liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Waltersson, Marie
Alternative names
Publications (10 of 15) Show all publications
Chow, J. A., Törnros, M. E., Waltersson, M., Richard, H., Kusoffsky, M., Lundström, C. & Kurti, A. (2017). A Design Study Investigating Augmented Reality and Photograph Annotation in a Digitalized Grossing Workstation. Journal of Pathology Informatics, 8(31)
Open this publication in new window or tab >>A Design Study Investigating Augmented Reality and Photograph Annotation in a Digitalized Grossing Workstation
Show others...
2017 (English)In: Journal of Pathology Informatics, ISSN 2229-5089, E-ISSN 2153-3539, Vol. 8, no 31Article in journal (Refereed) Published
Abstract [en]

Context: Within digital pathology, digitalization of the grossing procedure has been relatively underexplored in comparison to digitalization of pathology slides. 

Aims: Our investigation focuses on the interaction design of an augmented reality gross pathology workstation and refining the interface so that information and visualizations are easily recorded and displayed in a thoughtful view. 

Settings and Design: The work in this project occurred in two phases: the first phase focused on implementation of an augmented reality grossing workstation prototype while the second phase focused on the implementation of an incremental prototype in parallel with a deeper design study. 

Subjects and Methods: Our research institute focused on an experimental and “designerly” approach to create a digital gross pathology prototype as opposed to focusing on developing a system for immediate clinical deployment. 

Statistical Analysis Used: Evaluation has not been limited to user tests and interviews, but rather key insights were uncovered through design methods such as “rapid ethnography” and “conversation with materials”. 

Results: We developed an augmented reality enhanced digital grossing station prototype to assist pathology technicians in capturing data during examination. The prototype uses a magnetically tracked scalpel to annotate planned cuts and dimensions onto photographs taken of the work surface. This article focuses on the use of qualitative design methods to evaluate and refine the prototype. Our aims were to build on the strengths of the prototype's technology, improve the ergonomics of the digital/physical workstation by considering numerous alternative design directions, and to consider the effects of digitalization on personnel and the pathology diagnostics information flow from a wider perspective. A proposed interface design allows the pathology technician to place images in relation to its orientation, annotate directly on the image, and create linked information. 

Conclusions: The augmented reality magnetically tracked scalpel reduces tool switching though limitations in today's augmented reality technology fall short of creating an ideal immersive workflow by requiring the use of a monitor. While this technology catches up, we recommend focusing efforts on enabling the easy creation of layered, complex reports, linking, and viewing information across systems. Reflecting upon our results, we argue for digitalization to focus not only on how to record increasing amounts of data but also how these data can be accessed in a more thoughtful way that draws upon the expertise and creativity of pathology professionals using the systems.

Place, publisher, year, edition, pages
Medknow Publications, 2017
Keywords
Augmented reality; design methods; gross pathology; human–computer interaction; interface design; visualization
National Category
Media Engineering
Identifiers
urn:nbn:se:liu:diva-145037 (URN)10.4103/jpi.jpi_13_17 (DOI)28966831 (PubMedID)
Available from: 2018-02-08 Created: 2018-02-08 Last updated: 2018-05-07Bibliographically approved
Lundström, C., Waltersson, M., Persson, A. & Treanor, D. (2016). Summary of third Nordic symposium on digital pathology. Journal of Pathology Informatics, 7(12)
Open this publication in new window or tab >>Summary of third Nordic symposium on digital pathology
2016 (English)In: Journal of Pathology Informatics, ISSN 2229-5089, E-ISSN 2153-3539, Vol. 7, no 12Article in journal, Editorial material (Other academic) Published
Abstract [en]

Cross-disciplinary and cross-sectorial collaboration is a key success factor for turning the promise of digital pathology into actual clinical benefits. The Nordic symposium on digital pathology (NDP) was created to promote knowledge exchange in this area, among stakeholders in health care, industry, and academia. This article is a summary of the third NDP symposium in Linkφping, Sweden. The Nordic experiences, including several hospitals using whole-slide imaging for substantial parts of their primary reviews, formed a fertile base for discussions among the 190 NDP attendees originating from 15 different countries. This summary also contains results from a survey on adoption and validation aspects of clinical digital pathology use.

Place, publisher, year, edition, pages
Medknow Publications, 2016
Keywords
Implementation; pathology informatics; validation
National Category
Other Medical Engineering Human Computer Interaction
Identifiers
urn:nbn:se:liu:diva-130542 (URN)10.4103/2153-3539.179902 (DOI)27141318 (PubMedID)2-s2.0-85009253042 (Scopus ID)
Funder
VINNOVA, 2012-01121
Available from: 2016-08-15 Created: 2016-08-15 Last updated: 2018-01-10Bibliographically approved
Lundström, C., Thorstenson, S., Waltersson, M., Persson, A. & Treanor, D. (2015). Summary of 2nd Nordic symposium on digital pathology. Journal of Pathology Informatics, 6
Open this publication in new window or tab >>Summary of 2nd Nordic symposium on digital pathology
Show others...
2015 (English)In: Journal of Pathology Informatics, ISSN 2229-5089, E-ISSN 2153-3539, Vol. 6Article in journal, Editorial material (Refereed) Published
Abstract [en]

Techniques for digital pathology are envisioned to provide great benefits in clinical practice, but experiences also show that solutions must be carefully crafted. The Nordic countries are far along the path toward the use of whole-slide imaging in clinical routine. The Nordic Symposium on Digital Pathology (NDP) was created to promote knowledge exchange in this area, between stakeholders in health care, industry, and academia. This article is a summary of the NDP 2014 symposium, including conclusions from a workshop on clinical adoption of digital pathology among the 144 attendees.

Place, publisher, year, edition, pages
Medknow Publications, 2015
National Category
Other Medical Engineering
Identifiers
urn:nbn:se:liu:diva-118879 (URN)10.4103/2153-3539.151889 (DOI)25774316 (PubMedID)
Funder
VINNOVA
Available from: 2015-06-04 Created: 2015-06-04 Last updated: 2017-12-04
Perez-Tenorio, G., Karlsson, E., Ahnström, M., Olsson, B., Holmlund, B., Nordenskjöld, B., . . . Stål, O. (2011). Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer. Breast Cancer Research and Treatment, 128(3), 713-723
Open this publication in new window or tab >>Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer
Show others...
2011 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 128, no 3, p. 713-723Article in journal (Refereed) Published
Abstract [en]

The mammalian target of rapamycin (mTOR) and its substrates S6K1 and S6K2 regulate cell growth, proliferation, and metabolism through translational control. RPS6KB1 (S6K1) and RPS6KB2 (S6K2) are situated in the commonly amplified 17q21-23 and 11q13 regions. S6K1 amplification and protein overexpression have earlier been associated with a worse outcome in breast cancer, but information regarding S6K2 is scarce. The aim of this study was to evaluate the prognostic and treatment predictive relevance of S6K1/S6K2 gene amplification, as well as S6K2 protein expression in breast cancer. S6K1/S6K2 gene copy number was determined by real-time PCR in 207 stage II breast tumors and S6K2 protein expression was investigated by immunohistochemistry in 792 node-negative breast cancers. S6K1 amplification/gain was detected in 10.7%/21.4% and S6K2 amplification/gain in 4.3%/21.3% of the tumors. S6K2 protein was detected in the nucleus (38%) and cytoplasm (76%) of the tumor cells. S6K1 amplification was significantly associated with HER2 gene amplification and protein expression. S6K2 amplification correlated significantly with high S6K2 mRNA levels, ER+ status and CCND1 amplification. S6K1 and S6K2 gene amplification was associated with a worse prognosis independent of HER2 and CCND1. S6K2 gain and nuclear S6K2 expression was related to an improved benefit from tamoxifen among patients with ER+, respectively ER+/PgR+ tumors. In the ER+/PgR- subgroup, nuclear S6K2 rather indicated decreased tamoxifen responsiveness. S6K1 amplification predicted reduced benefit from radiotherapy. This is the first study showing that S6K2 amplification and overexpression, like S6K1 amplification, have prognostic and treatment predictive significance in breast cancer.

Place, publisher, year, edition, pages
Springer Science Business Media, 2011
Keywords
mTOR; S6 kinase; 17q21-23; 11q13; Gene amplification; Tamoxifen response
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-69784 (URN)10.1007/s10549-010-1058-x (DOI)000292557100013 ()
Note
The original publication is available at www.springerlink.com: Gizeh Perez-Tenorio, Elin Karlsson, Marie Ahnström, Birgit Olsson, Birgitta Holmlund, Bo Nordenskjöld, Tommy Fornander, Lambert Skoog and Olle Stål, Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer, 2011, Breast Cancer Research and Treatment, (128), 3, 713-723. http://dx.doi.org/10.1007/s10549-010-1058-x Copyright: Springer Science Business Media http://www.springerlink.com/Available from: 2011-08-10 Created: 2011-08-08 Last updated: 2017-12-08
Karlsson, E., Ahnström, M., Bostner, J., Perez-Tenorio, G., Olsson, B., Hallbeck, A.-L. & Stål, O. (2011). High-Resolution Genomic Analysis of the 11q13 Amplicon in Breast Cancers Identifies Synergy with 8p12 Amplification, Involving the mTOR Targets S6K2 and 4EBP1. Genes, Chromosomes and Cancer, 50(10), 775-787
Open this publication in new window or tab >>High-Resolution Genomic Analysis of the 11q13 Amplicon in Breast Cancers Identifies Synergy with 8p12 Amplification, Involving the mTOR Targets S6K2 and 4EBP1
Show others...
2011 (English)In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 50, no 10, p. 775-787Article in journal (Refereed) Published
Abstract [en]

The chromosomal region 11q13 is amplified in 15-20% of breast cancers; an event not only associated with estrogen receptor (ER) expression but also implicated in resistance to endocrine therapy. Coamplifications of the 11q13 and 8p12 regions are common, suggesting synergy between the amplicons. The aim was to identify candidate oncogenes in the 11q13 region based on recurrent amplification patterns and correlations to mRNA expression levels. Furthermore, the 11q13/8p12 coamplification and its prognostic value, was evaluated at the DNA and the mRNA levels. Affymetrix 250K NspI arrays were used for whole-genome screening of DNA copy number changes in 29 breast tumors. To identify amplicon cores at 11q13 and 8p12, genomic identification of significant targets in cancer (GISTIC) was applied. The mRNA expression levels of candidate oncogenes in the amplicons [ RAD9A, RPS6KB2 (S6K2), CCND1, FGF19, FGF4, FGF3, PAK1, GAB2 (11q13); EIF4EBP1 (4EBP1), PPAPDC1B, and FGFR1 (8p12)] were evaluated using real-time PCR. Resulting data revealed three main amplification cores at 11q13. ER expression was associated with the central 11q13 amplification core, encompassing CCND1, whereas 8p12 amplification/gene expression correlated to S6K2 in a proximal 11q13 core. Amplification of 8p12 and high expression of 4EBP1 or FGFR1 was associated with a poor outcome in the group. In conclusion, single nucleotide polymorphism arrays have enabled mapping of the 11q13 amplicon in breast tumors with high resolution. A proximal 11q13 core including S6K2 was identified as involved in the coamplification/coexpression with 8p12, suggesting synergy between the mTOR targets S6K2 and 4EBP1 in breast cancer development and progression.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2011
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-70514 (URN)10.1002/gcc.20900 (DOI)000294177300003 ()
Note

Funding Agencies|Swedish Cancer Foundation||Swedish Research Council||

Available from: 2011-09-12 Created: 2011-09-12 Last updated: 2017-12-08
Ahnström, M., Askmalm Stenmark, M., Nordenskjöld, B., Fornander, T., Skoog, L. & Stål, O. (2009). Altered expression of cyclin E and the retinoblastoma protein influences the effect of adjuvant therapy in breast cancer. International Journal of Oncology, 34(2), 441-448
Open this publication in new window or tab >>Altered expression of cyclin E and the retinoblastoma protein influences the effect of adjuvant therapy in breast cancer
Show others...
2009 (English)In: International Journal of Oncology, ISSN 1019-6439, Vol. 34, no 2, p. 441-448Article in journal (Refereed) Published
Abstract [en]

Cyclin E and the retinoblastoma protein (Rb) are both important regulators of the G(1) phase in the cell cycle. Overexpression of cyclin E and lost expression of Rb has previously been observed in breast tumours at frequencies of 10-50% and 20-30%, respectively. We explored the prognostic role of cyclin E and Rb in breast cancer patients randomised for tamoxifen (TAM), CMF (cyclophosphamide, metotrexate, 5-fluorouracil) chemotherapy and radiotherapy (RT) and how their expression affects the patients response to treatment. Protein expression was assessed with immunohistochemistry. We found overexpression of cyclin E in 32.1% (71/221) of the tumours and loss of Rb expression in 25.0% (59/236). Increased expression of cyclin E correlated to dysfunctional p53 (P=0.003) while loss of Rb correlated to normal p53 status (P=0.001). Our results suggest that patients with high cyclin E tumours have less benefit from tamoxifen (ER+, TAM vs. no TAM; RR=0.97; 95% CI, 0.36-2.60) than patients whose tumours show low expression (ER+, TAM vs. no TAM; RR =0.41; 95% CI, 0.24-0.72). Cyclin E also tended to predict the benefit from radiotherapy with a local recurrence rate of 0.31 (RT vs. CMF; 95% CI, 0.12-0.93) for patients with low expression and 0.68 (RT vs. CMF; 95% CI, 0.2-2.32) for patients with high expression of cyclin E. When the p53 status was taken in consideration the results showed that patients with both normal p53 and normal Rb expression had considerably lower locoregional recurrence rate when treated with radiotherapy instead of CMF (RR=0.17; 95% CI, 0.052-0.58) as compared to patients with either altered Rb or p53 or both (RR=0.70; 95% CI, 0.28-1.73).

Keywords
cell cycle, radiotherapy, chemotherapy, overexpression, Rb, p53
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-16619 (URN)10.3892/ijo_00000168 (DOI)
Available from: 2009-02-07 Created: 2009-02-06 Last updated: 2017-12-14Bibliographically approved
Ahnström Waltersson, M. (2009). Cell cycle alterations and 11q13 amplification in breast cancer: prediction of adjuvant treatment response. (Doctoral dissertation). Linköping: Linköping University Electronic Press
Open this publication in new window or tab >>Cell cycle alterations and 11q13 amplification in breast cancer: prediction of adjuvant treatment response
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The growth and development of the breast is to a large extent regulated by oestrogens through the oestrogen receptor (ER). Activation of the ERα triggers transcription of genes that are important for cell proliferation and stimulates entry into the G1 phase of the cell cycle. In breast cancer the ERα is often upregulated and is therefore a suitable target for adjuvant therapies such as tamoxifen. Although tamoxifen is an effective treatment in most cases, tumours sometimes acquire resistance to the drug. The aim of this thesis was to investigate the impact of G1 phase proteins and 11q13 amplification on prognosis and treatment response in breast cancer. The material used was from a clinical trial in which postmenopausal breast cancer patients were randomised to chemotherapy or radiotherapy and tamoxifen or no adjuvant treatment. We studied the expression of cyclin D1, cyclin E and Rb with immunohisochemistry and amplification of CCND1 and PAK1 with real time PCR. We found that among patients with high tumour expression of cyclin D1, overexpression of ErbB2 was associated with reduced recurrence-free survival. Both cyclin D1 and cyclin E overexpression were associated with reduced tamoxifen response. High expression of cyclin D1 has been found to induce ligand independent activation of ERα in breast cancer cells and might also switch tamoxifen from acting as an antagonist to an agonist. Overexpression of cyclin E has been shown to be associated with expression of low molecular weight isoforms of the protein that possess an increased kinase activity and are insensitive to p21 and p27 inhibition. Furthermore, amplification of 11q13, and in particular the gene PAK1, was a strong predictor of tamoxifen resistance. The pak1 protein is involved in phosphorylation and ligand independent activation of the ERα. We also found that lost expression of either p53 or Rb reduced the patients benefit from radiotherapy compared with patients with normal expression of both proteins. Normally, ionizing radiation upregulates p53 resulting in G1 arrest or apoptosis. If either functional p53 or Rb is missing the cells can proceed from G1 to the S phase despite damaged DNA. The expression of the microRNA, miR-206, was analysed with real time PCR, and the results showed that high expression of miR-206 correlated to low expression of ERα and 11q13 amplification. In vitro studies have shown that miR-206 negatively regulates the expression of ERα. Taken together the G1 regulators and amplification of 11q13 seem to have an important role in predicting the patient’s response to adjuvant therapy.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2009. p. 68
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1102
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-17458 (URN)978-91-7393-690-3 (ISBN)
Public defence
2009-04-17, Linden, Hälsouniversitetet, Campus HU, Linköpings universitet, Linköping, 09:00 (Swedish)
Opponent
Supervisors
Available from: 2009-03-25 Created: 2009-03-25 Last updated: 2009-08-21Bibliographically approved
Perez-Tenorio, G., Karlsson, E., Ahnström Waltersson, M., Olsson, B., Holmlund, B., Nordenskjöld, B., . . . Stål, O. (2008). Clinical Value of RPS6KB1 and RPS6KB2 Gene Amplification in Postmenopausal Breast Cancer.
Open this publication in new window or tab >>Clinical Value of RPS6KB1 and RPS6KB2 Gene Amplification in Postmenopausal Breast Cancer
Show others...
2008 (English)Article in journal (Refereed) Submitted
Abstract [en]

The mammalian target of rapamycin (mTOR) and its substrates the ribosomal S6 kinases (S6K)1 and 2 integrate nutrient and hormonal/growth factor mediated signals and are implicated indiabetes, obesity and cancer. The genes encoding S6K1 (RPS6KB1) and S6K2 (RPS6KB2) aresituated close to well known amplicons but information regarding its expression and clinicalvalue is scarce. In this study we quantified RPS6KB1/2 gene copy number, establishedassociations with other clinical factors and explored their clinical value in breast cancer. RPS6KB1/2 copy number was determined by fast real-time PCR in 207 breast tumors.RPS6KB1 was amplified (≥ 4 copies) in 10.7% (22/206) and RPS6KB2 in 4.3% (9/207) of thetumors. Amplification of RPS6KB1 was associated with HER2 gene amplification (P=0.025)and protein expression (P=0.014) while RPS6KB2 correlated with ER+ status (P=0.046) and CCND1 amplification (P<0.00001). In a multivariate analysis, both genes were independentprognostic factors indicating higher risk to develop recurrences. In terms of loco regionalcontrol, amplification of the RPS6KB1 gene predicted less response to radiotherapy (P=0.035) while RPS6KB2 gene copy gain (≥ 3 copies) indicated increased benefit from tamoxifen (P=0.03) among ER+ patients. S6K1/2 gene amplification could be used as an indicator oftherapy response among postmenopausal breast cancer patients.

Keywords
PI3K, AKT, mTOR, CCND1, HER2, ER, Tamoxifen
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-15042 (URN)
Available from: 2008-10-13 Created: 2008-10-13 Last updated: 2009-04-09
Bostner, J., Ahnström Waltersson, M., Fornander, T., Skoog, L., Nordenskjöld, B. & Stål, O. (2007). Amplification of CCND1 and PAK1 as predictors of recurrence and tamoxifen resistance in postmenopausal breast cancer.. Oncogene, 26(49), 6997-7005
Open this publication in new window or tab >>Amplification of CCND1 and PAK1 as predictors of recurrence and tamoxifen resistance in postmenopausal breast cancer.
Show others...
2007 (English)In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 26, no 49, p. 6997-7005Article in journal (Refereed) Published
Abstract [en]

The 11q13 region is amplified in approximately 15% of all breast tumors. Situated in this region are the cyclin D1 gene (CCND1) and the p-21-activated kinase 1 (PAK1) gene. Both genes encode proteins shown to activate the estrogen receptor (ER), leading to transcription of CCND1 and other ER-responsive genes. Here, we investigate the prognostic and treatment predictive role of CCND1 and PAK1 gene amplification in postmenopausal breast cancer patients randomized to tamoxifen treatment or no adjuvant treatment. Amplification of CCND1 and PAK1, assessed by real-time PCR, was observed in 12.5 and 9.3%, respectively. Amplification of PAK1 was seen in 37% of the CCND1-amplified tumors, indicating coamplification (P<0.001). In ER-positive patients, amplification of at least one of the genes indicated a reduced recurrence-free survival (P=0.025). When response to tamoxifen treatment was analysed, patients with PAK1 amplification showed decreased benefit from the drug (ER+; relative risk ratio (RR)=1.62; 95% confidence interval (CI), 0.47-5.55) compared to patients without amplification (ER+; RR=0.53; 95% CI, 0.32-0.88). This was not evident for CCND1 amplification. We show that PAK1 may be a predictor of tamoxifen resistance and furthermore, we do not discard PAK1 as a potential candidate oncogene in the 11q13 amplicon. In addition, we show that high pak1 protein levels may predict tamoxifen insensitivity.

Keywords
Cyclin D1, pak1, drug resistance, breast cancer, real-time PCR
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-17456 (URN)10.1038/sj.onc.1210506 (DOI)17486065 (PubMedID)
Available from: 2009-03-25 Created: 2009-03-25 Last updated: 2017-12-13Bibliographically approved
Yu, Q., Sicinska, E., Geng, Y., Ahnström, M., Zagozdzon, A., Kong, Y., . . . Sicinski, P. (2006). Requirement for CDK4 kinase function in breast cancer. Cancer Cell, 9(1), 23-32
Open this publication in new window or tab >>Requirement for CDK4 kinase function in breast cancer
Show others...
2006 (English)In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 9, no 1, p. 23-32Article in journal (Refereed) Published
Abstract [en]

Cyclin D1 is overexpressed in the majority of human breast cancers. We previously found that mice lacking cyclin D1 are resistant to mammary carcinomas triggered by the ErbB-2 oncogene. In this study, we investigated which function of cyclin D1 is required for ErbB-2-driven mammary oncogenesis. We report that the ability of cyclin D1 to activate cyclin-dependent kinase CDK4 underlies the critical role for cyclin D1 in breast cancer formation. We also found that the continued presence of CDK4-associated kinase activity is required to maintain breast tumorigenesis. We analyzed primary human breast cancers and found high cyclin D1 levels in a subset (∼25%) of ErbB-2-overexpressing tumors. We propose that this subset of breast cancer patients might benefit from inhibiting CDK4 kinase.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-36168 (URN)10.1016/j.ccr.2005.12.012 (DOI)30325 (Local ID)30325 (Archive number)30325 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13
Organisations

Search in DiVA

Show all publications