Interferon-induced transmembrane protein 1 (IFITM1) overexpression enhances the aggressive phenotype of SUM149 inflammatory breast cancer cells in a signal transducer and activator of transcription 2 (STAT2)-dependent manner
Conclusions: These findings indicate that overexpression of IFITM1 enhances the aggressive phenotype of triple-negative SUM149 IBC cells and that this effect is dependent on STAT2/BRG1 interaction. Further studies are necessary to explore the potential of IFITM1 as a novel therapeutic target and prognostic marker for some subtypes of IBCs. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 20, 2016 Category: Cancer & Oncology Authors: Joshua OgonyHye ChoiAsona LuiMassimo CristofanilliJoan Lewis-Wambi Source Type: research

Circulating insulin-like growth factor-I, insulin-like growth factor binding protein-3 and terminal duct lobular unit involution of the breast: a cross-sectional study of women with benign breast disease
Background: Terminal duct lobular units (TDLUs) are the primary structures from which breast cancers and their precursors arise. Decreased age-related TDLU involution and elevated mammographic density are both correlated and independently associated with increased breast cancer risk, suggesting that these characteristics of breast parenchyma might be linked to a common factor. Given data suggesting that increased circulating levels of insulin-like growth factors (IGFs) factors are related to reduced TDLU involution and increased mammographic density, we assessed these relationships using validated quantitative methods in a...
Source: Breast Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Hisani HorneMark ShermanRuth PfeifferJonine FigueroaZeina KhodrRoni FalkMichael PollakDeesha PatelMaya PalakalLaura LinvilleDaphne PapathomasBerta GellerPamela VacekDonald WeaverRachael ChicoineJohn ShepherdAmir MahmoudzadehJeff WangBo FanSerghei MalkovSa Source Type: research

Genetic predisposition to ductal carcinoma in situ of the breast
Background: Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. Methods: To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. Results: Most (67 %) of the 76 known breast ...
Source: Breast Cancer Research - February 17, 2016 Category: Cancer & Oncology Authors: Christos PetridisMark BrookVandna ShahKelly KohutPatricia GormanMichele CaneppeleDina LeviEfterpi PapouliNick OrrAngela CoxSimon CrossIsabel dos-Santos-SilvaJulian PetoAnthony SwerdlowMinouk SchoemakerManjeet BollaQin WangJoe DennisKyriaki MichailidouJavi Source Type: research

LIN7A is a major determinant of cell-polarity defects in breast carcinomas
Conclusion: This study therefore shows that LIN7A has a crucial role in the polarity abnormalities associated with breast carcinogenesis. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 17, 2016 Category: Cancer & Oncology Authors: Nadège GruelLaetitia FuhrmannCatalina LodillinskyVanessa BenhamoOdette MarianiAurélie CédenotLaurent ArnouldGaëtan MacgroganXavier Sastre-GarauPhilippe ChavrierOlivier DelattreAnne Vincent-Salomon Source Type: research

Computational pathology of pre-treatment biopsies identifies lymphocyte density as a predictor of response to neoadjuvant chemotherapy in breast cancer
Conclusions: A data-driven analysis of computational pathology reveals lymphocyte density as an independent predictor of pCR. Paradoxically an increase in lymphocyte density, following exposure to chemotherapy, is associated with a lack of pCR. Computational pathology can provide objective, quantitative and reproducible tissue metrics and represents a viable means of outcome prediction in breast cancer.Trial registrationClinicalTrials.gov NCT00070278; 03/10/2003 (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 16, 2016 Category: Cancer & Oncology Authors: H. AliAliakbar DariushElena ProvenzanoHelen BardwellJean AbrahamMahesh IddawelaAnne-Laure VallierLouise HillerJanet. DunnSarah BowdenTamas HickishKaren McAdamStephen HoustonMike IrwinPaul PharoahJames BrentonNicholas WaltonHelena EarlCarlos Caldas Source Type: research

Does primary neoadjuvant systemic therapy eradicate minimal residual disease? Analysis of disseminated and circulating tumor cells before and after therapy
Conclusions: Although CTCs were eradicated more effectively than DTCs, CTCs detected after treatment seemed to be associated with tumor cells showing tumor stem cell characteristics as well as with resistant tumor cell populations that might indicate a worse outcome in the future. Thus, these patients might benefit from additional second-line treatment protocols including bisphosphonates for the eradication of DTCs. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 12, 2016 Category: Cancer & Oncology Authors: Sabine Kasimir-BauerAnn-Kathrin BittnerLisa KönigKatharina ReiterThomas KellerRainer KimmigOliver Hoffmann Source Type: research

Male breast cancer in BRCA1 and BRCA2 mutation carriers: pathology data from the Consortium of Investigators of Modifiers of BRCA1/2
Conclusions: On the basis of the largest series analysed to date, our results show that BRCA1/2 MBCs display distinct pathologic characteristics compared with BRCA1/2 FBCs, and we identified a specific BRCA2-associated MBC phenotype characterised by a variable suggesting greater biological aggressiveness (i.e., high histologic grade). These findings could lead to the development of gender-specific risk prediction models and guide clinical strategies appropriate for MBC management. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 9, 2016 Category: Cancer & Oncology Authors: Valentina SilvestriDaniel BarrowdaleAnna MulliganSusan NeuhausenStephen FoxBeth KarlanGillian MitchellPaul JamesDarcy ThullKristin ZornNatalie CarterKatherine NathansonSusan DomchekTimothy RebbeckSusan RamusRobert NussbaumOlufunmilayo OlopadeJohanna Ranta Source Type: research

Targeting the cyclin-dependent kinases (CDK) 4/6 in estrogen receptor-positive breast cancers
Despite significant advances in early detection and treatment, breast cancer still remains a major cause of morbidity and mortality for women. Our understanding of the molecular heterogeneity of the disease has significantly expanded over the past decade and the role of cell cycle signaling in both breast cancer oncogenesis and anti-estrogen resistance has gained increasing attention. The mammalian cell cycle is driven by a complex interplay between cyclins and their associated cyclin-dependent kinase (CDK) partners, and dysregulation of this process is one of the hallmarks of cancer. Despite this, initial results with bro...
Source: Breast Cancer Research - February 9, 2016 Category: Cancer & Oncology Authors: Richard FinnAlexey AleshinDennis Slamon Source Type: research

High content screening application for cell-type specific behaviour in heterogeneous primary breast epithelial subpopulations
Conclusions: We demonstrate the practical application of a new method for assessing cell-type specific change in mixed cultures, especially the analysis of normal primary cultures, overcoming a major technical issue of dissecting the response of multiple cell types in a heterogeneous population. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 9, 2016 Category: Cancer & Oncology Authors: Rebecca JohnstonLeesa WocknerAmy McCart ReedAdrian WiegmansGeorgia Chenevix-TrenchKum KhannaSunil LakhaniChanel Smart Source Type: research

Downregulation of histone H2A and H2B pathways is associated with anthracycline sensitivity in breast cancer
Conclusions: This study revealed a key pathway that contributes to anthracycline resistance and established model systems for investigating drug resistance in all four major breast cancer subtypes. As the histone modification can be targeted with small-molecule inhibitors, it represents a possible means of reversing clinical anthracycline resistance.Trial registrationClinicalTrials.gov identifier NCT00003012. Registered on 1 November 1999. (Source: Breast Cancer Research)
Source: Breast Cancer Research - February 6, 2016 Category: Cancer & Oncology Authors: Marsela BraunsteinLinda LiaoNicola LyttleNazleen LoboKaren TaylorPaul KrzyzanowskiIrina KalatskayaCindy YaoLincoln SteinPaul BoutrosChristopher TwelvesRichard MarcellusJohn BartlettMelanie Spears Source Type: research

The fibroblast Tiam1-osteopontin pathway modulates breast cancer invasion and metastasis
Conclusions: These findings suggest a new therapeutic paradigm for preventing breast cancer metastasis. Pro-malignant signals from the tumor microenvironment with long-lasting effects on associated cancer cells may perpetuate the metastatic potential of developing cancers. Inhibition of these microenvironment signals represents a new therapeutic strategy against cancer metastasis that enables targeting of stromal cells with less genetic plasticity than associated cancer cells and opens new avenues for investigation of novel therapeutic targets and agents. (Source: Breast Cancer Research)
Source: Breast Cancer Research - January 28, 2016 Category: Cancer & Oncology Authors: Kun XuXuejun TianSun OhMohammad MovassaghiStephen NaberCharlotte KuperwasserRachel Buchsbaum Source Type: research

p53 deficiency linked to B cell translocation gene 2 (BTG2) loss enhances metastatic potential by promoting tumor growth in primary and metastatic sites in patient-derived xenograft (PDX) models of triple-negative breast cancer
Conclusions: Using paired isogenic PDX-derived metastatic TNBC cells, loss of p53 promoted tumor growth and consequently increased tumor cell shedding into the blood, thus enhancing metastasis. Loss of BTG2 expression in p53-deficient tumors contributed to this metastatic potential by enhancing tumor growth in primary and metastatic sites. Furthermore, clinical data support conclusions generated from PDX models and indicate that BTG2 expression is a candidate prognostic biomarker for TNBC. (Source: Breast Cancer Research)
Source: Breast Cancer Research - January 27, 2016 Category: Cancer & Oncology Authors: Emily PowellJiansu ShaoYuan YuanHsiang-Chun ChenShirong CaiGloria EcheverriaNipun MistryKeith DeckerChristopher SchlosbergKim-Anh DoJohn EdwardsHan LiangDavid Piwnica-WormsHelen Piwnica-Worms Source Type: research

Lymphocyte depletion and repopulation after chemotherapy for primary breast cancer
We examined circulating titres of antibodies against pneumococcal and tetanus antigens using ELISAs. Results: Levels of B, T and NK cells were significantly reduced 2 weeks after chemotherapy (p  (Source: Breast Cancer Research)
Source: Breast Cancer Research - January 26, 2016 Category: Cancer & Oncology Authors: Rashmi VermaRuth FosterKieran HorganKatherine MounseyHelen NixonNatuley SmalleThomas HughesClive Carter Source Type: research

Epigenetic silencing of CREB3L1 by DNA methylation is associated with high-grade metastatic breast cancers with poor prognosis and is prevalent in triple negative breast cancers
Conclusions: Our data further strengthens the role for CREB3L1 as a metastasis suppressor in breast cancer and demonstrates that epigenetic silencing is a major regulator of the loss of CREB3L1 expression. We also highlight that CREB3L1 expression is frequently altered in many cancer types suggesting that it could have a broader role in cancer progression and metastasis. (Source: Breast Cancer Research)
Source: Breast Cancer Research - January 25, 2016 Category: Cancer & Oncology Authors: Alison WardPaul MellorShari SmithStephanie KendallNatasha JustFrederick VizeacoumarSabuj SarkerZoe PhillipsRiaz AlviAnurag SaxenaFranco VizeacoumarSvein CarlsenDeborah Anderson Source Type: research

The cell surface mucin podocalyxin regulates collective breast tumor budding
Conclusions: Podocalyxin is a tumor cell-intrinsic regulator of experimental collective tumor cell invasion and tumor budding. (Source: Breast Cancer Research)
Source: Breast Cancer Research - January 22, 2016 Category: Cancer & Oncology Authors: Marcia GravesJane CipollonePamela AustinErin BellJulie NielsenC. GilksKelly McNagnyCalvin Roskelley Source Type: research