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breast carcinoma

MedGen UID:
146260
Concept ID:
C0678222
Neoplastic Process
Synonym: Breast carcinoma
SNOMED CT: CA - Carcinoma of breast (254838004); Carcinoma of breast (254838004)
Modes of inheritance:
heterogeneous
MedGen UID:
67020
Concept ID:
C0242960
Organism Attribute
Source: HPO
The presence of apparently similar characters for which the genetic evidence indicates that different genes or different genetic mechanisms are involved in different pedigrees. In clinical settings genetic heterogeneity refers to the presence of a variety of genetic defects which cause the same disease, often due to mutations at different loci on the same gene, a finding common to many human diseases including ALZHEIMER DISEASE; CYSTIC FIBROSIS; LIPOPROTEIN LIPASE DEFICIENCY, FAMILIAL; and POLYCYSTIC KIDNEY DISEASES. (Rieger, et al., Glossary of Genetics: Classical and Molecular, 5th ed; Segen, Dictionary of Modern Medicine, 1992)
autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
somatic mutation
MedGen UID:
107465
Concept ID:
C0544886
Cell or Molecular Dysfunction
Sources: HPO, OMIM
A mode of inheritance in which a trait or disorder results from a de novo mutation occurring after conception, rather than being inherited from a preceding generation.
somatic mutation (HPO, OMIM)
 
HPO: HP:0003002

Definition

A carcinoma arising from the breast, most commonly the terminal ductal-lobular unit. It is the most common malignant tumor in females. Risk factors include country of birth, family history, menstrual and reproductive history, fibrocystic disease and epithelial hyperplasia, exogenous estrogens, contraceptive agents, and ionizing radiation. The vast majority of breast carcinomas are adenocarcinomas (ductal or lobular). Breast carcinoma spreads by direct invasion, by the lymphatic route, and by the blood vessel route. The most common site of lymph node involvement is the axilla. [from NCI]

Clinical features

From HPO
breast carcinoma
MedGen UID:
146260
Concept ID:
C0678222
Neoplastic Process
A carcinoma arising from the breast, most commonly the terminal ductal-lobular unit. It is the most common malignant tumor in females. Risk factors include country of birth, family history, menstrual and reproductive history, fibrocystic disease and epithelial hyperplasia, exogenous estrogens, contraceptive agents, and ionizing radiation. The vast majority of breast carcinomas are adenocarcinomas (ductal or lobular). Breast carcinoma spreads by direct invasion, by the lymphatic route, and by the blood vessel route. The most common site of lymph node involvement is the axilla.
breast carcinoma
MedGen UID:
146260
Concept ID:
C0678222
Neoplastic Process
A carcinoma arising from the breast, most commonly the terminal ductal-lobular unit. It is the most common malignant tumor in females. Risk factors include country of birth, family history, menstrual and reproductive history, fibrocystic disease and epithelial hyperplasia, exogenous estrogens, contraceptive agents, and ionizing radiation. The vast majority of breast carcinomas are adenocarcinomas (ductal or lobular). Breast carcinoma spreads by direct invasion, by the lymphatic route, and by the blood vessel route. The most common site of lymph node involvement is the axilla.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVbreast carcinoma

Conditions with this feature

cowden syndrome
MedGen UID:
5420
Concept ID:
C0018553
Neoplastic Process
Cowden syndrome-1 is a hamartomatous disorder characterized by macrocephaly, facial trichilemmomas, acral keratoses, papillomatous papules, and an increased risk for the development of breast, thyroid, and endometrial carcinoma. Bannayan-Riley-Ruvalcaba syndrome (BRRS), previously thought be distinct, shared clinical characteristics with Cowden syndrome, such as hamartomatous polyps of the gastrointestinal tract, mucocutaneous lesions, and increased risk of developing neoplasms, but had the additional features of developmental delay, macrocephaly, lipomas, hemangiomas, and pigmented speckled macules of the glans penis in males. Because features of BRRS and Cowden syndrome have been found in individuals within the same family with the same PTEN mutation, Cowden syndrome-1 and BRRS are considered to be the same disorder with variable expression and age-related penetrance (summary by Marsh et al., 1999, Lachlan et al., 2007, and Blumenthal and Dennis, 2008). Approximately 80% of patients reported with Cowden syndrome and 60% with BRSS have PTEN mutations (Blumenthal and Dennis, 2008). Some patients with Cowden syndrome may have immune system defects resulting in increased susceptibility to infections (summary by Browning et al., 2015).
peutz-jeghers syndrome
MedGen UID:
18404
Concept ID:
C0031269
Disease or Syndrome
Peutz-Jeghers syndrome (PJS) is an autosomal dominant condition characterized by the association of gastrointestinal polyposis, mucocutaneous pigmentation, and cancer predisposition. Peutz-Jeghers-type hamartomatous polyps are most common in the small intestine (in order of prevalence: in the jejunum, ileum, and duodenum) but can also occur in the stomach, large bowel, and extraintestinal sites including the renal pelvis, bronchus, gall bladder, nasal passages, urinary bladder, and ureters. Gastrointestinal polyps can result in chronic bleeding and anemia and also cause recurrent obstruction and intussusception requiring repeated laparotomy and bowel resection. Mucocutaneous hyperpigmentation presents in childhood as dark blue to dark brown macules around the mouth, eyes, and nostrils, in the perianal area, and on the buccal mucosa. Hyperpigmented macules on the fingers are common. The macules may fade in puberty and adulthood. Individuals with Peutz-Jeghers syndrome are at increased risk for a wide variety of epithelial malignancies (colorectal, gastric, pancreatic, breast, and ovarian cancers). Females are at risk for sex cord tumors with annular tubules (SCTAT), a benign neoplasm of the ovaries, and adenoma malignum of the cervix, a rare aggressive cancer. Males occasionally develop large calcifying Sertoli cell tumors (LCST) of the testes, which secrete estrogen and can lead to gynecomastia, advanced skeletal age, and ultimately short stature, if untreated.
saethre-chotzen syndrome
MedGen UID:
64221
Concept ID:
C0175699
Disease or Syndrome
Classic Saethre-Chotzen syndrome (SCS) is characterized by coronal synostosis (unilateral or bilateral), facial asymmetry (particularly in individuals with unicoronal synostosis), strabismus, ptosis, and characteristic appearance of the ear (small pinna with a prominent superior and/or inferior crus). Syndactyly of digits two and three of the hand is variably present. Cognitive development is usually normal, although those with a large genomic deletion are at an increased risk for intellectual challenges. Less common manifestations of SCS include other skeletal findings (parietal foramina, vertebral segmentation defects, radioulnar synostosis, maxillary hypoplasia, ocular hypertelorism, hallux valgus, duplicated or curved distal hallux), hypertelorism, palatal anomalies, obstructive sleep apnea, increased intracranial pressure, short stature, and congenital heart malformations.
familial cancer of breast
MedGen UID:
87542
Concept ID:
C0346153
Neoplastic Process
BRCA1- and BRCA2-associated hereditary breast and ovarian cancer syndrome (HBOC) is characterized by an increased risk for female and male breast cancer, ovarian cancer (includes fallopian tube and primary peritoneal cancers), and to a lesser extent other cancers such as prostate cancer, pancreatic cancer, and melanoma primarily in individuals with a BRCA2 pathogenic variant. The exact cancer risks differ slightly depending on whether HBOC is caused by a BRCA1 or BRCA2 pathogenic variant.
lhermitte-duclos disease
MedGen UID:
140251
Concept ID:
C0391826
Neoplastic Process
A very rare disorder characterized by abnormal development and enlargement of the cerebellum, and an increased intracranial pressure.
breast carcinoma
MedGen UID:
146260
Concept ID:
C0678222
Neoplastic Process
A carcinoma arising from the breast, most commonly the terminal ductal-lobular unit. It is the most common malignant tumor in females. Risk factors include country of birth, family history, menstrual and reproductive history, fibrocystic disease and epithelial hyperplasia, exogenous estrogens, contraceptive agents, and ionizing radiation. The vast majority of breast carcinomas are adenocarcinomas (ductal or lobular). Breast carcinoma spreads by direct invasion, by the lymphatic route, and by the blood vessel route. The most common site of lymph node involvement is the axilla.
neoplasm of ovary
MedGen UID:
181539
Concept ID:
C0919267
Neoplastic Process
Ovarian cancer, the leading cause of death from gynecologic malignancy, is characterized by advanced presentation with loco-regional dissemination in the peritoneal cavity and the rare incidence of visceral metastases (Chi et al., 2001). These typical features relate to the biology of the disease, which is a principal determinant of outcome (Auersperg et al., 2001). Epithelial ovarian cancer is the most common form and encompasses 5 major histologic subtypes: papillary serous, endometrioid, mucinous, clear cell, and transitional cell. Epithelial ovarian cancer arises as a result of genetic alterations sustained by the ovarian surface epithelium (Stany et al., 2008; Soslow, 2008).
muir-torré syndrome
MedGen UID:
231157
Concept ID:
C1321489
Neoplastic Process
Lynch syndrome is characterized by an increased risk for colorectal cancer (CRC) and cancers of the endometrium, ovary, stomach, small bowel, urinary tract, biliary tract, brain (usually glioblastoma), skin (sebaceous adenomas, sebaceous carcinomas, and keratoacanthomas), pancreas, and prostate. Cancer risks and age of onset vary depending on the associated gene. Several other cancer types have been reported to occur in individuals with Lynch syndrome (e.g., breast, sarcomas, adrenocortical carcinoma). However, the data are not sufficient to demonstrate that the risk of developing these cancers is increased in individuals with Lynch syndrome.
cerebelloparenchymal disorder vi
MedGen UID:
331813
Concept ID:
C1834711
Disease or Syndrome
cerebellar granule cell hypertrophy and megalencephaly
MedGen UID:
371886
Concept ID:
C1834712
Disease or Syndrome
li-fraumeni syndrome 1
MedGen UID:
322656
Concept ID:
C1835398
Disease or Syndrome
Li-Fraumeni syndrome (LFS) is a cancer predisposition syndrome associated with high risks for a diverse spectrum of childhood- and adult-onset malignancies. The lifetime risk of cancer in individuals with LFS is =70% for men and =90% for women. Five cancer types account for the majority of LFS tumors: adrenocortical carcinomas, breast cancer, central nervous system tumors, osteosarcomas, and soft-tissue sarcomas. LFS is associated with an increased risk of several additional cancers including leukemia, lymphoma, gastrointestinal cancers, cancers of head and neck, kidney, larynx, lung, skin (e.g., melanoma), ovary, pancreas, prostate, testis, and thyroid. Individuals with LFS are at increased risk for cancer in childhood and young adulthood; survivors are at increased risk for multiple primary cancers.
li-fraumeni syndrome 2
MedGen UID:
322930
Concept ID:
C1836482
Disease or Syndrome
Li-Fraumeni syndrome is a rare disorder that greatly increases the risk of developing several types of cancer, particularly in children and young adults.\n\nA very similar condition called Li-Fraumeni-like syndrome shares many of the features of classic Li-Fraumeni syndrome. Both conditions significantly increase the chances of developing multiple cancers beginning in childhood; however, the pattern of specific cancers seen in affected family members is different.\n\nThe cancers most often associated with Li-Fraumeni syndrome include breast cancer, a form of bone cancer called osteosarcoma, and cancers of soft tissues (such as muscle) called soft tissue sarcomas. Other cancers commonly seen in this syndrome include brain tumors, cancers of blood-forming tissues (leukemias), and a cancer called adrenocortical carcinoma that affects the outer layer of the adrenal glands (small hormone-producing glands on top of each kidney). Several other types of cancer also occur more frequently in people with Li-Fraumeni syndrome.
pten hamartoma tumor syndrome with granular cell tumor
MedGen UID:
400984
Concept ID:
C1866376
Neoplastic Process
proteus-like syndrome
MedGen UID:
356222
Concept ID:
C1866398
Disease or Syndrome
Proteus like syndrome describes patients who do not meet the diagnostic criteria for Proteus syndrome but who share a multitude of characteristic clinical features of the disease. The prevalence is unknown. The main clinical features include skeletal overgrowth, hamartomatous overgrowth of multiple tissues, cerebriform connective tissue nevi, vascular malformations and linear epidermal nevi. Mutations in the PTEN gene are found in 50% of Proteus-like syndrome cases, making them a part of the PTEN hamartoma syndrome group.
pten hamartoma tumor syndrome
MedGen UID:
368366
Concept ID:
C1959582
Neoplastic Process
The PTEN hamartoma tumor syndrome (PHTS) includes Cowden syndrome (CS), Bannayan-Riley-Ruvalcaba syndrome (BRRS), PTEN-related Proteus syndrome (PS), and PTEN-related Proteus-like syndrome. CS is a multiple hamartoma syndrome with a high risk for benign and malignant tumors of the thyroid, breast, kidney, and endometrium. Affected individuals usually have macrocephaly, trichilemmomas, and papillomatous papules, and present by the late 20s. The lifetime risk of developing breast cancer is 85%, with an average age of diagnosis between 38 and 46 years. The lifetime risk for thyroid cancer (usually follicular, rarely papillary, but never medullary thyroid cancer) is approximately 35%. The lifetime risk for renal cell cancer (predominantly of papillary histology) is 34%. The risk for endometrial cancer may approach 28%. BRRS is a congenital disorder characterized by macrocephaly, intestinal hamartomatous polyposis, lipomas, and pigmented macules of the glans penis. PS is a complex, highly variable disorder involving congenital malformations and hamartomatous overgrowth of multiple tissues, as well as connective tissue nevi, epidermal nevi, and hyperostoses. Proteus-like syndrome is undefined but refers to individuals with significant clinical features of PS who do not meet the diagnostic criteria for PS.
breast-ovarian cancer, familial 2
MedGen UID:
382625
Concept ID:
C2675520
Finding
BRCA1- and BRCA2-associated hereditary breast and ovarian cancer syndrome (HBOC) is characterized by an increased risk for female and male breast cancer, ovarian cancer (includes fallopian tube and primary peritoneal cancers), and to a lesser extent other cancers such as prostate cancer, pancreatic cancer, and melanoma primarily in individuals with a BRCA2 pathogenic variant. The exact cancer risks differ slightly depending on whether HBOC is caused by a BRCA1 or BRCA2 pathogenic variant.
breast-ovarian cancer, familial 1
MedGen UID:
382914
Concept ID:
C2676676
Finding
BRCA1- and BRCA2-associated hereditary breast and ovarian cancer syndrome (HBOC) is characterized by an increased risk for female and male breast cancer, ovarian cancer (includes fallopian tube and primary peritoneal cancers), and to a lesser extent other cancers such as prostate cancer, pancreatic cancer, and melanoma primarily in individuals with a BRCA2 pathogenic variant. The exact cancer risks differ slightly depending on whether HBOC is caused by a BRCA1 or BRCA2 pathogenic variant.
breast-ovarian cancer, familial 3
MedGen UID:
462009
Concept ID:
C3150659
Finding
cutaneous telangiectasia and cancer syndrome, familial
MedGen UID:
482833
Concept ID:
C3281203
Neoplastic Process
Patients with this syndrome develop cutaneous telangiectases in infancy with patchy alopecia over areas of affected skin, thinning of the lateral eyebrows, and mild dental and nail anomalies. Affected individuals are at increased risk of developing oropharyngeal cancer, and other malignancies have been reported as well (Tanaka et al., 2012).
cowden syndrome 5
MedGen UID:
767432
Concept ID:
C3554518
Disease or Syndrome
Cowden syndrome is a genetic disorder characterized by multiple noncancerous, tumor-like growths called hamartomas and an increased risk of developing certain cancers.\n\nAlmost everyone with Cowden syndrome develops hamartomas. These growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but they can also occur in the intestine and other parts of the body. The growth of hamartomas on the skin and mucous membranes typically becomes apparent by a person's late twenties.\n\nCowden syndrome is associated with an increased risk of developing several types of cancer, particularly cancers of the breast, a gland in the lower neck called the thyroid, and the lining of the uterus (the endometrium). Other cancers that have been identified in people with Cowden syndrome include kidney cancer, colorectal cancer, and an agressive form of skin cancer called melanoma. Compared with the general population, people with Cowden syndrome develop these cancers at younger ages, often beginning in their thirties or forties. People with Cowden syndrome are also more likely to develop more than one cancer during their lifetimes compared to the general population. Other diseases of the breast, thyroid, and endometrium are also common in Cowden syndrome. Additional signs and symptoms can include an enlarged head (macrocephaly) and a rare, noncancerous brain tumor called Lhermitte-Duclos disease. A small percentage of affected individuals have delayed development, intellectual disability, or autism spectrum disorder, which can affect communication and social interaction.\n\nSome people do not meet the strict criteria for a clinical diagnosis of Cowden syndrome, but they have some of the characteristic features of the condition, particularly the cancers. These individuals are often described as having Cowden-like syndrome. Both Cowden syndrome and Cowden-like syndrome are caused by mutations in the same genes.\n\nThe features of Cowden syndrome overlap with those of another disorder called Bannayan-Riley-Ruvalcaba syndrome. People with Bannayan-Riley-Ruvalcaba syndrome also develop hamartomas and other noncancerous tumors.  Some people with Cowden syndrome have relatives diagnosed with Bannayan-Riley-Ruvalcaba syndrome, and other affected individuals have the characteristic features of both conditions. Based on these similarities, researchers have proposed that Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome represent a spectrum of overlapping features known as PTEN hamartoma tumor syndrome (named for the genetic cause of the conditions) instead of two distinct conditions.\n\n
cowden syndrome 6
MedGen UID:
767433
Concept ID:
C3554519
Disease or Syndrome
\n\nThe features of Cowden syndrome overlap with those of another disorder called Bannayan-Riley-Ruvalcaba syndrome. People with Bannayan-Riley-Ruvalcaba syndrome also develop hamartomas and other noncancerous tumors.  Some people with Cowden syndrome have relatives diagnosed with Bannayan-Riley-Ruvalcaba syndrome, and other affected individuals have the characteristic features of both conditions. Based on these similarities, researchers have proposed that Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome represent a spectrum of overlapping features known as PTEN hamartoma tumor syndrome (named for the genetic cause of the conditions) instead of two distinct conditions.\n\nSome people do not meet the strict criteria for a clinical diagnosis of Cowden syndrome, but they have some of the characteristic features of the condition, particularly the cancers. These individuals are often described as having Cowden-like syndrome. Both Cowden syndrome and Cowden-like syndrome are caused by mutations in the same genes.\n\nCowden syndrome is associated with an increased risk of developing several types of cancer, particularly cancers of the breast, a gland in the lower neck called the thyroid, and the lining of the uterus (the endometrium). Other cancers that have been identified in people with Cowden syndrome include kidney cancer, colorectal cancer, and an agressive form of skin cancer called melanoma. Compared with the general population, people with Cowden syndrome develop these cancers at younger ages, often beginning in their thirties or forties. People with Cowden syndrome are also more likely to develop more than one cancer during their lifetimes compared to the general population. Other diseases of the breast, thyroid, and endometrium are also common in Cowden syndrome. Additional signs and symptoms can include an enlarged head (macrocephaly) and a rare, noncancerous brain tumor called Lhermitte-Duclos disease. A small percentage of affected individuals have delayed development, intellectual disability, or autism spectrum disorder, which can affect communication and social interaction.\n\nAlmost everyone with Cowden syndrome develops hamartomas. These growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but they can also occur in the intestine and other parts of the body. The growth of hamartomas on the skin and mucous membranes typically becomes apparent by a person's late twenties.\n\nCowden syndrome is a genetic disorder characterized by multiple noncancerous, tumor-like growths called hamartomas and an increased risk of developing certain cancers.
familial adenomatous polyposis 3
MedGen UID:
902388
Concept ID:
C4225157
Disease or Syndrome
NTHL1 tumor syndrome is characterized by an increased lifetime risk for colorectal cancer (CRC), breast cancer, and colorectal polyposis. Colorectal polyps can be adenomatous, hyperplastic, and/or sessile serrated. Duodenal polyposis has also been reported. Additional cancers reported in individuals with NTHL1 tumor syndrome include endometrial cancer, cervical cancer, urothelial carcinoma of the bladder, meningiomas, unspecified brain tumors, basal cell carcinomas, head and neck squamous cell carcinomas, and hematologic malignancies. The cumulative lifetime risk of developing extracolonic cancer by age 60 years has been estimated at 35% to 78%.
cowden syndrome 7
MedGen UID:
908796
Concept ID:
C4225179
Disease or Syndrome
Cowden syndrome is a genetic disorder characterized by multiple noncancerous, tumor-like growths called hamartomas and an increased risk of developing certain cancers.\n\nAlmost everyone with Cowden syndrome develops hamartomas. These growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but they can also occur in the intestine and other parts of the body. The growth of hamartomas on the skin and mucous membranes typically becomes apparent by a person's late twenties.\n\nCowden syndrome is associated with an increased risk of developing several types of cancer, particularly cancers of the breast, a gland in the lower neck called the thyroid, and the lining of the uterus (the endometrium). Other cancers that have been identified in people with Cowden syndrome include kidney cancer, colorectal cancer, and an agressive form of skin cancer called melanoma. Compared with the general population, people with Cowden syndrome develop these cancers at younger ages, often beginning in their thirties or forties. People with Cowden syndrome are also more likely to develop more than one cancer during their lifetimes compared to the general population. Other diseases of the breast, thyroid, and endometrium are also common in Cowden syndrome. Additional signs and symptoms can include an enlarged head (macrocephaly) and a rare, noncancerous brain tumor called Lhermitte-Duclos disease. A small percentage of affected individuals have delayed development, intellectual disability, or autism spectrum disorder, which can affect communication and social interaction.\n\nSome people do not meet the strict criteria for a clinical diagnosis of Cowden syndrome, but they have some of the characteristic features of the condition, particularly the cancers. These individuals are often described as having Cowden-like syndrome. Both Cowden syndrome and Cowden-like syndrome are caused by mutations in the same genes.\n\nThe features of Cowden syndrome overlap with those of another disorder called Bannayan-Riley-Ruvalcaba syndrome. People with Bannayan-Riley-Ruvalcaba syndrome also develop hamartomas and other noncancerous tumors.  Some people with Cowden syndrome have relatives diagnosed with Bannayan-Riley-Ruvalcaba syndrome, and other affected individuals have the characteristic features of both conditions. Based on these similarities, researchers have proposed that Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome represent a spectrum of overlapping features known as PTEN hamartoma tumor syndrome (named for the genetic cause of the conditions) instead of two distinct conditions.\n\n
fanconi anemia, complementation group s
MedGen UID:
1632414
Concept ID:
C4554406
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.

Recent clinical studies

Etiology

Mukama T, Fallah M, Brenner H, Xu X, Sundquist K, Sundquist J, Kharazmi E
BMC Med 2020 Nov 5;18(1):295. doi: 10.1186/s12916-020-01772-x. PMID: 33148280Free PMC Article
Wijesinghe HD, Fernando J, Senarath U, Wijesinghe GK, S Lokuhetty MD
Indian J Pathol Microbiol 2020 Jul-Sep;63(3):388-396. doi: 10.4103/IJPM.IJPM_657_19. PMID: 32769327
Paramita S, Raharjo EN, Niasari M, Azizah F, Hanifah NA
Asian Pac J Cancer Prev 2019 Aug 1;20(8):2247-2252. doi: 10.31557/APJCP.2019.20.8.2247. PMID: 31450891Free PMC Article
Dintzis SM, Hansen S, Harrington KM, Tan LC, Miller DM, Ishak L, Parrish-Novak J, Kittle D, Perry J, Gombotz C, Fortney T, Porenta S, Hales L, Calhoun KE, Anderson BO, Javid SH, Byrd DR
Arch Pathol Lab Med 2019 Sep;143(9):1076-1083. Epub 2018 Dec 14 doi: 10.5858/arpa.2018-0197-OA. PMID: 30550350
Fan X, Huang X, Li Z, Ma X
J BUON 2018 Sep-Oct;23(5):1309-1315. PMID: 30570852

Diagnosis

Zhang Z, Chen X, Zhang J, Dai X
Breast Cancer Res Treat 2021 Feb;186(1):89-98. Epub 2021 Jan 3 doi: 10.1007/s10549-020-06045-y. PMID: 33389402
Mukama T, Fallah M, Brenner H, Xu X, Sundquist K, Sundquist J, Kharazmi E
BMC Med 2020 Nov 5;18(1):295. doi: 10.1186/s12916-020-01772-x. PMID: 33148280Free PMC Article
Tsuji W
Breast Dis 2020;39(3-4):149-153. doi: 10.3233/BD-200452. PMID: 33074216
Mawaribuchi S, Haramoto Y, Tateno H, Onuma Y, Aiki Y, Ito Y
FEBS Open Bio 2020 Jun;10(6):1056-1064. Epub 2020 May 5 doi: 10.1002/2211-5463.12852. PMID: 32237061Free PMC Article
Na K, Lee JY, Sung JY, Kim GM, Koo JS, Kim HS
Virchows Arch 2018 Aug;473(2):165-175. Epub 2018 Jun 20 doi: 10.1007/s00428-018-2390-5. PMID: 29926183

Therapy

Trevisi E, La Salvia A, Daniele L, Brizzi MP, De Rosa G, Scagliotti GV, Di Maio M
Med Oncol 2020 Jul 25;37(8):70. doi: 10.1007/s12032-020-01396-4. PMID: 32712767Free PMC Article
Mawaribuchi S, Haramoto Y, Tateno H, Onuma Y, Aiki Y, Ito Y
FEBS Open Bio 2020 Jun;10(6):1056-1064. Epub 2020 May 5 doi: 10.1002/2211-5463.12852. PMID: 32237061Free PMC Article
Dintzis SM, Hansen S, Harrington KM, Tan LC, Miller DM, Ishak L, Parrish-Novak J, Kittle D, Perry J, Gombotz C, Fortney T, Porenta S, Hales L, Calhoun KE, Anderson BO, Javid SH, Byrd DR
Arch Pathol Lab Med 2019 Sep;143(9):1076-1083. Epub 2018 Dec 14 doi: 10.5858/arpa.2018-0197-OA. PMID: 30550350
Luo Z, Cai Q, Zhao Y, Wang X, Fu S, Zhai L
Medicine (Baltimore) 2018 May;97(20):e10754. doi: 10.1097/MD.0000000000010754. PMID: 29768356Free PMC Article
Bayhan Z, Zeren S, Kocak C, Kocak FE, Duzgun SA, Algin MC, Taskoylu BY, Yaylak F
Ann Ital Chir 2016 Sep 19;87(6):517-524. PMID: 27830671

Prognosis

Mukama T, Fallah M, Brenner H, Xu X, Sundquist K, Sundquist J, Kharazmi E
BMC Med 2020 Nov 5;18(1):295. doi: 10.1186/s12916-020-01772-x. PMID: 33148280Free PMC Article
Wijesinghe HD, Fernando J, Senarath U, Wijesinghe GK, S Lokuhetty MD
Indian J Pathol Microbiol 2020 Jul-Sep;63(3):388-396. doi: 10.4103/IJPM.IJPM_657_19. PMID: 32769327
Zheng YQ, Miao X, Li J, Hu MF, Zhu YS, Li XR, Zhang YJ
Eur Rev Med Pharmacol Sci 2020 Jun;24(11):6417-6425. doi: 10.26355/eurrev_202006_21540. PMID: 32572939
Paramita S, Raharjo EN, Niasari M, Azizah F, Hanifah NA
Asian Pac J Cancer Prev 2019 Aug 1;20(8):2247-2252. doi: 10.31557/APJCP.2019.20.8.2247. PMID: 31450891Free PMC Article
Na K, Lee JY, Sung JY, Kim GM, Koo JS, Kim HS
Virchows Arch 2018 Aug;473(2):165-175. Epub 2018 Jun 20 doi: 10.1007/s00428-018-2390-5. PMID: 29926183

Clinical prediction guides

Tsuji W
Breast Dis 2020;39(3-4):149-153. doi: 10.3233/BD-200452. PMID: 33074216
Wijesinghe HD, Fernando J, Senarath U, Wijesinghe GK, S Lokuhetty MD
Indian J Pathol Microbiol 2020 Jul-Sep;63(3):388-396. doi: 10.4103/IJPM.IJPM_657_19. PMID: 32769327
Zheng YQ, Miao X, Li J, Hu MF, Zhu YS, Li XR, Zhang YJ
Eur Rev Med Pharmacol Sci 2020 Jun;24(11):6417-6425. doi: 10.26355/eurrev_202006_21540. PMID: 32572939
Fan X, Huang X, Li Z, Ma X
J BUON 2018 Sep-Oct;23(5):1309-1315. PMID: 30570852
Na K, Lee JY, Sung JY, Kim GM, Koo JS, Kim HS
Virchows Arch 2018 Aug;473(2):165-175. Epub 2018 Jun 20 doi: 10.1007/s00428-018-2390-5. PMID: 29926183

Recent systematic reviews

Fitzpatrick SE, Lam TC
Plast Reconstr Surg 2020 Aug;146(2):117e-126e. doi: 10.1097/PRS.0000000000006965. PMID: 32740565
Lloyd AJ, Ryan ÉJ, Boland MR, Elwahab SA, Malone C, Sweeney KJ, Barry KM, McLaughlin R, Kerin MJ, Lowery AJ
Breast Cancer Res Treat 2020 Oct;183(3):503-514. Epub 2020 Jul 24 doi: 10.1007/s10549-020-05810-3. PMID: 32710280
Gibbons CE, Quinn CM, Gibbons D
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