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17 beta-hydroxysteroid dehydrogenase gene expression in human breast cancer cells: regulation of expression by a progestin.

https://arctichealth.org/en/permalink/ahliterature24541
Source
Cancer Res. 1992 Jan 15;52(2):290-4
Publication Type
Article
Date
Jan-15-1992
Author
M. Poutanen
B. Moncharmont
R. Vihko
Author Affiliation
Department of Clinical Chemistry, University of Oulu, Finland.
Source
Cancer Res. 1992 Jan 15;52(2):290-4
Date
Jan-15-1992
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - genetics - metabolism
Breast Neoplasms - enzymology - genetics
Gene Expression Regulation, Neoplastic - drug effects
Humans
Isoenzymes - genetics
Placenta - enzymology
Pregnenediones - pharmacology
Progesterone Congeners - pharmacology
RNA, Messenger - genetics
RNA, Neoplasm - genetics
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
The expression of the 17 beta-hydroxysteroid dehydrogenase (17-HSD) gene in a series of human breast cancer cell lines was studied by Northern blot hybridization with a cDNA probe and by a time-resolved immunofluorometric assay using polyclonal antibodies against the enzyme protein. The 17-HSD enzyme protein concentration was measured in the 800 x g cell extract. A high concentration was measured in the BT-20 cell line, corresponding to one-fourth of the average concentration in placental tissue. Western blot analysis indicated that the antigen corresponded to a single Mr 35,000 band. In 2 other cell lines (MDA-MB-361 and T-47D), the 17-HSD protein concentration was much lower, but still measurable, whereas in the remaining 5 cell lines (HBL-100, MCF-7, MDA-MB-231, MDA-MB-468, and ZR-75-1) it was below the detection limit of the assay. Treatment of the cells for 5 days with the synthetic progestin, ORG2058, resulted in an increase of the 17-HSD protein concentration only in the T-47D cell line. By Northern blot analysis, a low level of 2.3-kilobase mRNA transcripts was detected in all 8 cell lines. In addition, a 1.3-kilobase 17-HSD mRNA was present in the samples from the 3 cell lines containing measurable amounts of 17-HSD protein in the cell extract, and the band intensities were proportional to the amount of protein measured with the immunofluorometric assay. Only in the T-47D cell line did progestin treatment correspond to an increased amount of the 17-HSD 1.3-kilobase mRNA. These results suggest that the 1.3-kilobase mRNA for 17-HSD is the form most closely associated with protein expression and is also the only form responding to the progestin induction of the 17-HSD gene.
PubMed ID
1728403 View in PubMed
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Adjuvant Capecitabine in Combination With Docetaxel, Epirubicin, and Cyclophosphamide for Early Breast Cancer: The Randomized Clinical FinXX Trial.

https://arctichealth.org/en/permalink/ahliterature285225
Source
JAMA Oncol. 2017 Jun 01;3(6):793-800
Publication Type
Article
Date
Jun-01-2017
Author
Heikki Joensuu
Pirkko-Liisa Kellokumpu-Lehtinen
Riikka Huovinen
Arja Jukkola-Vuorinen
Minna Tanner
Riitta Kokko
Johan Ahlgren
Päivi Auvinen
Outi Lahdenperä
Sanna Kosonen
Kenneth Villman
Paul Nyandoto
Greger Nilsson
Paula Poikonen-Saksela
Vesa Kataja
Jouni Junnila
Petri Bono
Henrik Lindman
Source
JAMA Oncol. 2017 Jun 01;3(6):793-800
Date
Jun-01-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
Capecitabine - administration & dosage
Chemotherapy, Adjuvant - methods - mortality
Cyclophosphamide - administration & dosage
Epirubicin - administration & dosage
Female
Finland - epidemiology
Fluorouracil - administration & dosage
Humans
Middle Aged
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Sweden - epidemiology
Taxoids - administration & dosage
Treatment Outcome
Triple Negative Breast Neoplasms - drug therapy - mortality
Young Adult
Abstract
Capecitabine is not considered a standard agent in the adjuvant treatment of early breast cancer. The results of this study suggest that addition of adjuvant capecitabine to a regimen that contains docetaxel, epirubicin, and cyclophosphamide improves survival outcomes of patients with triple-negative breast cancer (TNBC).
To investigate the effect of capecitabine on long-term survival outcomes of patients with early breast cancer, particularly in subgroups defined by cancer estrogen receptor (ER) and progesterone receptor (PR) content, and HER2 content (human epidermal growth factor receptor 2).
This is an exploratory analysis of the multicenter FinXX randomized clinical trial that accrued 1500 women in Finland and Sweden between January 27, 2004, and May 29, 2007. About half received 3 cycles of docetaxel followed by 3 cycles of cyclophosphamide, epirubicin, and fluorouracil (T+CEF), while the other half received 3 cycles of docetaxel plus capecitabine followed by 3 cycles of cyclophosphamide, epirubicin, and capecitabine (TX+CEX). Data analysis took place between January 27, 2004, and December 31, 2015.
Recurrence-free survival (RFS).
Following random allocation, 747 women received T+CEF, and 753 women received TX+CEX. Five patients were excluded from the intention-to-treat population (3 had overt distant metastases at the time of randomization; 2 withdrew consent). The median age of the remaining 1495 patients was 53 years at the time of study entry; 157 (11%) had axillary node-negative disease; 1142 (76%) had ER-positive cancer; and 282 (19%) had HER2-positive cancer. The median follow-up time after random allocation was 10.3 years. There was no significant difference in RFS or overall survival between the groups (hazard ratio [HR], 0.88; 95% CI, 0.71-1.08; P?=?.23; and HR, 0.84, 95% CI, 0.66-1.07; P?=?.15; respectively). Breast cancer-specific survival tended to favor the capecitabine group (HR, 0.79; 95% CI, 0.60-1.04; P?=?.10). When RFS and survival of the patients were compared within the subgroups defined by cancer steroid hormone receptor status (ER and/or PR positive vs ER and PR negative) and HER2 status (positive vs negative), TX+CEX was more effective than T+CEF in the subset of patients with TNBC (HR, 0.53; 95% CI, 0.31-0.92; P?=?.02; and HR, 0.55, 95% CI, 0.31-0.96; P?=?.03; respectively).
Capecitabine administration with docetaxel, epirubicin, and cyclophosphamide did not prolong RFS or survival compared with a regimen that contained only standard agents. Patients with TNBC had favorable survival outcomes when treated with the capecitabine-containing regimen in an exploratory subgroup analysis.
clinicaltrials.gov Identifier: NCT00114816.
PubMed ID
28253390 View in PubMed
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Adjuvant denosumab in breast cancer (ABCSG-18): a multicentre, randomised, double-blind, placebo-controlled trial.

https://arctichealth.org/en/permalink/ahliterature265750
Source
Lancet. 2015 Aug 1;386(9992):433-43
Publication Type
Article
Date
Aug-1-2015
Author
Michael Gnant
Georg Pfeiler
Peter C Dubsky
Michael Hubalek
Richard Greil
Raimund Jakesz
Viktor Wette
Marija Balic
Ferdinand Haslbauer
Elisabeth Melbinger
Vesna Bjelic-Radisic
Silvia Artner-Matuschek
Florian Fitzal
Christian Marth
Paul Sevelda
Brigitte Mlineritsch
Günther G Steger
Diether Manfreda
Ruth Exner
Daniel Egle
Jonas Bergh
Franz Kainberger
Susan Talbot
Douglas Warner
Christian Fesl
Christian F Singer
Source
Lancet. 2015 Aug 1;386(9992):433-43
Date
Aug-1-2015
Language
English
Publication Type
Article
Keywords
Absorptiometry, Photon
Adult
Aged
Aged, 80 and over
Antibodies, Monoclonal, Humanized - therapeutic use
Aromatase Inhibitors - therapeutic use
Austria
Bone Density - physiology
Breast Neoplasms - complications - drug therapy
Double-Blind Method
Female
Fractures, Bone - complications - prevention & control
Humans
Middle Aged
Postmenopause
Prospective Studies
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Sweden
Treatment Outcome
Abstract
Adjuvant endocrine therapy compromises bone health in patients with breast cancer, causing osteopenia, osteoporosis, and fractures. Antiresorptive treatments such as bisphosphonates prevent and counteract these side-effects. In this trial, we aimed to investigate the effects of the anti-RANK ligand antibody denosumab in postmenopausal, aromatase inhibitor-treated patients with early-stage hormone receptor-positive breast cancer.
In this prospective, double-blind, placebo-controlled, phase 3 trial, postmenopausal patients with early hormone receptor-positive breast cancer receiving treatment with aromatase inhibitors were randomly assigned in a 1:1 ratio to receive either denosumab 60 mg or placebo administered subcutaneously every 6 months in 58 trial centres in Austria and Sweden. Patients were assigned by an interactive voice response system. The randomisation schedule used a randomly permuted block design with block sizes 2 and 4, stratified by type of hospital regarding Hologic device for DXA scans, previous aromatase inhibitor use, and baseline bone mineral density. Patients, treating physicians, investigators, data managers, and all study personnel were masked to treatment allocation. The primary endpoint was time from randomisation to first clinical fracture, analysed by intention to treat. As an additional sensitivity analysis, we also analysed the primary endpoint on the per-protocol population. Patients were treated until the prespecified number of 247 first clinical fractures was reached. This trial is ongoing (patients are in follow-up) and is registered with the European Clinical Trials Database, number 2005-005275-15, and with ClinicalTrials.gov, number NCT00556374.
Between Dec 18, 2006, and July 22, 2013, 3425 eligible patients were enrolled into the trial, of whom 3420 were randomly assigned to receive denosumab 60 mg (n=1711) or placebo (n=1709) subcutaneously every 6 months. Compared with the placebo group, patients in the denosumab group had a significantly delayed time to first clinical fracture (hazard ratio [HR] 0·50 [95% CI 0·39-0·65], p
Notes
Comment In: Lancet. 2015 Aug 1;386(9992):409-1026040500
PubMed ID
26040499 View in PubMed
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Anthropometric factors and risk of molecular breast cancer subtypes among postmenopausal Norwegian women.

https://arctichealth.org/en/permalink/ahliterature258863
Source
Int J Cancer. 2014 Dec 1;135(11):2678-86
Publication Type
Article
Date
Dec-1-2014
Author
Julie Horn
Mirjam D K Alsaker
Signe Opdahl
Monica J Engstrøm
Steinar Tretli
Olav A Haugen
Anna M Bofin
Lars J Vatten
Bjørn Olav Asvold
Source
Int J Cancer. 2014 Dec 1;135(11):2678-86
Date
Dec-1-2014
Language
English
Publication Type
Article
Keywords
Adult
Body Height
Body mass index
Breast Neoplasms - classification - epidemiology - metabolism - pathology
Female
Follow-Up Studies
Humans
Immunoenzyme Techniques
Middle Aged
Neoplasm Staging
Norway - epidemiology
Postmenopause
Prognosis
Prospective Studies
Receptor, erbB-2 - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Risk factors
Tissue Array Analysis
Tumor Markers, Biological - analysis
Abstract
Adult height and body weight are positively associated with breast cancer risk after menopause, but few studies have investigated these factors according to molecular breast cancer subtype. A total of 18,562 postmenopausal Norwegian women who were born between 1886 and 1928 were followed up for breast cancer incidence from the time (between 1963 and 1975) height and weight were measured until 2008. Immunohistochemical and in situ hybridization techniques were used to subtype 734 incident breast cancer cases into Luminal A, Luminal B [human epidermal growth factor receptor 2 (HER2-)], Luminal B (HER2+), HER2 subtype, basal-like phenotype (BP) and five-negative phenotype (5NP). We used Cox regression analysis to assess adult height and body mass index (BMI) in relation to risk of these subtypes. We found a positive association of height with risk of Luminal A breast cancer (ptrend , 0.004), but there was no clear association of height with any other subtype. BMI was positively associated with risk of all luminal breast cancer subtypes, including Luminal A (ptrend , 0.002), Luminal B (HER2-) (ptrend , 0.02), Luminal B (HER2+) (ptrend , 0.06), and also for the HER2 subtype (ptrend , 0.04), but BMI was not associated with risk of the BP or 5NP subtypes. Nonetheless, statistical tests for heterogeneity did not provide evidence that associations of height and BMI differed across breast cancer subtypes. This study of breast cancer risk among postmenopausal women suggests that height is positively associated with risk of Luminal A breast cancer. BMI is positively associated with risk of all luminal subtypes and for the HER2 subtype.
PubMed ID
24752603 View in PubMed
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An update review of cellular mechanisms conferring the indirect and direct effects of estrogen on articular cartilage.

https://arctichealth.org/en/permalink/ahliterature87075
Source
Climacteric. 2008 Feb;11(1):4-16
Publication Type
Article
Date
Feb-2008
Author
Tankó L B
Søndergaard B-C
Oestergaard S.
Karsdal M A
Christiansen C.
Author Affiliation
Nordic Bioscience, Herlev, Denmark.
Source
Climacteric. 2008 Feb;11(1):4-16
Date
Feb-2008
Language
English
Publication Type
Article
Keywords
Cartilage, Articular - cytology - drug effects
Chondrocytes - drug effects
Estrogens - pharmacology - physiology
Female
Humans
Osteoarthritis - blood - prevention & control
Postmenopause
Progestins - pharmacology - physiology
Receptors, Estrogen - metabolism
Abstract
OBJECTIVE: To review cellular mechanisms that have been proposed to mediate the indirect and direct effects of estrogen on articular cartilage, and to outline the remaining clinical questions that need to be clarified before utilizing the beneficial effects of estrogen for the prevention of osteoarthritis in early postmenopausal women. DESIGN: Summary of original research papers and reviews listed in Pubmed (1980-2007). RESULTS: Estrogen receptors have been identified in articular chondrocytes from various animals and humans. Molecular studies showed that estrogen can elicit genomic and rapid non-genomic effects on various cell types, including chondrocytes, and the latter effects are only inducible in females. In addition to direct effects, estrogen can also affect the homeostasis of articular cartilage by modulating the expression/production of different molecules such as various growth factors, inflammatory cytokines, matrix metalloproteinases, and reactive oxygen species. Moreover, in vivo observation argues for the notion that inhibition of subchondral bone turnover is also part of the mechanisms by which estrogen (and antiresorptive agents in general) can protect against joint degradation. Published studies undertaken at cellular, tissue, and in vivo levels illustrate that the effect of estrogen on cartilage may depend on the dose applied, the administration route, the time of initiation, and whether it is combined with a progestin. CONCLUSIONS: The herein reviewed direct and indirect effects of estrogen on articular cartilage further corroborate the due consideration of estrogen therapy for maintaining not only bone but also cartilage health in postmenopausal women. Future studies in postmenopausal women are needed to clarify whether the efficacy of estrogen therapy can be further optimized by using other forms of estrogen, other progestins, or by initiating the therapy in the peri- or early postmenopausal period.
PubMed ID
18202960 View in PubMed
Less detail

Breast cancer biological subtypes and protein expression predict for the preferential distant metastasis sites: a nationwide cohort study.

https://arctichealth.org/en/permalink/ahliterature131332
Source
Breast Cancer Res. 2011;13(5):R87
Publication Type
Article
Date
2011
Author
Harri Sihto
Johan Lundin
Mikael Lundin
Tiina Lehtimäki
Ari Ristimäki
Kaija Holli
Liisa Sailas
Vesa Kataja
Taina Turpeenniemi-Hujanen
Jorma Isola
Päivi Heikkilä
Heikki Joensuu
Author Affiliation
Laboratory of Molecular Oncology, University of Helsinki, Biomedicum Helsinki, Haartmaninkatu 8, 00290, Helsinki, Finland. harri.sihto@helsinki.fi
Source
Breast Cancer Res. 2011;13(5):R87
Date
2011
Language
English
Publication Type
Article
Keywords
Antigens, CD - metabolism
Bone Neoplasms - metabolism - secondary
Brain Neoplasms - metabolism - secondary
Breast Neoplasms - metabolism - pathology
Cadherins - metabolism
Cohort Studies
Cyclooxygenase 2 - metabolism
Female
Finland
Follow-Up Studies
Glycoproteins - metabolism
Humans
Intermediate Filament Proteins - metabolism
Keratin-5 - metabolism
Liver Neoplasms - metabolism - secondary
Lung Neoplasms - metabolism - secondary
Nerve Tissue Proteins - metabolism
Nestin
Peptides - metabolism
Proteins - analysis - metabolism
Receptor, Epidermal Growth Factor - metabolism
Receptor, erbB-2 - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Skin Neoplasms - metabolism - secondary
Transcription Factors - metabolism
Abstract
Some molecular subtypes of breast cancer have preferential sites of distant relapse. The protein expression pattern of the primary tumor may influence the first distant metastasis site.
We identified from the files of the Finnish Cancer Registry patients diagnosed with breast cancer in five geographical regions Finland in 1991-1992, reviewed the hospital case records, and collected primary tumor tissue. Out of the 2,032 cases identified, 234 developed distant metastases after a median follow-up time of 2.7 years and had the first metastatic site documented (a total of 321 sites). Primary tumor microarray (TMA) cores were analyzed for 17 proteins using immunohistochemistry and for erbB2 using chromogenic in situ hybridization, and their associations with the first metastasis site were examined. The cancers were classified into luminal A, luminal B, HER2+ enriched, basal-like or non-expressor subtypes.
A total of 3,886 TMA cores were analyzed. Luminal A cancers had a propensity to give rise first to bone metastases, HER2-enriched cancers to liver and lung metastases, and basal type cancers to liver and brain metastases. Primary tumors that gave first rise to bone metastases expressed frequently estrogen receptor (ER) and SNAI1 (SNAIL) and rarely COX2 and HER2, tumors with first metastases in the liver expressed infrequently SNAI1, those with lung metastases expressed frequently the epidermal growth factor receptor (EGFR), cytokeratin-5 (CK5) and HER2, and infrequently progesterone receptor (PgR), tumors with early skin metastases expressed infrequently E-cadherin, and breast tumors with first metastases in the brain expressed nestin, prominin-1 and CK5 and infrequently ER and PgR.
Breast tumor biological subtypes have a tendency to give rise to first distant metastases at certain body sites. Several primary tumor proteins were associated with homing of breast cancer cells.
Notes
Cites: Cancer. 2011 May 1;117(9):1837-4621509760
Cites: Clin Cancer Res. 2008 Jul 1;14(13):4103-1018593987
Cites: Cell Tissue Res. 2005 Jan;319(1):15-2615558321
Cites: Lancet. 2005 Feb 19-25;365(9460):671-915721472
Cites: CA Cancer J Clin. 2005 Mar-Apr;55(2):74-10815761078
Cites: Clin Cancer Res. 2005 Aug 15;11(16):5678-8516115903
Cites: Ann Oncol. 2006 Jun;17(6):935-4416603601
Cites: JAMA. 2006 Jun 7;295(21):2492-50216757721
Cites: Oncol Rep. 2006 Jul;16(1):119-2216786133
Cites: Cancer. 2006 Aug 15;107(4):696-70416826579
Cites: J Pathol. 2007 Mar;211(4):481-817294421
Cites: Nature. 2007 Apr 12;446(7137):765-7017429393
Cites: Clin Cancer Res. 2008 Apr 1;14(7):1938-4618381931
Cites: Cancer. 2000 Jan 1;88(1):95-10710618611
Cites: Breast Cancer Res Treat. 2000 Feb;59(3):271-810832597
Cites: J Clin Oncol. 2001 Jan 1;19(1):28-3611134192
Cites: Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-7411553815
Cites: Cancer Res. 2002 Feb 1;62(3):632-511830510
Cites: N Engl J Med. 2002 Dec 19;347(25):1999-200912490681
Cites: Breast Cancer Res Treat. 2003 Mar;78(1):105-1812611463
Cites: Clin Cancer Res. 2003 Mar;9(3):923-3012631589
Cites: Cancer Res. 2008 May 1;68(9):3108-1418451135
Cites: Cancer. 1983 Dec 15;52(12):2349-546640506
Cites: Breast. 2008 Aug;17(4):323-3418455396
Cites: Neurochem Res. 2008 Dec;33(12):2407-1518493853
Cites: Ann Oncol. 2008 Dec;19(12):2012-918641006
Cites: Am J Surg Pathol. 2009 Feb;33(2):163-7518936692
Cites: J Clin Oncol. 2009 Mar 10;27(8):1168-7619204205
Cites: Cancer Metastasis Rev. 2009 Jun;28(1-2):151-6619153669
Cites: Clin Cancer Res. 2009 Jun 1;15(11):3733-919458057
Cites: Eur J Cancer. 2009 Jul;45(11):1916-2319398327
Cites: Ann Oncol. 2009 Sep;20(9):1499-50419299408
Cites: J Clin Oncol. 2009 Nov 1;27(31):5278-8619770385
Cites: Clin Breast Cancer. 2009 Nov;9(4):225-3019933077
Cites: Ann Oncol. 2010 May;21(5):942-819840953
Cites: Hum Pathol. 2010 Jun;41(6):914-720338615
Cites: Ann Oncol. 2010 Jun;21(6):1254-6119858088
Cites: J Clin Oncol. 2010 Jun 1;28(16):2784-9520404251
Cites: J Clin Oncol. 2010 Jul 10;28(20):3271-720498394
Cites: Breast Cancer Res. 2010;12(4):R4620604919
Cites: Nature. 2004 Nov 18;432(7015):396-40115549107
PubMed ID
21914172 View in PubMed
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Breast cancer during follow-up and progression - A population based cohort on new cancers and changed biology.

https://arctichealth.org/en/permalink/ahliterature259835
Source
Eur J Cancer. 2014 Nov;50(17):2916-24
Publication Type
Article
Date
Nov-2014
Author
E. Karlsson
J. Appelgren
A. Solterbeck
M. Bergenheim
V. Alvariza
J. Bergh
Source
Eur J Cancer. 2014 Nov;50(17):2916-24
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biopsy, Needle
Breast Neoplasms - metabolism - mortality - therapy
Chemoradiotherapy, Adjuvant
Disease Progression
Female
Humans
Immunohistochemistry
Kaplan-Meier Estimate
Ki-67 Antigen - metabolism
Middle Aged
Neoplasm Metastasis
Neoplasm Recurrence, Local - metabolism - mortality - therapy
Neoplasms, Second Primary - metabolism - mortality
Receptor, erbB-2 - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Retrospective Studies
Sweden - epidemiology
Tumor Markers, Biological - metabolism
Abstract
Emerging data indicate an important role for biopsies of clinically/radiologically defined breast cancer 'recurrences'. The present study investigates tumour related events (relapses, other malignancies, benign conditions) after a primary breast cancer diagnosis.
The cohort includes 2102 women, representing all patients, with primary invasive breast cancer during 2000-2011 in the county of Värmland, Sweden. A comparative analysis of oestrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and proliferation (Ki67) between the primary tumour and the relapse was performed and related to outcome.
With a mean follow-up time of 4.8 years, 1060 out of 2102 patients have had a biopsy taken after the initial breast cancer diagnosis demonstrating 177 recurrences, 93 other malignancies (colorectal, lung, skin), 40 cancer in situ (skin, breast) and 857 benign lesions. Approximately 70% (177 out of 245) of all cases of relapsed breast cancer underwent a biopsy during this time period. For patients with recurrences, ER (n=127), PR (n=101), HER2 (n=73) and Ki67 (n=55) status in both primary tumour and the corresponding relapse were determined. The discordance of receptor status was 14.2%, 39.6%, 9.6% and 36.3%, respectively. Loss of ER or PR in the relapse resulted in a significant increased risk of death (hazard ratio (HR) 3.62; 95% confidence interval (CI), 1.65-7.94) and (HR 2.34; 95% CI, 1.01-5.47) compared with patients with stable ER or PR positive tumours. The proportion of patients losing ER was bigger in the group treated with endocrine therapy alone or in combination with chemotherapy, 16.7% and 13.3%, respectively, compared with the group treated with chemotherapy alone or that which received no treatment 4.3% and 7.7%, respectively.
Discordance of biomarkers between the primary tumour and the corresponding relapse was seen in 10-40% of the patients, adjuvant therapies seem to drive clonal selections. Patients with tumours losing ER or PR during progression have worse survival compared with patients with retained receptor expression.
PubMed ID
25241230 View in PubMed
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Breast cancer incidence by estrogen receptor status in Denmark from 1996 to 2007.

https://arctichealth.org/en/permalink/ahliterature119973
Source
Breast Cancer Res Treat. 2012 Nov;136(2):559-64
Publication Type
Article
Date
Nov-2012
Author
J. Bigaard
C. Stahlberg
M-B Jensen
M. Ewertz
N. Kroman
Author Affiliation
Department of Breast Surgery, Ringsted Hospital, Ringsted, Denmark. j.bigaard@dadlnet.dk
Source
Breast Cancer Res Treat. 2012 Nov;136(2):559-64
Date
Nov-2012
Language
English
Publication Type
Article
Keywords
Adult
Breast Neoplasms - epidemiology - metabolism
Denmark - epidemiology
Female
Humans
Incidence
Middle Aged
Receptors, Estrogen - metabolism
Retrospective Studies
Young Adult
Abstract
During the past 50 years, breast cancer incidence has increased by 2-3 % annually. Despite many years of testing for estrogen receptors (ER), evidence is scarce on breast cancer incidence by ER status. The aim of this paper was to investigate the increase in breast cancer incidence by ER status. Data were obtained from the clinical database of the Danish Breast Cancer Cooperative Group which holds nationwide data on diagnosis, including pathology, treatment, and follow-up on primary breast cancers since 1977. All Danish women
PubMed ID
23053655 View in PubMed
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Breast cancer incidence in ex-smokers in relation to body mass index, weight gain and blood lipid levels.

https://arctichealth.org/en/permalink/ahliterature19708
Source
Eur J Cancer Prev. 2001 Jun;10(3):281-7
Publication Type
Article
Date
Jun-2001
Author
J. Manjer
J. Malina
G. Berglund
L. Bondeson
J P Garne
L. Janzon
Author Affiliation
Department of Community Medicine, Lund University, Malmö University Hospital, Malmö, Sweden. jonas.manjer@smi.mas.lu.se
Source
Eur J Cancer Prev. 2001 Jun;10(3):281-7
Date
Jun-2001
Language
English
Publication Type
Article
Keywords
Adult
Body Height
Body mass index
Body Weight
Breast Neoplasms - blood - epidemiology
Cholesterol - blood
Female
Follow-Up Studies
Humans
Incidence
Lipids - blood
Lipoproteins - blood
Middle Aged
Neoplasm Staging
Receptors, Estrogen - metabolism
Risk assessment
Risk factors
Smoking Cessation
Sweden - epidemiology
Triglycerides - blood
Abstract
According to several studies breast cancer is more common among former smokers. This study explores whether this association has any relationship with anthropometric measurements or blood lipid levels. The 2082 ex-smokers (mean age 49.9 years) in the Malmö Preventive Cohort were followed for an average of 13.3 years using official cancer registries. This yielded 93 incident breast cancer cases. Oestrogen receptor (ER) status was assessed by an immunological method. Incidence of breast cancer covaried with height, body mass index, weight gain and cholesterol levels. None of these associations reached statistical significance. Incidence of breast cancer increased over quartiles of serum triglycerides, Ptrend: 0.02, relative risk (RR) for triglycerides as a continuous variable: 1.46 (1.21-1.77). Nineteen tumours were ER negative; this subgroup was similarly related to high triglycerides, 1.76 (1.40-2.21). All results were similar when BMI and cholesterol levels were entered into the model. It is concluded that breast cancer incidence covaries with triglyceride levels in ex-smokers.
PubMed ID
11432717 View in PubMed
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Breast cancer in women using digoxin: tumor characteristics and relapse risk.

https://arctichealth.org/en/permalink/ahliterature261130
Source
Breast Cancer Res. 2013;15(1):R13
Publication Type
Article
Date
2013
Author
Robert J Biggar
Elisabeth W Andersen
Niels Kroman
Jan Wohlfahrt
Mads Melbye
Source
Breast Cancer Res. 2013;15(1):R13
Date
2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aromatase Inhibitors - administration & dosage - adverse effects
Breast Neoplasms - chemically induced - drug therapy - epidemiology - pathology
Denmark
Digoxin - administration & dosage - adverse effects
Female
Heart Diseases - drug therapy - pathology
Humans
Middle Aged
Neoplasm Recurrence, Local - chemically induced - epidemiology - pathology
Prognosis
Receptors, Estrogen - metabolism
Risk factors
Tamoxifen - administration & dosage - adverse effects
Abstract
Digoxin use is associated with increased incidence of breast and uterus cancers. We postulated that digoxin use might affect tumor characteristics and increase relapse risk in women with breast cancer.
Incident breast cancer cases in Danish women (n = 49,312; 1995 to 2008) were identified. Analyses were conducted in women 20 to 74 years old. Relapse hazard ratios (HR) were compared in women using and not using digoxin, adjusting for age, calendar period, protocol, tumor size, nodal involvement, histology grade, estrogen-receptor (ER) status, and anti-estrogen therapy in Cox regression models.
At diagnosis, tumors in digoxin users were more likely ER+ (85.4% vs. 78.6%: P = 0.002) and have grade 1 ductal histology (37.2% vs. 25.7%; P = 0.004), compared to non-users. 45 relapses occurred in women already using digoxin at breast cancer diagnosis (1,487 person-years); 24 relapses occurred in women later starting digoxin (384 person-years). Overall relapse risk HR in digoxin users was 1.13 (95% confidence interval: 0.88, 1.46) compared to non-users. Relapse risk in digoxin users was significantly increased in the first year (2.19; 1.26, 3.78) but not thereafter (0.99; 0.74, 1.32) (P = 0.02 for difference in HRs). First-year relapse hazard was high in digoxin-using women with ER+ tumors (2.51; 1.39, 4.55) but not ER- tumors (0.72; 0.10, 5.27). Recurrence hazard was not significantly changed among digoxin-using women also using tamoxifen.
Breast cancers arising in digoxin-using women had better prognostic features. After adjustment for markers, overall breast cancer relapse risk in digoxin users was not increased significantly, although recurrence hazards for ER+ tumors were higher in the first year following diagnosis.
Notes
Cites: Arch Surg. 2002 Sep;137(9):1015-9; discussion 1019-2112215151
Cites: JAMA. 2002 Jul 17;288(3):321-3312117397
Cites: Obes Rev. 2003 Aug;4(3):157-7312916817
Cites: J Natl Cancer Inst. 2003 Oct 1;95(19):1467-7614519753
Cites: Lancet. 2004 Feb 7;363(9407):453-514962527
Cites: Obstet Gynecol. 1995 Jan;85(1):11-77800305
Cites: Dan Med Bull. 1997 Sep;44(4):445-89377907
Cites: Lancet. 1997 Oct 11;350(9084):1047-5910213546
Cites: J Natl Cancer Inst. 2005 Apr 6;97(7):471-215812065
Cites: Br J Cancer. 2005 Aug 22;93(4):392-816106246
Cites: Acta Obstet Gynecol Scand. 2007;86(11):1342-5117963062
Cites: J Natl Cancer Inst. 2008 Apr 2;100(7):475-8218364505
Cites: Breast Cancer Res. 2008;10(6):R10219055760
Cites: Acta Oncol. 2008;47(4):506-2418465317
Cites: Cancer Epidemiol Biomarkers Prev. 2008 Apr;17(4):864-7118381475
Cites: Prim Care. 2009 Jun;36(2):271-8519501243
Cites: Breast Cancer Res Treat. 2010 Jan;119(1):145-5319731015
Cites: Oncologist. 2010;15(6):556-6520507889
Cites: Breast Cancer Res Treat. 2010 Oct;123(3):627-3520571870
Cites: J Clin Oncol. 2011 Jan 1;29(1):25-3121115856
Cites: Breast Cancer Res Treat. 2011 Apr;126(3):729-3820872242
Cites: Recent Pat Anticancer Drug Discov. 2011 May;6(2):237-4521247404
Cites: J Clin Oncol. 2011 Jun 1;29(16):2165-7021422417
Cites: J Steroid Biochem Mol Biol. 2011 May;125(1-2):13-2221335088
Cites: Clin Cancer Res. 2012 Apr 15;18(8):2133-722368159
Cites: J Clin Oncol. 2012 Apr 20;30(12):1268-7322393101
Cites: Int J Cancer. 2012 Aug 1;131(3):716-2121913187
Cites: Cancer. 2012 Dec 1;118(23):5937-4622926690
Cites: Basic Res Cardiol. 2002;97 Suppl 1:I19-2412479229
PubMed ID
23421975 View in PubMed
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