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5. Distinct mechanisms of resistance to fulvestrant treatment dictate level of ER independence and selective response to CDK inhibitors in metastatic breast cancer

Author

Kaminska K, Akrap N, Staaf J, Alves C, Ehinger A, Ebbesson A, Hedenfalk I, Beumers L, Veerla S, Harbst K, Ehmsen S, Borgquist S, Borg A, Perez-Fidalgo A, Ditzel H, Bosch A, and Honeth G

Subjects
Endocrine treatment resistance, Cell cycle inhibitors, Cyclin E2, Metastatic breast cancer, Fulvestrant
Abstract

Background Resistance to endocrine treatment in metastatic breast cancer is a major clinical challenge. Clinical tools to predict both drug resistance and possible treatment combination approaches to overcome it are lacking. This unmet need is mainly due to the heterogeneity underlying both the mechanisms involved in resistance development and breast cancer itself. Methods To study the complexity of the mechanisms involved in the resistance to the selective estrogen receptor degrader (SERD) fulvestrant, we performed comprehensive biomarker analyses using several in vitro models that recapitulate the heterogeneity of developed resistance. We further corroborated our findings in tissue samples from patients treated with fulvestrant. Results We found that different in vitro models of fulvestrant resistance show variable stability in their phenotypes, which corresponded with distinct genomic alterations. Notably, the studied models presented adaptation at different cell cycle nodes to facilitate progression through the cell cycle and responded differently to CDK inhibitors. Cyclin E2 overexpression was identified as a biomarker of a persistent fulvestrant-resistant phenotype. Comparison of pre- and post-treatment paired tumor biopsies from patients treated with fulvestrant revealed an upregulation of cyclin E2 upon development of resistance. Moreover, overexpression of this cyclin was found to be a prognostic factor determining resistance to fulvestrant and shorter progression-free survival. Conclusions These data highlight the complexity of estrogen receptor positive breast cancer and suggest that the development of diverse resistance mechanisms dictate levels of ER independence and potentially cross-resistance to CDK inhibitors.

Published
2021

7. Correction:VersicanV1 promotes proliferation and metastasis of hepatocellular carcinoma through the activation of EGFR–PI3K–AKT pathway (Oncogene, (2018), 37, 41, (5585-5586), 10.1038/s41388-018-0495-6)

Author

Elias, D., Vever, Henriette, Lænkholm, A. V., Gjerstorff, M. F., Yde, C. W., Lykkesfeldt, A. E., and Ditzel, H. J.

Abstract

Since the publication of this Erratum, the Authors noticed a further error in Fig. 1c. The same image was inserted twice next to each other (second row: PRKCA, image for RamR7 and TamR8) instead of the correct image for TamR8. The corrected Fig. 1c has been provided below.

Published
2020

11. Pathological chemotherapy response score is prognostic in tubo-ovarian high-grade serous carcinoma: A systematic review and meta-analysis of individual patient data

Author

Cohen, P. A., Powell, A., Bohm, S., Gilks, C. B., Stewart, C. J. R., Meniawy, T. M., Bulsara, M., Avril, S., Brockbank, E. C., Bosse, T., de Azevedo Focchi, G. R., Ganesan, R., Glasspool, R. M., Howitt, B. E., Kim, H. -S., Lee, J. -Y., Le, N. D., Lockley, M., Manchanda, R., Mandalia, T., Mccluggage, W. G., Mcneish, I., Midha, D., Srinivasan, R., Tan, Y. Y., van der Griend, R., Yunokawa, M., Zannoni, Gian Franco, Aggarwal, S., Bronger, H., Brown, E. B., Buck, M., Bukhari, S. A., Coghlan, E., Cope, N., de Almeida, M. S., De Kroon, C. D., Dean, A., Devlin, M. -J., Ditzel, H. M., Drecoll, E., Fagotti, Anna, Faruqi, A., Feeney, L., Gupta, K., Harley, I., Inzani, Frediano, Jeyarajah, A. R., Koay, M. H. E., Kroep, J. R., Leung, Y., Loft, A. R., Magee, D., Mckenna, S., Millan, D., Millar, J., Miller, R., Mohan, G. R., Mughal, S., Nicolau, S. M., Nevin, J., Oakley, A. S., Quigley, Michelle, Praitano, Barbara, Rajwanshi, A., Salfinger, S. G., Scambia, Giovanni, Scatchard, K., Schmalfeldt, B., Simcock, B., Singh, P., Strickland, K. C., Suri, V., Syed, S., Sykes, P., Tan, A., Tan, J., Thompson, E., Tinker, A. V., Trevisani, Gian Rolando, Uyeda, M. G. B. K., Vaughan, M. M., Weichert, W., Williams, A., Williams, S., Zorzato, P. C., Singh, Manprietkaur, Zannoni G. F. (ORCID:0000-0003-1809-129X), Fagotti A. (ORCID:0000-0001-5579-335X), Inzani F., Quigley M., Rai B., Scambia G. (ORCID:0000-0003-2758-1063), Trevisan G., Singh N., Cohen, P. A., Powell, A., Bohm, S., Gilks, C. B., Stewart, C. J. R., Meniawy, T. M., Bulsara, M., Avril, S., Brockbank, E. C., Bosse, T., de Azevedo Focchi, G. R., Ganesan, R., Glasspool, R. M., Howitt, B. E., Kim, H. -S., Lee, J. -Y., Le, N. D., Lockley, M., Manchanda, R., Mandalia, T., Mccluggage, W. G., Mcneish, I., Midha, D., Srinivasan, R., Tan, Y. Y., van der Griend, R., Yunokawa, M., Zannoni, Gian Franco, Aggarwal, S., Bronger, H., Brown, E. B., Buck, M., Bukhari, S. A., Coghlan, E., Cope, N., de Almeida, M. S., De Kroon, C. D., Dean, A., Devlin, M. -J., Ditzel, H. M., Drecoll, E., Fagotti, Anna, Faruqi, A., Feeney, L., Gupta, K., Harley, I., Inzani, Frediano, Jeyarajah, A. R., Koay, M. H. E., Kroep, J. R., Leung, Y., Loft, A. R., Magee, D., Mckenna, S., Millan, D., Millar, J., Miller, R., Mohan, G. R., Mughal, S., Nicolau, S. M., Nevin, J., Oakley, A. S., Quigley, Michelle, Praitano, Barbara, Rajwanshi, A., Salfinger, S. G., Scambia, Giovanni, Scatchard, K., Schmalfeldt, B., Simcock, B., Singh, P., Strickland, K. C., Suri, V., Syed, S., Sykes, P., Tan, A., Tan, J., Thompson, E., Tinker, A. V., Trevisani, Gian Rolando, Uyeda, M. G. B. K., Vaughan, M. M., Weichert, W., Williams, A., Williams, S., Zorzato, P. C., Singh, Manprietkaur, Zannoni G. F. (ORCID:0000-0003-1809-129X), Fagotti A. (ORCID:0000-0001-5579-335X), Inzani F., Quigley M., Rai B., Scambia G. (ORCID:0000-0003-2758-1063), Trevisan G., and Singh N.

Abstract

Objective: There is a need to develop and validate biomarkers for treatment response and survival in tubo-ovarian high-grade serous carcinoma (HGSC). The chemotherapy response score (CRS) stratifies patients into complete/near-complete (CRS3), partial (CRS2), and no/minimal (CRS1) response after neoadjuvant chemotherapy (NACT). Our aim was to review current evidence to determine whether the CRS is prognostic in women with tubo-ovarian HGSC treated with NACT. Methods: We established an international collaboration to conduct a systematic review and meta-analysis, pooling individual patient data from 16 sites in 11 countries. Patients had stage IIIC/IV HGSC, 3–4 NACT cycles and >6-months follow-up. Random effects models were used to derive combined odds ratios in the pooled population to investigate associations between CRS and progression free and overall survival (PFS and OS). Results: 877 patients were included from published and unpublished studies. Median PFS and OS were 15 months (IQR 5–65) and 28 months (IQR 7–92) respectively. CRS3 was seen in 249 patients (28%). The pooled hazard ratios (HR) for PFS and OS for CRS3 versus CRS1/CRS2 were 0·55 (95% CI, 0·45–0·66; P < 0·001) and 0·65 (95% CI 0·50–0·85, P = 0·002) respectively; no heterogeneity was identified (PFS: Q = 6·42, P = 0·698, I2 = 0·0%; OS: Q = 6·89, P = 0·648, I2 = 0·0%). CRS was significantly associated with PFS and OS in multivariate models adjusting for age and stage. Of 306 patients with known germline BRCA1/2 status, those with BRCA1/2 mutations (n = 80) were more likely to achieve CRS3 (P = 0·027). Conclusions: CRS3 was significantly associated with improved PFS and OS compared to CRS1/2. This validation of CRS in a real-world setting demonstrates it to be a robust and reproducible biomarker with potential to be incorporated into therapeutic decision-making and clinical trial design.

Published
2019

13. Editorial Acknowledgment

Author

Aarvak, T., Abedi-Valugerdi, M., Abrahamsen, T., Akdis, C., Akuffo, H.O., Alarcon-Riquelme, M., Andersen, P., Arstila, P., Austgulen, R., Baecker-Allan, C., Baggiolini, M., Baker, B.S., Bakke, O., Bakken, V., Barclay, A.N., Bemark, M., Benestad, H.B., Berzins, K., Bjerkvik, R., Bjørge, L., Bland, P., Bolstad, A.I., Born, W., Bowman, S., Brinchmann, J., Britton, S., Brokstad, K.A., Brunet, L.R., Bruserud, Ø., Cardona, P.J., Ceyppens, J.L., Cirino, G., Cohn, M., Cox, R.J., Cunliffe, J., Dahlgren, U., Dellacasagrande, J., Ditzel, H., Dobryszycka, E., Dyrhol-Riise, A.M., Edwards, J.C., Egeland, T., Elsayed, S., Eray, M., Erb, K.J., Esch, T., Eugen-Olsen, J., Everse, L.A., Fagerhol, M., Farstad, I., Feldmann, M., Fernandez, C., Fleck, M., Franksson, R., Freitas, A., Garred, P., Gidlund, M., Gilhus, N.E., Goldbach-Mansky, R., Gordon, J., Gordon, T., Grandien, A., Gregerson, P., Grewal, H., Hakulinen, J., Halstensen, T., Haneberg, B., Hanej, S.H.E., Hansen, T., Harley, J.B., Haukenes, G., Hengartner, H., Henz, B.M., Holen, E., Hurme, M., Husby, G., Husby, S., Hörnqvist-Hultgren, E., Haaheim, L.R., Isenberg, D., Jahnson, F., Jakobsen, H., James, J.A., Jansson, J.O., Jarva, H., Jeansson, S., Johannessen, A.C., Johansen, F.E., Julkunen, I., Kalland, K.H., Kaye, J., Kazatchkine, M., Kihlström, E., Kohler, L., Konttinen, Y., Kotenko, S., Koutzov, S., Krammer, P., Kristoffersen, E., Kunzendorf, U., Lachmann, P., Langman, R., Langner, J., Lanzavecchia, L., Lappalainen, M., Laskay, T., Lea, T., Lefvert, A.K., Lehmann, A.C., Louka, A, Lúdviksson, B.R., Mariette, X., Marion, T., Marker-Herrmann, E., Mattsson, R., McAdam, S., Mellbye, O.J., Mellgren, G., Mellgren, S.I., Mestecky, J., Michaelsen, T., Michalek, S., Miettinen, A., Moestrup, S.K., Moretta, A., Moser, M., Mountz, J., Moutsopoulos, H., Munthe, L.A., Mustafa, T., Myrmel, H., Nannemark, G., Netea, M.G., Nilsen, R., Notarangelo, L.D., Ögmundsdóttir, H., Olsson, I., Olweus, J., Osland, A., Paludan, S.R., Parsons, K.R., Patarroyo, M., Paul, W.E., Perlman, P., Pollock, J.M., Puolakkainen, M., Quale, A., Rajewsky, K., Raman, C., Reichlin, M., Renkonen, R., Rese Shadidi, K., Ricciardi-Castagnoli, P., Rickinson, A.B., Ringdén, O., Risto, R., Rodinov, D., Rosenkrands, I., Rottenberg, M., Russel, M., Rygaard, J., Rødahl, E., Röllinghof, M., Sandberg, M., Schenk, K., Seppälä, I., Shevach, E., Shortman, K., Siegrist, C.A., Sigurdardóttir, S., Silvennoinen, O., Sinigaglia, F., Sistonen, L., Skarstein, K., Skogh, T., Smith, E., Spurkland, A., Stendahl, O., Sugden, B., Suri-Payer, E., Svennerholm, A.M., Szodoray, P., Theofilopoulos, A., Thorley-Lawson, D.A., Timonen, T., Trowsdale, J., Tuomo, T., Ulmer, A.J., Ulvestad, E., Ulvik, R., Vaerman, J.P., van, der Merwe J.P., van Eden, W., Vedeler, C., Vintermyr, O.K., Vyse, J., Wahlgren, M., Wahren-Herlenius, M., Walsh, L.J., Weetman, A.P., Westermark, P., Wiker, H., Yang, J., Yewdell, J.W., Youinou, P., and Zouali, M.

Published
2002

14. Correction to:Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy (Oncogene, (2015), 34, 15, (1919-1927), 10.1038/onc.2014.138)

Author

Elias, D., Vever, H., Lænkholm, A. V., Gjerstorff, M. F., Yde, C. W., Lykkesfeldt, A. E., and Ditzel, H. J.

Abstract

Since the online publication of the above article, the authors have noted errors in subfigures 1c and 3b. Therefore, new images of the original immmunocytochemistry stainings have been obtained for Fig. 1c, and the Western blots for siRNA-mediated FYN knockdown in Fig. 3b were repeated. The amended versions of Figs. 1c and 3b are now provided.

Published
2018

17. Role of Miro1 adaptor protein in mitochondrial mobility between cancer and stromal cells

Author

Novák Jaromír, Nahacka Zuzana, Oliveira Gabriela, Brisudova Petra, Dvorakova Sarka, Dalecka Marketa, Puttrich Verena, Grycova Lenka, Stepanek Ludek, Zobalova Renata, Terp Mikkel, Lansky Zdenek, Oliveira Paulo, Ditzel Henrik, Berridge Michael, Rohlena Jakub, and Neuzil Jiri

Subjects
horizontal mitochondrial transfer, miro1, cancer, Microbiology, QR1-502, Physiology, QP1-981, Zoology, QL1-991
Published
2024
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18. SSX2-4 expression in early-stage non-small cell lung cancer

Author

Greve, K B V, Pøhl, M, Olsen, K E, Nielsen, O, Ditzel, H J, and Gjerstorff, M F

Subjects
Cancer/testis antigen, Immunotherapy, Lung cancer, SSX, respiratory tract diseases
Abstract

The expression of cancer/testis antigens SSX2, SSX3, and SSX4 in non-small cell lung cancers (NSCLC) was examined, since they are considered promising targets for cancer immunotherapy due to their immunogenicity and testis-restricted normal tissue expression. We characterized three SSX antibodies and performed immunohistochemical staining of 25 different normal tissues and 143 NSCLCs. The antibodies differed in binding to two distinctive splice variants of SSX2 that exhibited different subcellular staining patterns, suggesting that the two splice variants display different functions. SSX2-4 expression was only detected in 5 of 143 early-stage NSCLCs, which is rare compared to other cancer/testis antigens (e.g. MAGE-A and GAGE). However, further studies are needed to determine whether SSX can be used as a prognostic or predictive biomarker in NSCLC.

Published
2014

21. Limited SP17 expression within tumors diminishes its therapeutic potential

Author

Gjerstorff, M F and Ditzel, H J

Subjects
endocrine system
Abstract

In this study, we have investigated the expression of the tumor antigen sperm protein 17 (SP17) in a large panel of human cancers and compared it with the expression of two well-characterized families of tumor antigens, melanoma-associated antigen-A (MAGE-A) and G antigen (GAGE). We found that SP17 was expressed in many cancer types with an overall frequency of 12%. SP17 was most frequently expressed in a different set of cancer types than MAGE-A and GAGE antigens and rarely overlapped with these proteins. Importantly, SP17 expression was limited to a small number of scattered cancer cells in most positive tumors in contrast to MAGE-A and GAGE proteins, which were homogenously expressed in large foci. Our results suggest that SP17 may not be an optimal target for cancer vaccines.

Published
2012

23. Independent validation of Genomic Grade in the BIG 1-98 study

Author

Sotiriou, Christos, Ignatiadis, Michail, Desmedt, Christine, Abdel Azim, Hatem Hamdy, Veys, Isabelle, Larsimont, Denis, Lyng, M, Viale, Giuseppe, Leyland-Jones, Brian, Ditzel, H, Giobbie-Hurder, Anita, Regan, Meredith, Piccart-Gebhart, Martine, Michiels, Stefan, Sotiriou, Christos, Ignatiadis, Michail, Desmedt, Christine, Abdel Azim, Hatem Hamdy, Veys, Isabelle, Larsimont, Denis, Lyng, M, Viale, Giuseppe, Leyland-Jones, Brian, Ditzel, H, Giobbie-Hurder, Anita, Regan, Meredith, Piccart-Gebhart, Martine, and Michiels, Stefan

Abstract

General Session 4 - Oral Abstract S4-4, info:eu-repo/semantics/published

Published
2012

24. Independent validation of Genomic Grade in the BIG 1-98 study.

Author

San Antonio Breast Cancer Symposium (December 6, 2012: San Antonio, TX, USA), Sotiriou, Christos, Ignatiadis, Michail, Desmedt, Christine, Abdel Azim, Hatem Hamdy, Veys, Isabelle, Larsimont, Denis, Lyng, M, Viale, G, Leyland-Jones, Brian, Ditzel, H, Giobbie-Hurder, Anita, Regan, Meredith, Piccart-Gebhart, Martine, Michiels, Stefan, San Antonio Breast Cancer Symposium (December 6, 2012: San Antonio, TX, USA), Sotiriou, Christos, Ignatiadis, Michail, Desmedt, Christine, Abdel Azim, Hatem Hamdy, Veys, Isabelle, Larsimont, Denis, Lyng, M, Viale, G, Leyland-Jones, Brian, Ditzel, H, Giobbie-Hurder, Anita, Regan, Meredith, Piccart-Gebhart, Martine, and Michiels, Stefan

Abstract

info:eu-repo/semantics/nonPublished

Published
2012

27. Abstract S4-4: Independent validation of Genomic Grade in the BIG 1-98 study

Author

Sotiriou, C, primary, Ignatiadis, M, additional, Desmedt, C, additional, Azim, Jr HA, additional, Veys, I, additional, Larsimont, D, additional, Lyng, M, additional, Viale, G, additional, Leyland-Jones, B, additional, Ditzel, H, additional, Giobbie-Hurder, A, additional, Regan, M, additional, Piccart, M, additional, and Michiels, S, additional

Published
2012
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