Breast lumps pathophysiology: Difference between revisions

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Latest revision as of 20:42, 29 July 2020

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

Mammary gland development, maturation, and differentiation is controlled by hormones through their action on epithelial and stromal cells:^[1]^[2]^[3]
- Estrogen: Development of ductal tissue
- Progesterone: Ductal branching and lobulo-alveolar development
- Prolactin: Milk protein production
- Estradiol and progesterone: Breast development at puberty
- Estrogen and progesterone: Cell proliferation during luteal phase

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

Specific changes during the period of times:
- Early reproductive ages^[5]
  - Stromal hyperplasia, unilateral or bilateral macromastia
- Middle reproductive ages^[6]
  - Substantial changes in glandular breast tissue result in adenosis
  - Stromal hyperplasia may result into ill-defined fullness areas called lumpy-bumpy consistency or firm areas which may require biopsy
  - No ductal changes
- Late reproductive period^[6]
  - Hyperplastic glandular tissue with sclerosing adenosis or lobular hyperplasia
    - Hyperplastic glandular lesions may require biopsy
  - Hyperplastic ductal tissue

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]	Consist of disposed compressed glands within collagenous stroma. Complex fibroadenomas: containing sclerosing adenosis, calcifications, papillary hyperplasia.
Phyllodes tumor^[17]	Prominent and hypercellular stromal feature expanded to epithelial of tumor. Classified to benign, borderline, and malignant on the basis of stromal mitotic rate, cytology and degree of stromal overgrowth.
Pseudoangiomatous Stromal Hyperplasia^[18]	Composed of dense collagen, slit like spaces resulting from fibroblast proliferation resembling blood vessels in the stroma between lobular units.
Sclerosing adenosis^[19]	Increase in lobular acini number, enriched in myoepithelial cells.

Pathogenesis

It is understood that breast lumps are the result of hormonal events:^[20]
- Prevalence of benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold.
- Estrogen and progesterone increase rate of benign proliferative breast disease to 74%.^[21]
- Anti-estrogen drugs such as tamoxifen, decrease prevalence of breast lesions such as adenosis, cysts, hyperplasia, duct ectasia to 28%.^[22]

Although estrogen receptors (ER) and progesterone-receptor (PR) attributed to weak prognosis, they may predict patients' response to endocrine therapy.^[23]
- Assessment of presence of ER and PR are required in invasive breast cancers.
- ER-positive result is present in 70% of breast cancers and PR-positive result is present in 60% of breast cancers.^[24]
HER2/neu is a proto-oncogene which involves in breast regulatory pathways such as proliferation, cell motility and invasion.^[25]^[26]
- In 10% to 34% of breast cancers, overexpression and amplification of HER2 is reported.
- In 90% of cases, overexpression, amplification, and surface membrane protein expressions of HER2/neu may be seen.

Genetics

Breast lumps is associated with deletion of small segments of DNA (loss of heterozigosity).^[27]
The development of breast lumps is the result of multiple genetic mutations such as:
- High risk genes mutations:^[28]
  - BRCA1
  - BRCA2
  - TP53 resulting in Li-Fraumeni syndrome
  - PTEN resulting in Cowden syndrome
  - STK11 resulting in Peutz-Jegher’s syndrome, Neurofibromatosis (NF1) and (CDH-1) E-Cadherin
- Moderate risk genes mutations:^[29]^[30]^[31]
  - Homozygous ataxia-telangiectasia (ATM)
  - Somatic mutations in CHEK2
  - BRIP1: BRCA1 modifier
  - PALB2: BRCA2 modifier
- Low risk genes mutations:^[32]
  - Clinical determination of these genes have not determined yet

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
Phyllodes tumor is a tumor of the intralobular breast stroma and it may be benign or malignant with large slit-like spaces. It is a type of fibroepithelial tumor.	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
ADH, based on a molecular basis, is a low-grade DCIS with localized proliferation.	Histopathologic image of atypical ductal hyperplasia Source: Nephron, from Wikimedia Commons

References

↑ 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.
↑ 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.
↑ 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/
↑ 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.
↑ Pearlman MD, Griffin JL (2010). "Benign breast disease". Obstet Gynecol. 116 (3): 747–58. doi:10.1097/AOG.0b013e3181ee9fc7. PMID 20733462.
↑ ^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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ Schnitt SJ, Vincent-Salomon A (2003). "Columnar cell lesions of the breast". Adv Anat Pathol. 10 (3): 113–24. PMID 12717115.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ Ferrara A (2011). "Benign breast disease". Radiol Technol. 82 (5): 447M–62M. PMID 21572066.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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

[pmid3337211-1] 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.

[pmid2890912-2] 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/

[LoveSue_Gelman1982-4] 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.

[pmid20733462-5] Pearlman MD, Griffin JL (2010). "Benign breast disease". Obstet Gynecol. 116 (3): 747–58. doi:10.1097/AOG.0b013e3181ee9fc7. PMID 20733462.

[pmid26941287-6] 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.

[pmid25636589-7] 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.

[pmid7560165-8] 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.

[pmid11474285-9] 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.

[pmid2986821-10] 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.

[pmid24639339-11] 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.

[pmid16720843-12] 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.

[pmid12717115-13] Schnitt SJ, Vincent-Salomon A (2003). "Columnar cell lesions of the breast". Adv Anat Pathol. 10 (3): 113–24. PMID 12717115.

[pmid18716096-14] 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.

[pmid22268202-15] 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.

[pmid16034008-16] 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.

[pmid19329316-17] 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.

[pmid15569209-18] 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.

[pmid21572066-19] Ferrara A (2011). "Benign breast disease". Radiol Technol. 82 (5): 447M–62M. PMID 21572066.

[pmid10335458-20] 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.

[pmid18725513-21] 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.

[pmid12591986-22] 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.

[pmid10888772-23] 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.

[pmid9504686-24] 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.

[pmid17159189-25] 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.

[pmid18208807-26] 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.

[pmid9586667-27] 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.

[pmid17369502-28] 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.

[pmid17033622-29] 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.

[pmid21409391-30] 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.

[pmid15928302-31] 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.

[pmid22356477-32] 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.

[pmid19946485-33] 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.

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@@ Line 1: / Line 1: @@
 __NOTOC__
+{{Breast lumps}}
+{{CMG}}; {{AE}} {{S.M}}
-{{CMG}}; {{AE}}
 ==Overview==
-The exact pathogenesis of [disease name] is not fully understood.
-OR
-It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
-OR
-[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
-OR
-Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
-OR
-[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
-OR
+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 [[Progesterone|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|ataxia-telangiectasia]], somatic mutation in [[CHEK2]], [[BRIP1]], [[PALB2]]  moderate risk mutations, and low risk genes mutation are not determined yet.
-The progression to [disease name] usually involves the [molecular pathway].
-OR
-The pathophysiology of [disease/malignancy] depends on the histological subtype.
 ==Pathophysiology==
 ===Physiology===
-* Mammary gland development, maturation and differentiation controlled by hormones through acting on epithelial and stromal cells<ref name="pmid3337211">{{cite journal| author=Going JJ, Anderson TJ, Battersby S, MacIntyre CC| title=Proliferative and secretory activity in human breast during natural and artificial menstrual cycles. | journal=Am J Pathol | year= 1988 | volume= 130 | issue= 1 | pages= 193-204 | pmid=3337211 | doi= | pmc=1880536 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3337211  }} </ref><ref name="pmid2890912">{{cite journal| author=Hughes LE, Mansel RE, Webster DJ| title=Aberrations of normal development and involution (ANDI): a new perspective on pathogenesis and nomenclature of benign breast disorders. | journal=Lancet | year= 1987 | volume= 2 | issue= 8571 | pages= 1316-9 | pmid=2890912 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2890912  }} </ref><ref>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/</ref>
+* Mammary gland development, maturation, and differentiation is controlled by [[hormones]] through their action on [[epithelial]] and [[stromal cells]]:<ref name="pmid3337211">{{cite journal| author=Going JJ, Anderson TJ, Battersby S, MacIntyre CC| title=Proliferative and secretory activity in human breast during natural and artificial menstrual cycles. | journal=Am J Pathol | year= 1988 | volume= 130 | issue= 1 | pages= 193-204 | pmid=3337211 | doi= | pmc=1880536 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3337211  }} </ref><ref name="pmid2890912">{{cite journal| author=Hughes LE, Mansel RE, Webster DJ| title=Aberrations of normal development and involution (ANDI): a new perspective on pathogenesis and nomenclature of benign breast disorders. | journal=Lancet | year= 1987 | volume= 2 | issue= 8571 | pages= 1316-9 | pmid=2890912 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2890912  }} </ref><ref>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/</ref>
-**Estrogen: Development of ductal tissue
+**[[Estrogen]]: Development of ductal tissue
-**Progestrone:ductal branching and lobulo-alveolar development
+**[[Progesterone]]: Ductal branching and lobulo-alveolar development
-**Prolactine:Milk protein production
+**[[Prolactin]]: Milk protein production
-**Estradiol and progestrone: breast development at puberty
+**[[Estradiol]] and [[progesterone]]: Breast development at [[puberty]]
-**Estrogen and Progestron: cell proliferation during luteal phase
+**[[Estrogen]] and [[progesterone]]: Cell proliferation during [[luteal phase]]
 ===Histological changes of breast===
-Histological changes of breast undergo some changes throughout aging<ref name="LoveSue Gelman1982">{{cite journal|last1=Love|first1=Susan M.|last2=Sue Gelman|first2=Rebecca|last3=silen|first3=William|title=Fibrocystic Disease of the Breast — A Nondisease?|journal=New England Journal of Medicine|volume=307|issue=16|year=1982|pages=1010–1014|issn=0028-4793|doi=10.1056/NEJM198210143071611}}</ref>
-*Fibrocystic disease
-**Histological apperance change from predominance of ducts, lobules to fibrous change and cyst formation
-**Fibrocystic changes donot associated with breast cancer
-Specific changes in period of times:
+Histological changes of breast undergo continuous changes throughout the life:<ref name="LoveSue Gelman1982">{{cite journal|last1=Love|first1=Susan M.|last2=Sue Gelman|first2=Rebecca|last3=silen|first3=William|title=Fibrocystic Disease of the Breast — A Nondisease?|journal=New England Journal of Medicine|volume=307|issue=16|year=1982|pages=1010–1014|issn=0028-4793|doi=10.1056/NEJM198210143071611}}</ref>
-*Early reproductive ages<ref name="pmid20733462">{{cite journal| author=Pearlman MD, Griffin JL| title=Benign breast disease. | journal=Obstet Gynecol | year= 2010 | volume= 116 | issue= 3 | pages= 747-58 | pmid=20733462 | doi=10.1097/AOG.0b013e3181ee9fc7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20733462  }} </ref>
+*'''Fibrocystic disease'''
-**Stromal hyperplasia, unilateral or bilateral macromastia
+**Histological apperance change from predominance of ducts, lobules to [[fibrous]] change, and [[cyst]] formation
-*Middle reproductive ages<ref name="pmid26941287">{{cite journal| author=Huh SJ, Oh H, Peterson MA, Almendro V, Hu R, Bowden M et al.| title=The Proliferative Activity of Mammary Epithelial Cells in Normal Tissue Predicts Breast Cancer Risk in Premenopausal Women. | journal=Cancer Res | year= 2016 | volume= 76 | issue= 7 | pages= 1926-34 | pmid=26941287 | doi=10.1158/0008-5472.CAN-15-1927 | pmc=4873436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26941287  }} </ref>
+**Fibrocystic changes are not associated with [[breast cancer]]
-**Substantial changes in glandular breast tissue result in adenosis
-**Stromal hyperplasia may turn into ill-defined fullness areas called lumpy-bumpy consistency or firm areas which require biopsy
-**No ductalchanges
-*Late reproductive period<ref name="pmid26941287" />
-**Hyperplastic glandular tissue with sclerosing adenosis or lobular hyperplasia
-***Hyperplastic glandular lesions may require biopsy
-**Hyperplastic ductal tissue
-Diagnostic subtypesand histologic subtypes <ref name="pmid25636589">{{cite journal| author=Dyrstad SW, Yan Y, Fowler AM, Colditz GA| title=Breast cancer risk associated with benign breast disease: systematic review and meta-analysis. | journal=Breast Cancer Res Treat | year= 2015 | volume= 149 | issue= 3 | pages= 569-75 | pmid=25636589 | doi=10.1007/s10549-014-3254-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25636589  }} </ref>
+* Specific changes during the period of times:
+**Early [[reproductive]] ages<ref name="pmid20733462">{{cite journal| author=Pearlman MD, Griffin JL| title=Benign breast disease. | journal=Obstet Gynecol | year= 2010 | volume= 116 | issue= 3 | pages= 747-58 | pmid=20733462 | doi=10.1097/AOG.0b013e3181ee9fc7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20733462  }} </ref>
+***[[Stromal]] [[hyperplasia]], unilateral or bilateral macromastia
+**Middle [[reproductive]] ages<ref name="pmid26941287">{{cite journal| author=Huh SJ, Oh H, Peterson MA, Almendro V, Hu R, Bowden M et al.| title=The Proliferative Activity of Mammary Epithelial Cells in Normal Tissue Predicts Breast Cancer Risk in Premenopausal Women. | journal=Cancer Res | year= 2016 | volume= 76 | issue= 7 | pages= 1926-34 | pmid=26941287 | doi=10.1158/0008-5472.CAN-15-1927 | pmc=4873436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26941287  }} </ref>
+***Substantial changes in glandular breast tissue result in adenosis
+***[[Stromal]] [[hyperplasia]] may result into ill-defined fullness areas called lumpy-bumpy consistency or firm areas which may require [[biopsy]]
+***No ductal changes
+**Late [[reproductive]] period<ref name="pmid26941287" />
+***[[Hyperplastic]] [[glandular]] tissue with sclerosing adenosis or [[lobular]] [[hyperplasia]]
+****[[Hyperplastic]] [[glandular]] lesions may require [[biopsy]]
+***Hyperplastic ductal tissue
-Diagnostic subtypes:
+* Diagnostic subtypes and histologic subtypes are described according to their [[relative risk]] for cancer as below:<ref name="pmid25636589">{{cite journal| author=Dyrstad SW, Yan Y, Fowler AM, Colditz GA| title=Breast cancer risk associated with benign breast disease: systematic review and meta-analysis. | journal=Breast Cancer Res Treat | year= 2015 | volume= 149 | issue= 3 | pages= 569-75 | pmid=25636589 | doi=10.1007/s10549-014-3254-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25636589  }} </ref>
-*Non-proliferative disease
-**Relative risk (RR)of breast cancer is 1.17
-*Proliferative disease without atypia
-**RR is 1.76
-*Benign breast disease
-**RR is 2.07
-*Atypical hyperplasia
-**RR is 3.93
-Histologic subtypes:
-*Adenosis
-**RR is 2.00
-*Atypical ductal hyperplasia
-**RR is 3.28
-*Atypical lobular hyperplassia
-** RR is 3.92
-*Cysts
-**RR is 1.55
-*Fibroadenoma
-**RR is 1.41
-*Papilloma
-**RR is 2.06
 {| class="wikitable"
 |+
-!Breast lumps
+Diagnostic Subtypes
-!Histological findings
+! style="background:#4479BA; color: #FFFFFF;" align="center" + | Diagnostic Subtypes
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Breast cancer relative risk
 |-
-|Atypical hyperplasia<ref name="pmid7560165">{{cite journal| author=Lakhani SR, Collins N, Stratton MR, Sloane JP| title=Atypical ductal hyperplasia of the breast: clonal proliferation with loss of heterozygosity on chromosomes 16q and 17p. | journal=J Clin Pathol | year= 1995 | volume= 48 | issue= 7 | pages= 611-5 | pmid=7560165 | doi= | pmc=502709 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7560165  }}</ref>
+| style="background:#DCDCDC;" align="center" + |Non-proliferative disease
-|Clonal neoplastic proliferations
+| style="background:#F5F5F5;" +|1.17
 |-
-|Atypical ductal hyperplasia (ADH)<ref name="pmid11474285">{{cite journal| author=Ely KA, Carter BA, Jensen RA, Simpson JF, Page DL| title=Core biopsy of the breast with atypical ductal hyperplasia: a probabilistic approach to reporting. | journal=Am J Surg Pathol | year= 2001 | volume= 25 | issue= 8 | pages= 1017-21 | pmid=11474285 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11474285  }}</ref>
+| style="background:#DCDCDC;" align="center" + |Proliferative disease without [[atypia]]
-|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.
+| style="background:#F5F5F5;" + |1.76
-Differentiation of ADH from DCIS : ADH has less cytological atypia in than DCIS. But in
+|-
+| style="background:#DCDCDC;" align="center" + |Benign breast disease
+| style="background:#F5F5F5;" + |2.07
+|-
+| style="background:#DCDCDC;" align="center" + |Atypical [[hyperplasia]]
+| style="background:#F5F5F5;" + |3.93
+|}
-severe ADH as compared to DCIS ,distribution is restricted to less than 3 contiguous ducts and its size is less than 0.2 cm.
+{| class="wikitable"
+|+
+Histologic Subtypes
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Histological subtypes
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Relative risk|Breast cancer relative risk
 |-
-|Lobular neoplasia<ref name="pmid2986821">{{cite journal| author=Page DL, Dupont WD, Rogers LW, Rados MS| title=Atypical hyperplastic lesions of the female breast. A long-term follow-up study. | journal=Cancer | year= 1985 | volume= 55 | issue= 11 | pages= 2698-708 | pmid=2986821 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2986821  }}</ref>
+| style="background:#DCDCDC;" align="center" + |Adenosis
-|Associated to decrease expression or missing expression of E-cadherine, LN is considered to be as incidental findings in biopsies for assessment of microcalcification
+| style="background:#F5F5F5;" + |2.00
 |-
-|Atypical lobular hyperplasi (ALH)<ref name="pmid24639339">{{cite journal| author=Middleton LP, Sneige N, Coyne R, Shen Y, Dong W, Dempsey P et al.| title=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. | journal=Cancer Med | year= 2014 | volume= 3 | issue= 3 | pages= 492-9 | pmid=24639339 | doi=10.1002/cam4.223 | pmc=4101740 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24639339  }}</ref>
+| style="background:#DCDCDC;" align="center" + |Atypical ductal [[hyperplasia]]
-|ALH is containing monomorphic cells and has tendency to distend lobular acini and spread into adjacent terminal ducts.
+| style="background:#F5F5F5;" + |3.28
-Differentiation between ALH and lobular carcinoma in situ (LCIS) associated with quantitative degrees about lobules and architecture feature.
 |-
-|Apocrine proliferative lesions<ref name="pmid16720843">{{cite journal| author=Guray M, Sahin AA| title=Benign breast diseases: classification, diagnosis, and management. | journal=Oncologist | year= 2006 | volume= 11 | issue= 5 | pages= 435-49 | pmid=16720843 | doi=10.1634/theoncologist.11-5-435 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16720843  }}</ref>
+| style="background:#DCDCDC;" align="center" + |Atypical [[lobular]] [[hyperplasia]]
-|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
+| style="background:#F5F5F5;" + |3.92
 |-
-|Columnar cell lesions (CCL)<ref name="pmid12717115">{{cite journal| author=Schnitt SJ, Vincent-Salomon A| title=Columnar cell lesions of the breast. | journal=Adv Anat Pathol | year= 2003 | volume= 10 | issue= 3 | pages= 113-24 | pmid=12717115 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12717115  }}</ref>
+| style="background:#DCDCDC;" align="center" + |[[Cysts]]
-|Ubiquitousand and heterogeneous set of lesions characterized by reduplication and microcystic change in lobular acini,elevated estrogen receptor expression, increased proliferative rate, associated with sclerosing adenosis, calcifications and  pleomorphic appearnace
+| style="background:#F5F5F5;" + |1.55
 |-
-|
+| style="background:#DCDCDC;" align="center" + |[[Fibroadenoma]]
-|
+| style="background:#F5F5F5;" + |1.41
+|-
+| style="background:#DCDCDC;" align="center" + |[[Papilloma]]
+| style="background:#F5F5F5;" + |2.06
+|}
+{| class="wikitable"
+|+
+Histological findings of breast lumps
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Breast lumps
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Histological findings
+|-
+| style="background:#DCDCDC;" align="center" + |Atypical [[hyperplasia]]<ref name="pmid7560165">{{cite journal| author=Lakhani SR, Collins N, Stratton MR, Sloane JP| title=Atypical ductal hyperplasia of the breast: clonal proliferation with loss of heterozygosity on chromosomes 16q and 17p. | journal=J Clin Pathol | year= 1995 | volume= 48 | issue= 7 | pages= 611-5 | pmid=7560165 | doi= | pmc=502709 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7560165  }}</ref>
+| style="background:#F5F5F5;" + |
+* Clonal neoplastic proliferations is present.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Atypical AVNRT|Atypical]] [[Ductal carcinoma|ductal]] [[hyperplasia]] (ADH)<ref name="pmid11474285">{{cite journal| author=Ely KA, Carter BA, Jensen RA, Simpson JF, Page DL| title=Core biopsy of the breast with atypical ductal hyperplasia: a probabilistic approach to reporting. | journal=Am J Surg Pathol | year= 2001 | volume= 25 | issue= 8 | pages= 1017-21 | pmid=11474285 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11474285  }}</ref>
+| style="background:#F5F5F5;" + |
+* 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.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Lobular]] [[neoplasia]]<ref name="pmid2986821">{{cite journal| author=Page DL, Dupont WD, Rogers LW, Rados MS| title=Atypical hyperplastic lesions of the female breast. A long-term follow-up study. | journal=Cancer | year= 1985 | volume= 55 | issue= 11 | pages= 2698-708 | pmid=2986821 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2986821  }}</ref>
+| style="background:#F5F5F5;" + |
+* Associated to decrease expression or missing expression of E-cadherine, [[lobular]] [[neoplasia]] is considered to be as incidental findings in during [[microcalcification]] evaluation.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Atypical AVNRT|Atypical]] [[lobular]] [[hyperplasia]] (ALH)<ref name="pmid24639339">{{cite journal| author=Middleton LP, Sneige N, Coyne R, Shen Y, Dong W, Dempsey P et al.| title=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. | journal=Cancer Med | year= 2014 | volume= 3 | issue= 3 | pages= 492-9 | pmid=24639339 | doi=10.1002/cam4.223 | pmc=4101740 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24639339  }}</ref>
+| style="background:#F5F5F5;" + |
+* 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.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Apocrine]] proliferative lesions<ref name="pmid16720843">{{cite journal| author=Guray M, Sahin AA| title=Benign breast diseases: classification, diagnosis, and management. | journal=Oncologist | year= 2006 | volume= 11 | issue= 5 | pages= 435-49 | pmid=16720843 | doi=10.1634/theoncologist.11-5-435 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16720843  }}</ref>
+| style="background:#F5F5F5;" + |
+* [[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.
+|-
+| style="background:#DCDCDC;" align="center" + |Columnar cell lesions (CCL)<ref name="pmid12717115">{{cite journal| author=Schnitt SJ, Vincent-Salomon A| title=Columnar cell lesions of the breast. | journal=Adv Anat Pathol | year= 2003 | volume= 10 | issue= 3 | pages= 113-24 | pmid=12717115 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12717115  }}</ref>
+| style="background:#F5F5F5;" + |
+* 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.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Papillary]] lesions<ref name="pmid18716096">{{cite journal| author=Muttarak M, Lerttumnongtum P, Chaiwun B, Peh WC| title=Spectrum of papillary lesions of the breast: clinical, imaging, and pathologic correlation. | journal=AJR Am J Roentgenol | year= 2008 | volume= 191 | issue= 3 | pages= 700-7 | pmid=18716096 | doi=10.2214/AJR.07.3483 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18716096  }}</ref>
+| style="background:#F5F5F5;" + |
+* Arborescent fibrovascular stalk lined to the myoepithelium are present.
+|-
+| style="background:#DCDCDC;" align="center" + |Radical scars and complex sclerosing lesions<ref name="pmid22268202">{{cite journal| author=Krishnamurthy S, Bevers T, Kuerer H, Yang WT| title=Multidisciplinary considerations in the management of high-risk breast lesions. | journal=AJR Am J Roentgenol | year= 2012 | volume= 198 | issue= 2 | pages= W132-40 | pmid=22268202 | doi=10.2214/AJR.11.7799 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22268202  }}</ref>
+| style="background:#F5F5F5;" + |
+* 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.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Fibroadenoma]]<ref name="pmid16034008">{{cite journal| author=Hartmann LC, Sellers TA, Frost MH, Lingle WL, Degnim AC, Ghosh K et al.| title=Benign breast disease and the risk of breast cancer. | journal=N Engl J Med | year= 2005 | volume= 353 | issue= 3 | pages= 229-37 | pmid=16034008 | doi=10.1056/NEJMoa044383 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16034008  }}</ref>
+| style="background:#F5F5F5;" + |
+* Consist of  disposed compressed glands within collagenous stroma.
+* Complex [[Fibroadenoma|fibroadenomas]]: containing [[sclerosing  adenosis]], calcifications, [[papillary]] [[hyperplasia]].
+|-
+| style="background:#DCDCDC;" align="center" + |[[Phyllodes tumor]]<ref name="pmid19329316">{{cite journal| author=Karim RZ, Gerega SK, Yang YH, Spillane A, Carmalt H, Scolyer RA et al.| title=Phyllodes tumours of the breast: a clinicopathological analysis of 65 cases from a single institution. | journal=Breast | year= 2009 | volume= 18 | issue= 3 | pages= 165-70 | pmid=19329316 | doi=10.1016/j.breast.2009.03.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19329316  }}</ref>
+| style="background:#F5F5F5;" + |
+* Prominent and hypercellular [[stromal]] feature expanded to [[epithelial]] of tumor.
+* Classified to [[benign]], borderline, and [[malignant]] on the basis of [[stromal]] [[mitotic]] rate, [[cytology]] and degree of [[stromal]] overgrowth.
+|-
+| style="background:#DCDCDC;" align="center" + |Pseudoangiomatous [[Stromal]] [[Hyperplasia]]<ref name="pmid15569209">{{cite journal| author=Hoda SA, Rosen PP| title=Observations on the pathologic diagnosis of selected unusual lesions in needle core biopsies of breast. | journal=Breast J | year= 2004 | volume= 10 | issue= 6 | pages= 522-7 | pmid=15569209 | doi=10.1111/j.1075-122X.2004.21412.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15569209  }}</ref>
+| style="background:#F5F5F5;" + |
+* Composed of dense [[collagen]], slit like spaces resulting from [[fibroblast]] proliferation resembling blood vessels in the [[stroma]] between [[lobular]] units.
+|-
+| style="background:#DCDCDC;" align="center" + |[[Sclerosing adenosis]]<ref name="pmid21572066">{{cite journal| author=Ferrara A| title=Benign breast disease. | journal=Radiol Technol | year= 2011 | volume= 82 | issue= 5 | pages= 447M-62M | pmid=21572066 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21572066  }}</ref>
+| style="background:#F5F5F5;" + |
+* Increase in [[lobular]] acini number, enriched in [[myoepithelial cells]].
 |}
 ===Pathogenesis===
-*The exact pathogenesis of [disease name] is not completely understood.
+*It is understood that [[breast lumps]] are the result of [[hormonal]] events:<ref name="pmid10335458">{{cite journal| author=Rohan TE, Miller AB| title=Hormone replacement therapy and risk of benign proliferative epithelial disorders of the breast. | journal=Eur J Cancer Prev | year= 1999 | volume= 8 | issue= 2 | pages= 123-30 | pmid=10335458 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10335458  }}</ref>
-OR
+**Prevalence of benign breast lesion in post-menopausal women receiving [[estrogen]] with or without [[Progesterone|progesteron]] for more than 8 years raise by 1.7 fold.
-*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
+** [[Estrogen]] and  [[progesterone]] increase rate of benign proliferative breast disease to 74%.<ref name="pmid18725513">{{cite journal| author=Rohan TE, Negassa A, Chlebowski RT, Lasser NL, McTiernan A, Schenken RS et al.| title=Estrogen plus progestin and risk of benign proliferative breast disease. | journal=Cancer Epidemiol Biomarkers Prev | year= 2008 | volume= 17 | issue= 9 | pages= 2337-43 | pmid=18725513 | doi=10.1158/1055-9965.EPI-08-0380 | pmc=2584343 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18725513  }} </ref>
-*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
+**Anti-[[estrogen]] drugs such as [[tamoxifen]], decrease prevalence of breast lesions such as adenosis, [[cysts]], [[hyperplasia]], [[duct ectasia]] to 28%.<ref name="pmid12591986">{{cite journal| author=Tan-Chiu E, Wang J, Costantino JP, Paik S, Butch C, Wickerham DL et al.| title=Effects of tamoxifen on benign breast disease in women at high risk for breast cancer. | journal=J Natl Cancer Inst | year= 2003 | volume= 95 | issue= 4 | pages= 302-7 | pmid=12591986 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12591986  }} </ref>
-*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
-*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
+* Although [[estrogen receptors]] (ER) and [[Progesterone receptor|progesterone-receptor]] (PR) attributed to weak prognosis, they may predict patients' response to endocrine therapy.<ref name="pmid10888772">{{cite journal| author=Fitzgibbons PL, Page DL, Weaver D, Thor AD, Allred DC, Clark GM et al.| title=Prognostic factors in breast cancer. College of American Pathologists Consensus Statement 1999. | journal=Arch Pathol Lab Med | year= 2000 | volume= 124 | issue= 7 | pages= 966-78 | pmid=10888772 | doi=10.1043/0003-9985(2000)124<0966:PFIBC>2.0.CO;2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10888772  }}</ref>
-*The progression to [disease name] usually involves the [molecular pathway].
+**Assessment of presence of ER and PR are required in invasive [[breast cancers]].
-*The pathophysiology of [disease/malignancy] depends on the histological subtype.
+** ER-positive result is present in 70% of [[Breast cancer|breast cancers]] and PR-positive result is present in 60% of [[breast cancers]].<ref name="pmid9504686">{{cite journal| author=Allred DC, Harvey JM, Berardo M, Clark GM| title=Prognostic and predictive factors in breast cancer by immunohistochemical analysis. | journal=Mod Pathol | year= 1998 | volume= 11 | issue= 2 | pages= 155-68 | pmid=9504686 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9504686  }} </ref>
+*[[HER2/neu]] is a [[proto-oncogene]] which involves in breast regulatory pathways such as [[proliferation]], [[cell]] [[motility]] and [[invasion]].<ref name="pmid17159189">{{cite journal| author=Wolff AC, Hammond ME, Schwartz JN, Hagerty KL, Allred DC, Cote RJ et al.| title=American Society of Clinical Oncology/College of American Pathologists guideline recommendations for human epidermal growth factor receptor 2 testing in breast cancer. | journal=J Clin Oncol | year= 2007 | volume= 25 | issue= 1 | pages= 118-45 | pmid=17159189 | doi=10.1200/JCO.2006.09.2775 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17159189  }} </ref><ref name="pmid18208807">{{cite journal| author=Hicks DG, Kulkarni S| title=HER2+ breast cancer: review of biologic relevance and optimal use of diagnostic tools. | journal=Am J Clin Pathol | year= 2008 | volume= 129 | issue= 2 | pages= 263-73 | pmid=18208807 | doi=10.1309/99AE032R9FM8WND1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18208807  }}</ref>
+**In 10% to 34% of [[Breast cancer|breast cancers]], [[overexpression]] and [[amplification]] of [[HER2/neu|HER2]] is reported.
+**In 90% of cases, [[overexpression]], [[amplification]], and surface membrane protein expressions of [[HER2/neu]] may be seen.
 ==Genetics==
-[Disease name] is transmitted in [mode of genetic transmission] pattern.
+* [[Breast lumps]] is associated with deletion of small segments of [[DNA]] (loss of heterozigosity).<ref name="pmid9586667">{{cite journal| author=O'Connell P, Pekkel V, Fuqua SA, Osborne CK, Clark GM, Allred DC| title=Analysis of loss of heterozygosity in 399 premalignant breast lesions at 15 genetic loci. | journal=J Natl Cancer Inst | year= 1998 | volume= 90 | issue= 9 | pages= 697-703 | pmid=9586667 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9586667  }} </ref>
+* The development of breast lumps is the result of multiple genetic mutations such as:
+**High risk genes mutations:<ref name="pmid17369502">{{cite journal| author=Sharif S, Moran A, Huson SM, Iddenden R, Shenton A, Howard E et al.| title=Women with neurofibromatosis 1 are at a moderately increased risk of developing breast cancer and should be considered for early screening. | journal=J Med Genet | year= 2007 | volume= 44 | issue= 8 | pages= 481-4 | pmid=17369502 | doi=10.1136/jmg.2007.049346 | pmc=2597938 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17369502  }} </ref>
+***[[BRCA1]]
+***[[BRCA2]]
+***[[TP53]] resulting in [[Li-Fraumeni syndrome]]
+***[[PTEN]] resulting in [[Cowden syndrome]]
+***[[STK11]] resulting in Peutz-Jegher’s syndrome, [[Neurofibromatosis 1|Neurofibromatosis]] (NF1) and (CDH-1) E-Cadherin
+**Moderate risk genes mutations:<ref name="pmid17033622">{{cite journal| author=Seal S, Thompson D, Renwick A, Elliott A, Kelly P, Barfoot R et al.| title=Truncating mutations in the Fanconi anemia J gene BRIP1 are low-penetrance breast cancer susceptibility alleles. | journal=Nat Genet | year= 2006 | volume= 38 | issue= 11 | pages= 1239-41 | pmid=17033622 | doi=10.1038/ng1902 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17033622  }} </ref><ref name="pmid21409391">{{cite journal| author=Wong MW, Nordfors C, Mossman D, Pecenpetelovska G, Avery-Kiejda KA, Talseth-Palmer B et al.| title=BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer. | journal=Breast Cancer Res Treat | year= 2011 | volume= 127 | issue= 3 | pages= 853-9 | pmid=21409391 | doi=10.1007/s10549-011-1443-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21409391  }} </ref><ref name="pmid15928302">{{cite journal| author=Thompson D, Duedal S, Kirner J, McGuffog L, Last J, Reiman A et al.| title=Cancer risks and mortality in heterozygous ATM mutation carriers. | journal=J Natl Cancer Inst | year= 2005 | volume= 97 | issue= 11 | pages= 813-22 | pmid=15928302 | doi=10.1093/jnci/dji141 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15928302  }} </ref>
+***[[Homozygous]] [[Ataxia telangiectasia|ataxia-telangiectasia]] (ATM)
+***Somatic mutations in [[CHEK2]]
+***[[BRIP1]]: [[BRCA1]] modifier
+***[[PALB2]]: [[BRCA2]] modifier
+**Low risk genes mutations:<ref name="pmid22356477">{{cite journal| author=Lalloo F, Evans DG| title=Familial breast cancer. | journal=Clin Genet | year= 2012 | volume= 82 | issue= 2 | pages= 105-14 | pmid=22356477 | doi=10.1111/j.1399-0004.2012.01859.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22356477  }} </ref>
+***Clinical determination of these genes have not determined yet
-OR
+== Associated Conditions ==
+*There are no other associated conditions with breast lumps.
-Genes involved in the pathogenesis of [disease name] include:
+== Gross pathology ==
-*[Gene1]
+{| class="wikitable"
-*[Gene2]
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Gross findings
-*[Gene3]
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Gross pathology
+|-
+|style="background:#DCDCDC;" align="left" + |
+* Fibrotic capsule and infiltrated the surrounding tissue<ref name="pmid19946485">{{cite journal| author=Gashi-Luci LH, Limani RA, Kurshumliu FI| title=Invasive ductal carcinoma within fibroadenoma: a case report. | journal=Cases J | year= 2009 | volume= 2 | issue=  | pages= 174 | pmid=19946485 | doi=10.1186/1757-1626-2-174 | pmc=2783130 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19946485  }} </ref>
+* Gray-white color and moderately increased consistency
+|style="background:#F5F5F5;" + |[[File:FibroAdenoma of the breast.JPG|thumb|none|300px|Gross feature of fibroadenoma [https://commons.wikimedia.org/wiki/File:FibroAdenoma_of_the_breast.JPG Source: Netha Hussain , from Wikimedia Commons]]]
+|-
+|style="background:#DCDCDC;" align="left" + |
+* Stellate area of cancer 2cm in diameter
+* Felt as a hard mobile mass
+* Histology as a moderately well differentiated duct carcinoma
+|style="background:#F5F5F5;" + |[[File:800px-Breast cancer.JPG|thumb|none|300px| Gross image of breast cancer [https://commons.wikimedia.org/wiki/File:Breast_cancer.JPG Source: John Hayman , from Wikimedia Commons]]]
+|}
-OR
+== Microscopic Pathology ==
+{| class="wikitable"
-The development of [disease name] is the result of multiple genetic mutations such as:
+|+
+!style="background:#4479BA; color: #FFFFFF;" align="center" + | Pathologic findings
-*[Mutation 1]
+!style="background:#4479BA; color: #FFFFFF;" align="center" + |Microscopic image
-*[Mutation 2]
+|-
-*[Mutation 3]
+|style="background:#DCDCDC;" align="left" + |
+* [[Phyllodes tumor]] is a tumor of the intralobular breast [[stroma]]<br>and it may be benign or malignant with large slit-like spaces.<br>It is a type of [[fibroepithelial tumor]].
-==Associated Conditions==
+|style="background:#F5F5F5;" + |[[File:800px-Phyllodes tumour - very low mag.jpg|thumb|none|300px|Histopathologic image of Phyllodes tumor [https://commons.wikimedia.org/wiki/File:Phyllodes_tumour_-_very_low_mag.jpg Source: Nephron, from Wikimedia Commons]]]
-Conditions associated with [disease name] include:
+|-
+|style="background:#DCDCDC;" align="left" + |
-*[Condition 1]
+* Sclerosing adenosis microscopic pathology has increased numbers of small<br>breast acini with collapsed lumens, [[fibrosis]] surrounds the acini,<br>considered as benign lesion with increased risk of [[breast cancer]].
-*[Condition 2]
+|style="background:#F5F5F5;" + |[[File:Microscopic feature of Sclerosing adenosis.jpg|thumb|none|300px|Histopathologic image of sclerosing adenosis [https://commons.wikimedia.org/wiki/File:Sclerosing_adenosis_--_intermed_mag.jpg Source: Nephron, from Wikimedia Commons]]]
-*[Condition 3]
+|-
+|style="background:#DCDCDC;" align="left" + |
-==Gross Pathology==
+* [[ADH]], based on a molecular basis, is a low-grade [[DCIS]] with localized<br>[[proliferation]].
-On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
+|style="background:#F5F5F5;" + |[[File:Atypical ductal hyperplasia.jpg|thumb|none|300px|Histopathologic image of atypical ductal hyperplasia [https://commons.wikimedia.org/wiki/File:Atypical_ductal_hyperplasia_-_high_mag.jpg Source: Nephron, from Wikimedia Commons]]]
+|}
-==Microscopic Pathology==
-On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 ==References==
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