Breast lumps pathophysiology: Difference between revisions

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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>
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>
*'''Fibrocystic disease'''
*'''Fibrocystic disease'''
**Histological apperance change from predominance of ducts, lobules to [[fibrous]] change and [[cyst]] formation
**Histological apperance change from predominance of ducts, lobules to [[fibrous]] change, and [[cyst]] formation
**Fibrocystic changes are not associated with [[breast cancer]]
**Fibrocystic changes are not associated with [[breast cancer]]


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|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>
|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>
|Clonal neoplastic proliferations
|
* Clonal neoplastic proliferations is present.
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|-
|[[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>
|[[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>
|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.
* 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.
* Distribution in severe ADH is restricted to less than 3 contiguous ducts and less than 0.2 cm in size.
|-
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|[[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>
|[[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>
|Associated to decrease expression or missing expression of E-cadherine, [[lobular]] [[neoplasia]] is considered to be as incidental findings in during [[microcalcification]] evaluation.
|
* Associated to decrease expression or missing expression of E-cadherine, [[lobular]] [[neoplasia]] is considered to be as incidental findings in during [[microcalcification]] evaluation.
|-
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|[[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>
|[[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>
|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.
* 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.
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|[[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>
|[[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>
|[[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
|
* [[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.
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|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>
|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>
|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
|
* 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.
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|[[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>
|[[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>
|Arborescent fibrovascular stalk lined to the myoepithelium
|
* Arborescent fibrovascular stalk lined to the myoepithelium are present.
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|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>
|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>
|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
|
* 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.
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|[[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>
|[[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>
|Consist of  disposed compressed glands within collagenous stroma.  
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Complex [[Fibroadenoma|fibroadenomas]]: containing [[sclerosing  adenosis]], calcifications, [[papillary]] [[hyperplasia]]
* Consist of  disposed compressed glands within collagenous stroma.
* Complex [[Fibroadenoma|fibroadenomas]]: containing [[sclerosing  adenosis]], calcifications, [[papillary]] [[hyperplasia]].
|-
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|[[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>
|[[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>
|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.
|
* 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.
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|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>
|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>
|Composed of dense [[collagen]], slit like spaces resulting from [[fibroblast]] proliferation resembling
|
blood vessels in the [[stroma]] between [[lobular]] units
* Composed of dense [[collagen]], slit like spaces resulting from [[fibroblast]] proliferation resembling blood vessels in the [[stroma]] between [[lobular]] units.
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|[[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>
|[[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>
|Increase in [[lobular]] acini number, enriched in [[myoepithelial cells]]
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* Increase in [[lobular]] acini number, enriched in [[myoepithelial cells]].
|}
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===Pathogenesis===
===Pathogenesis===
*It is understood that [[breast lumps]] is 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>
*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>
**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.
**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.
** [[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>
** [[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>
**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>
**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>


==Genetics==
==Genetics==
[[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>
* [[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
 
== Associated Conditions ==


The development of breast lumps is the result of multiple genetic mutations such as:
== Gross pathology ==
*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


== Microscopic Pathology ==


==References==
==References==

Revision as of 20:29, 2 January 2019

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

Overview

It is thought that breast lumps is the result of hormonal events and genetic mutations. The pathophysiology of breast lumps depends on the histological subtypes.

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
  • Specific changes during the period of times:
  • 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 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

  • Breast lumps is associated with deletion of small segments of DNA (loss of heterozigosity).[23]
  • The development of breast lumps is the result of multiple genetic mutations such as:

Associated Conditions

Gross pathology

Microscopic Pathology

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. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ 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.

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