4]

  • Fibrocystic disease
    • Histological apperance change from predominance of ducts, lobules to fibrous change, and cyst formation
    • Fibrocystic changes are not associated with breast cancer
  • Diagnostic subtypes and histologic subtypes are described according to their relative risk for cancer as below:[7]
Diagnostic Subtypes
Diagnostic Subtypes Breast cancer relative risk
Non-proliferative disease 1.17
Proliferative disease without atypia 1.76
Benign breast disease 2.07
Atypical hyperplasia 3.93
Histologic Subtypes
Histological subtypes Relative risk|Breast cancer relative risk
Adenosis 2.00
Atypical ductal hyperplasia 3.28
Atypical lobular hyperplasia 3.92
Cysts 1.55
Fibroadenoma 1.41
Papilloma 2.06
Histological findings of breast lumps
Breast lumps Histological findings
Atypical hyperplasia[8]
  • Clonal neoplastic proliferations is present.
Atypical ductal hyperplasia (ADH)[9]
  • Localized intraductal proliferations,having some microscopic features of ductal carcinoma in situ (DCIS), usually associated with calcification, duct spaces consist of complex proliferation of monotonous luminal-type cells by creating bridging feature.
  • Differentiation of ADH from DCIS : ADH has less cytological atypia than DCIS.
  • Distribution in severe ADH is restricted to less than 3 contiguous ducts and less than 0.2 cm in size.
Lobular neoplasia[10]
  • Associated to decrease expression or missing expression of E-cadherine, lobular neoplasia is considered to be as incidental findings in during microcalcification evaluation.
Atypical lobular hyperplasia (ALH)[11]
  • ALH is containing monomorphic cells and distend into lobular acini and adjacent terminal ducts.
  • Differentiation between ALH and lobular carcinoma in situ (LCIS) associated with quantitative degrees about lobules and architecture feature.
Apocrine proliferative lesions[12]
  • Apocrine atypia is described by a 3-fold variation in nuclear size or by cribriform structures with nuclear atypia, associated with sclerosing adenosis or complex sclerosing lesion.
Columnar cell lesions (CCL)[13]
  • CCL has heterogeneous set of lesions distinguished by reduplication and microcystic changes in lobular acini, elevated estrogen receptor expression, increased proliferative rate, associated with sclerosing adenosis, clacification and pleomorphic appearnace.
Papillary lesions[14]
  • Arborescent fibrovascular stalk lined to the myoepithelium are present.
Radical scars and complex sclerosing lesions[15]
  • Radial scars are tumor like lesions with stellate nidus of dense elastotic collagen, surrounding with epithelial elements and sclerosing adenosis.
  • Complex sclerosing lesions are kind of radial scars larger than 1 cm which has distorted glandular tissue.
Fibroadenoma[16]
Phyllodes tumor[17]
Pseudoangiomatous Stromal Hyperplasia[18]
Sclerosing adenosis[19]

Pathogenesis

Genetics

Associated Conditions

  • There are no other associated conditions with breast lumps.

Gross pathology

Gross findings Gross pathology
  • Fibrotic capsule and infiltrated the surrounding tissue[33]
  • Gray-white color and moderately increased consistency
Gross feature of fibroadenoma Source: Netha Hussain , from Wikimedia Commons
  • Stellate area of cancer 2cm in diameter
  • Felt as a hard mobile mass
  • Histology as a moderately well differentiated duct carcinoma
Gross image of breast cancer Source: John Hayman , from Wikimedia Commons

Microscopic Pathology

Pathologic findings Microscopic image
Histopathologic image of Phyllodes tumor Source: Nephron, from Wikimedia Commons
  • Sclerosing adenosis microscopic pathology has increased numbers of small
    breast acini with collapsed lumens, fibrosis surrounds the acini,
    considered as benign lesion with increased risk of breast cancer.
Histopathologic image of sclerosing adenosis Source: Nephron, from Wikimedia Commons
Histopathologic image of atypical ductal hyperplasia Source: Nephron, from Wikimedia Commons

References

  1. ↑ Going JJ, Anderson TJ, Battersby S, MacIntyre CC (1988). "Proliferative and secretory activity in human breast during natural and artificial menstrual cycles". Am J Pathol. 130 (1): 193–204. PMC 1880536. PMID 3337211.
  2. ↑ Hughes LE, Mansel RE, Webster DJ (1987). "Aberrations of normal development and involution (ANDI): a new perspective on pathogenesis and nomenclature of benign breast disorders". Lancet. 2 (8571): 1316–9. PMID 2890912.
  3. ↑ Santen RJ. Benign Breast Disease in Women. [Updated 2018 May 25]. In: De Groot LJ, Chrousos G, Dungan K, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK278994/
  4. ↑ Love, Susan M.; Sue Gelman, Rebecca; silen, William (1982). "Fibrocystic Disease of the Breast — A Nondisease?". New England Journal of Medicine. 307 (16): 1010–1014. doi:10.1056/NEJM198210143071611. ISSN 0028-4793.
  5. ↑ Pearlman MD, Griffin JL (2010). "Benign breast disease". Obstet Gynecol. 116 (3): 747–58. doi:10.1097/AOG.0b013e3181ee9fc7. PMID 20733462.
  6. ↑ 6.0 6.1 Huh SJ, Oh H, Peterson MA, Almendro V, Hu R, Bowden M; et al. (2016). "The Proliferative Activity of Mammary Epithelial Cells in Normal Tissue Predicts Breast Cancer Risk in Premenopausal Women". Cancer Res. 76 (7): 1926–34. doi:10.1158/0008-5472.CAN-15-1927. PMC 4873436. PMID 26941287.
  7. ↑ Dyrstad SW, Yan Y, Fowler AM, Colditz GA (2015). "Breast cancer risk associated with benign breast disease: systematic review and meta-analysis". Breast Cancer Res Treat. 149 (3): 569–75. doi:10.1007/s10549-014-3254-6. PMID 25636589.
  8. ↑ Lakhani SR, Collins N, Stratton MR, Sloane JP (1995). "Atypical ductal hyperplasia of the breast: clonal proliferation with loss of heterozygosity on chromosomes 16q and 17p". J Clin Pathol. 48 (7): 611–5. PMC 502709. PMID 7560165.
  9. ↑ Ely KA, Carter BA, Jensen RA, Simpson JF, Page DL (2001). "Core biopsy of the breast with atypical ductal hyperplasia: a probabilistic approach to reporting". Am J Surg Pathol. 25 (8): 1017–21. PMID 11474285.
  10. ↑ Page DL, Dupont WD, Rogers LW, Rados MS (1985). "Atypical hyperplastic lesions of the female breast. A long-term follow-up study". Cancer. 55 (11): 2698–708. PMID 2986821.
  11. ↑ Middleton LP, Sneige N, Coyne R, Shen Y, Dong W, Dempsey P; et al. (2014). "Most lobular carcinoma in situ and atypical lobular hyperplasia diagnosed on core needle biopsy can be managed clinically with radiologic follow-up in a multidisciplinary setting". Cancer Med. 3 (3): 492–9. doi:10.1002/cam4.223. PMC 4101740. PMID 24639339.
  12. ↑ Guray M, Sahin AA (2006). "Benign breast diseases: classification, diagnosis, and management". Oncologist. 11 (5): 435–49. doi:10.1634/theoncologist.11-5-435. PMID 16720843.
  13. ↑ Schnitt SJ, Vincent-Salomon A (2003). "Columnar cell lesions of the breast". Adv Anat Pathol. 10 (3): 113–24. PMID 12717115.
  14. ↑ Muttarak M, Lerttumnongtum P, Chaiwun B, Peh WC (2008). "Spectrum of papillary lesions of the breast: clinical, imaging, and pathologic correlation". AJR Am J Roentgenol. 191 (3): 700–7. doi:10.2214/AJR.07.3483. PMID 18716096.
  15. ↑ Krishnamurthy S, Bevers T, Kuerer H, Yang WT (2012). "Multidisciplinary considerations in the management of high-risk breast lesions". AJR Am J Roentgenol. 198 (2): W132–40. doi:10.2214/AJR.11.7799. PMID 22268202.
  16. ↑ Hartmann LC, Sellers TA, Frost MH, Lingle WL, Degnim AC, Ghosh K; et al. (2005). "Benign breast disease and the risk of breast cancer". N Engl J Med. 353 (3): 229–37. doi:10.1056/NEJMoa044383. PMID 16034008.
  17. ↑ Karim RZ, Gerega SK, Yang YH, Spillane A, Carmalt H, Scolyer RA; et al. (2009). "Phyllodes tumours of the breast: a clinicopathological analysis of 65 cases from a single institution". Breast. 18 (3): 165–70. doi:10.1016/j.breast.2009.03.001. PMID 19329316.
  18. ↑ Hoda SA, Rosen PP (2004). "Observations on the pathologic diagnosis of selected unusual lesions in needle core biopsies of breast". Breast J. 10 (6): 522–7. doi:10.1111/j.1075-122X.2004.21412.x. PMID 15569209.
  19. ↑ Ferrara A (2011). "Benign breast disease". Radiol Technol. 82 (5): 447M–62M. PMID 21572066.
  20. ↑ Rohan TE, Miller AB (1999). "Hormone replacement therapy and risk of benign proliferative epithelial disorders of the breast". Eur J Cancer Prev. 8 (2): 123–30. PMID 10335458.
  21. ↑ Rohan TE, Negassa A, Chlebowski RT, Lasser NL, McTiernan A, Schenken RS; et al. (2008). "Estrogen plus progestin and risk of benign proliferative breast disease". Cancer Epidemiol Biomarkers Prev. 17 (9): 2337–43. doi:10.1158/1055-9965.EPI-08-0380. PMC 2584343. PMID 18725513.
  22. ↑ Tan-Chiu E, Wang J, Costantino JP, Paik S, Butch C, Wickerham DL; et al. (2003). "Effects of tamoxifen on benign breast disease in women at high risk for breast cancer". J Natl Cancer Inst. 95 (4): 302–7. PMID 12591986.
  23. ↑ Fitzgibbons PL, Page DL, Weaver D, Thor AD, Allred DC, Clark GM; et al. (2000). "Prognostic factors in breast cancer. College of American Pathologists Consensus Statement 1999". Arch Pathol Lab Med. 124 (7): 966–78. doi:10.1043/0003-9985(2000)124<0966:PFIBC>2.0.CO;2. PMID 10888772.
  24. ↑ Allred DC, Harvey JM, Berardo M, Clark GM (1998). "Prognostic and predictive factors in breast cancer by immunohistochemical analysis". Mod Pathol. 11 (2): 155–68. PMID 9504686.
  25. ↑ Wolff AC, Hammond ME, Schwartz JN, Hagerty KL, Allred DC, Cote RJ; et al. (2007). "American Society of Clinical Oncology/College of American Pathologists guideline recommendations for human epidermal growth factor receptor 2 testing in breast cancer". J Clin Oncol. 25 (1): 118–45. doi:10.1200/JCO.2006.09.2775. PMID 17159189.
  26. ↑ Hicks DG, Kulkarni S (2008). "HER2+ breast cancer: review of biologic relevance and optimal use of diagnostic tools". Am J Clin Pathol. 129 (2): 263–73. doi:10.1309/99AE032R9FM8WND1. PMID 18208807.
  27. ↑ O'Connell P, Pekkel V, Fuqua SA, Osborne CK, Clark GM, Allred DC (1998). "Analysis of loss of heterozygosity in 399 premalignant breast lesions at 15 genetic loci". J Natl Cancer Inst. 90 (9): 697–703. PMID 9586667.
  28. ↑ Sharif S, Moran A, Huson SM, Iddenden R, Shenton A, Howard E; et al. (2007). "Women with neurofibromatosis 1 are at a moderately increased risk of developing breast cancer and should be considered for early screening". J Med Genet. 44 (8): 481–4. doi:10.1136/jmg.2007.049346. PMC 2597938. PMID 17369502.
  29. ↑ Seal S, Thompson D, Renwick A, Elliott A, Kelly P, Barfoot R; et al. (2006). "Truncating mutations in the Fanconi anemia J gene BRIP1 are low-penetrance breast cancer susceptibility alleles". Nat Genet. 38 (11): 1239–41. doi:10.1038/ng1902. PMID 17033622.
  30. ↑ Wong MW, Nordfors C, Mossman D, Pecenpetelovska G, Avery-Kiejda KA, Talseth-Palmer B; et al. (2011). "BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer". Breast Cancer Res Treat. 127 (3): 853–9. doi:10.1007/s10549-011-1443-0. PMID 21409391.
  31. ↑ Thompson D, Duedal S, Kirner J, McGuffog L, Last J, Reiman A; et al. (2005). "Cancer risks and mortality in heterozygous ATM mutation carriers". J Natl Cancer Inst. 97 (11): 813–22. doi:10.1093/jnci/dji141. PMID 15928302.
  32. ↑ Lalloo F, Evans DG (2012). "Familial breast cancer". Clin Genet. 82 (2): 105–14. doi:10.1111/j.1399-0004.2012.01859.x. PMID 22356477.
  33. ↑ Gashi-Luci LH, Limani RA, Kurshumliu FI (2009). "Invasive ductal carcinoma within fibroadenoma: a case report". Cases J. 2: 174. doi:10.1186/1757-1626-2-174. PMC 2783130. PMID 19946485.


Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Breast_lumps_pathophysiology&oldid=1635432"