Breast lumps pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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
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[1][2][3]
- Estrogen: Development of ductal tissue
- Progestrone:ductal branching and lobulo-alveolar development
- Prolactine:Milk protein production
- Estradiol and progestrone: breast development at puberty
- Estrogen and Progestron: cell proliferation during luteal phase
Histological changes of breast
Histological changes of breast undergo some changes throughout aging[4]
- 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
- 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 turn into ill-defined fullness areas called lumpy-bumpy consistency or firm areas which require biopsy
- No ductalchanges
- Late reproductive period[6]
- Hyperplastic glandular tissue with sclerosing adenosis or lobular hyperplasia
- Hyperplastic glandular lesions may require biopsy
- Hyperplastic ductal tissue
- Hyperplastic glandular tissue with sclerosing adenosis or lobular hyperplasia
Diagnostic subtypesand histologic subtypes [7]
Diagnostic subtypes:
- 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
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- 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].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- 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].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.