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1. The tale of TILs in breast cancer: A report from The International Immuno-Oncology Biomarker Working Group

Author

Khalid El Bairi, Harry R. Haynes, Elizabeth Blackley, Susan Fineberg, Jeffrey Shear, Sophia Turner, Juliana Ribeiro de Freitas, Daniel Sur, Luis Claudio Amendola, Masoumeh Gharib, Amine Kallala, Indu Arun, Farid Azmoudeh-Ardalan, Luciana Fujimoto, Luz F. Sua, Shi-Wei Liu, Huang-Chun Lien, Pawan Kirtani, Marcelo Balancin, Hicham El Attar, Prerna Guleria, Wenxian Yang, Emad Shash, I-Chun Chen, Veronica Bautista, Jose Fernando Do Prado Moura, Bernardo L. Rapoport, Carlos Castaneda, Eunice Spengler, Gabriela Acosta-Haab, Isabel Frahm, Joselyn Sanchez, Miluska Castillo, Najat Bouchmaa, Reena R. Md Zin, Ruohong Shui, Timothy Onyuma, Wentao Yang, Zaheed Husain, Karen Willard-Gallo, An Coosemans, Edith A. Perez, Elena Provenzano, Paula Gonzalez Ericsson, Eduardo Richardet, Ravi Mehrotra, Sandra Sarancone, Anna Ehinger, David L. Rimm, John M. S. Bartlett, Giuseppe Viale, Carsten Denkert, Akira I. Hida, Christos Sotiriou, Sibylle Loibl, Stephen M. Hewitt, Sunil Badve, William Fraser Symmans, Rim S. Kim, Giancarlo Pruneri, Shom Goel, Prudence A. Francis, Gloria Inurrigarro, Rin Yamaguchi, Hernan Garcia-Rivello, Hugo Horlings, Said Afqir, Roberto Salgado, Sylvia Adams, Marleen Kok, Maria Vittoria Dieci, Stefan Michiels, Sandra Demaria, Sherene Loi, and The International Immuno-Oncology Biomarker Working Group

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract The advent of immune-checkpoint inhibitors (ICI) in modern oncology has significantly improved survival in several cancer settings. A subgroup of women with breast cancer (BC) has immunogenic infiltration of lymphocytes with expression of programmed death-ligand 1 (PD-L1). These patients may potentially benefit from ICI targeting the programmed death 1 (PD-1)/PD-L1 signaling axis. The use of tumor-infiltrating lymphocytes (TILs) as predictive and prognostic biomarkers has been under intense examination. Emerging data suggest that TILs are associated with response to both cytotoxic treatments and immunotherapy, particularly for patients with triple-negative BC. In this review from The International Immuno-Oncology Biomarker Working Group, we discuss (a) the biological understanding of TILs, (b) their analytical and clinical validity and efforts toward the clinical utility in BC, and (c) the current status of PD-L1 and TIL testing across different continents, including experiences from low-to-middle-income countries, incorporating also the view of a patient advocate. This information will help set the stage for future approaches to optimize the understanding and clinical utilization of TIL analysis in patients with BC.

Published
2021
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2. Spatial immunophenotypes predict response to anti-PD1 treatment and capture distinct paths of T cell evasion in triple negative breast cancer

Author

Dora Hammerl, John W. M. Martens, Mieke Timmermans, Marcel Smid, Anita M. Trapman-Jansen, Renée Foekens, Olga I. Isaeva, Leonie Voorwerk, Hayri E. Balcioglu, Rebecca Wijers, Iris Nederlof, Roberto Salgado, Hugo Horlings, Marleen Kok, and Reno Debets

Subjects
Science
Abstract

Only a subset of triple negative breast cancer patients respond to immunotherapy. Here, the authors analysed spatial immune contextures, which can be captured by a gene classifier, in relation to genomic alterations, mechanisms of T cell evasion and response to anti-PD1 treatment.

Published
2021
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3. Abstract P3-06-01: Unleashing NK- and CD8 T cells by combining monalizumab (anti-NKG2A) and trastuzumab for metastatic HER2+ breast cancer: first results MIMOSA trial

Author

Veerle Geurts, Leonie Voorwerk, Karolina Sikorska, Roberto Salgado, Koen van de Vijver, Marloes van Dongen, Inge Kemper, Ingrid A. Mandjes, Martine Heuver-mes, John Haanen, Gabe S. Sonke, Hugo Horlings, and Marleen Kok

Subjects
Cancer Research, Oncology
Abstract

Background Although treatment options and survival of HER2+ metastatic breast cancer (MBC) patients have greatly improved, the majority of MBC-patients still die of this disease. The relatively high levels of TILs observed in this BC subtype provide a rationale for immunomodulatory strategies, however, PD1-blockade has only shown modest response rates in this setting. While PD-1 blockade mainly acts on T cells, monalizumab targets the inhibitory immune checkpoint NKG2A which interacts with HLA-E on tumor cells, thereby unleashing NK- as well as CD8 T cells. We hypothesize that monalizumab can promote antibody-dependent cell-mediated cytotoxicity (ADCC) which is critical for trastuzumab efficacy. Clinical activity was shown in patients with head and neck cancer when monalizumab was combined with cetuximab (anti-EGFR). Here, we present the first results of the MIMOSA-trial investigating the efficacy of the novel combination monalizumab and trastuzumab in patients with HER2+ MBC. Methods In the phase II MIMOSA-trial (NTC04307329), HER2+ MBC patients were treated biweekly with 4mg/kg trastuzumab and 750mg monalizumab. Key eligibility criteria were progressive disease despite anti-HER2 therapy, had received a minimum of one and a maximum of three lines of palliative chemotherapy, had measurable disease according to RECIST1.1, and a serum LDH-level below 500U/L. Primary endpoint was objective response rate according to RECIST1.1. Secondary endpoints included clinical benefit rate (complete response CR, partial response PR or stable disease SD for at least 6 months) according to RECIST1.1, progression-free survival, overall survival and safety. Dose-limiting toxicities were continuously monitored throughout the trial and evaluated using a pre-defined Pocock-type boundary rule. Following a Simon’s two-stage design, 11 patients were included in stage I of the trial. If two or more responders were observed, further exploration is warranted in stage II. Results Between January 2021 and April 2022, eleven women of which ten are currently evaluable were enrolled in the trial. Patients received a median of two lines of prior treatment for MBC, of which 6 out of 11 patients were treated with trastuzumab emtansine (T-DM1). The majority of patients had hormone receptor positive BC (72% of the patients) and had low levels of tumor-infiltrating lymphocytes (TILs) with a median of 1% (ranging from 1% to 20%). Patients received a median of four cycles of trastuzumab and monalizumab. Treatment was well tolerated with no dose-limiting toxicities. No objective responses were observed in the first ten out of eleven evaluable patients. Therefore, MIMOSA stage I did not meet its primary endpoint, leading to discontinuation of the trial. Conclusions The novel combination of trastuzumab and monalizumab did not induce objective responses in heavily pre-treated HER2+ MBC patients. Citation Format: Veerle Geurts, Leonie Voorwerk, Karolina Sikorska, Roberto Salgado, Koen van de Vijver, Marloes van Dongen, Inge Kemper, Ingrid A. Mandjes, Martine Heuver-mes, John Haanen, Gabe S. Sonke, Hugo Horlings, Marleen Kok. Unleashing NK- and CD8 T cells by combining monalizumab (anti-NKG2A) and trastuzumab for metastatic HER2+ breast cancer: first results MIMOSA trial [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P3-06-01.

Published
2023
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4. Supplemental Methods, Supplemental Tables 1-2, Supplemental Figures 1-4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium

Author

Hongxin Zhang, Ahmet Zehir, Emily Yu, Thomas V. Yu, Celeste Yu, Stuart Watt, Chetna Wathoo, Lucy L. Wang, Emile E. Voest, Carl Virtanen, Victor E. Velculescu, Harm van Tinteren, Tony van de Velde, Laura J. Van 'T Veer, Eliezer M. Van Allen, Stacy B. Thomas, Jelle J. ten Hoeve, Barry S. Taylor, Shawn M. Sweeney, Thomas P. Stricker, Natalie H. Stickle, Parin Sripakdeevong, Jean Charles Soria, Gabe S. Sonke, David B. Solit, Lillian L. Siu, Priyanka Shivdasani, Kenna R Mills Shaw, Nikolaus Schultz, Deborah Schrag, Charles L. Sawyers, Mark J. Routbort, Barrett J. Rollins, Brendan Reardon, Trevor J. Pugh, Ben Ho Park, John A. Orechia, Larsson Omberg, Petra M. Nederlof, Nathanael D. Moore, Gordon Mills, Clinton Miller, Christine M. Micheel, Funda Meric-Bernstam, Gerrit A. Meijer, David S. Maxwell, Ian Maurer, Laura E. MacConaill, Zhibin Lu, David Liu, James Lindsay, Neal I. Lindeman, Mia A. Levy, Eva M. Lepisto, Michele L. LeNoue-Newton, Céline Lefebvre, Marc Ladanyi, Ritika Kundra, Priti Kumari, Walter Kinyua, Cyriac Kandoth, Suzanne Kamel-Reid, David M. Hyman, Jan Hudeček, Hugo Horlings, Stephanie Hintzen, Zachary J. Heins, Justin Guinney, Benjamin E. Gross, Christopher D. Gocke, Stu Gardos, Francisco Garcia, Jianjiong Gao, P. Andrew Futreal, Matthew D. Ducar, Raymond N. DuBois, Semih Dogan, Catherine Del Vecchio Fitz, Nancy E. Davidson, Kristen K. Dang, Debyani Chakravarty, Ethan Cerami, Fabien Calvo, Mariska Bierkens, Michael F. Berger, Philippe L. Bedard, José Baselga, Alexander S. Baras, Monica Arnedos, and Fabrice André

Abstract

Supplemental Methods. Supplemental Table 1: ââ,¬â€¹Genomic Data Characterization by Center. Supplemental Table 2: ââ,¬â€¹Gene Panels Submitted by Each Center. Figure S1: Number of putative germline SNPs per sample, before and after uniform germline filtering. Figure S2ââ,¬â€¹. Distribution of total somatic mutation burden per sample stratified by sequencing panel. Figure S3: ââ,¬â€¹Log-scale comparison of mutation frequencies at hotspot sites between GENIE (data aggregated from all sequencing panels) and cancerhotspots.org (CHS) using a binomial test. Figure S4:ââ,¬â€¹ Comparison of mutation frequencies at hotspot sites in each GENIE sequencing panel with cancerhotspots.org (CHS) using a binomial test.

Published
2023
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5. Table S4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium

Author

Hongxin Zhang, Ahmet Zehir, Emily Yu, Thomas V. Yu, Celeste Yu, Stuart Watt, Chetna Wathoo, Lucy L. Wang, Emile E. Voest, Carl Virtanen, Victor E. Velculescu, Harm van Tinteren, Tony van de Velde, Laura J. Van 'T Veer, Eliezer M. Van Allen, Stacy B. Thomas, Jelle J. ten Hoeve, Barry S. Taylor, Shawn M. Sweeney, Thomas P. Stricker, Natalie H. Stickle, Parin Sripakdeevong, Jean Charles Soria, Gabe S. Sonke, David B. Solit, Lillian L. Siu, Priyanka Shivdasani, Kenna R Mills Shaw, Nikolaus Schultz, Deborah Schrag, Charles L. Sawyers, Mark J. Routbort, Barrett J. Rollins, Brendan Reardon, Trevor J. Pugh, Ben Ho Park, John A. Orechia, Larsson Omberg, Petra M. Nederlof, Nathanael D. Moore, Gordon Mills, Clinton Miller, Christine M. Micheel, Funda Meric-Bernstam, Gerrit A. Meijer, David S. Maxwell, Ian Maurer, Laura E. MacConaill, Zhibin Lu, David Liu, James Lindsay, Neal I. Lindeman, Mia A. Levy, Eva M. Lepisto, Michele L. LeNoue-Newton, Céline Lefebvre, Marc Ladanyi, Ritika Kundra, Priti Kumari, Walter Kinyua, Cyriac Kandoth, Suzanne Kamel-Reid, David M. Hyman, Jan Hudeček, Hugo Horlings, Stephanie Hintzen, Zachary J. Heins, Justin Guinney, Benjamin E. Gross, Christopher D. Gocke, Stu Gardos, Francisco Garcia, Jianjiong Gao, P. Andrew Futreal, Matthew D. Ducar, Raymond N. DuBois, Semih Dogan, Catherine Del Vecchio Fitz, Nancy E. Davidson, Kristen K. Dang, Debyani Chakravarty, Ethan Cerami, Fabien Calvo, Mariska Bierkens, Michael F. Berger, Philippe L. Bedard, José Baselga, Alexander S. Baras, Monica Arnedos, and Fabrice André

Abstract

Table S4

Published
2023
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6. Supplemental File 1 from AACR Project GENIE: Powering Precision Medicine through an International Consortium

Author

Hongxin Zhang, Ahmet Zehir, Emily Yu, Thomas V. Yu, Celeste Yu, Stuart Watt, Chetna Wathoo, Lucy L. Wang, Emile E. Voest, Carl Virtanen, Victor E. Velculescu, Harm van Tinteren, Tony van de Velde, Laura J. Van 'T Veer, Eliezer M. Van Allen, Stacy B. Thomas, Jelle J. ten Hoeve, Barry S. Taylor, Shawn M. Sweeney, Thomas P. Stricker, Natalie H. Stickle, Parin Sripakdeevong, Jean Charles Soria, Gabe S. Sonke, David B. Solit, Lillian L. Siu, Priyanka Shivdasani, Kenna R Mills Shaw, Nikolaus Schultz, Deborah Schrag, Charles L. Sawyers, Mark J. Routbort, Barrett J. Rollins, Brendan Reardon, Trevor J. Pugh, Ben Ho Park, John A. Orechia, Larsson Omberg, Petra M. Nederlof, Nathanael D. Moore, Gordon Mills, Clinton Miller, Christine M. Micheel, Funda Meric-Bernstam, Gerrit A. Meijer, David S. Maxwell, Ian Maurer, Laura E. MacConaill, Zhibin Lu, David Liu, James Lindsay, Neal I. Lindeman, Mia A. Levy, Eva M. Lepisto, Michele L. LeNoue-Newton, Céline Lefebvre, Marc Ladanyi, Ritika Kundra, Priti Kumari, Walter Kinyua, Cyriac Kandoth, Suzanne Kamel-Reid, David M. Hyman, Jan Hudeček, Hugo Horlings, Stephanie Hintzen, Zachary J. Heins, Justin Guinney, Benjamin E. Gross, Christopher D. Gocke, Stu Gardos, Francisco Garcia, Jianjiong Gao, P. Andrew Futreal, Matthew D. Ducar, Raymond N. DuBois, Semih Dogan, Catherine Del Vecchio Fitz, Nancy E. Davidson, Kristen K. Dang, Debyani Chakravarty, Ethan Cerami, Fabien Calvo, Mariska Bierkens, Michael F. Berger, Philippe L. Bedard, José Baselga, Alexander S. Baras, Monica Arnedos, and Fabrice André

Abstract

AACR GENIE Data Guide

Published
2023
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7. Supplementary Data from Characteristics and Outcome of AKT1E17K-Mutant Breast Cancer Defined through AACR Project GENIE, a Clinicogenomic Registry

Author

David M. Hyman, Deborah Schrag, Alexia Iasonos, Philippe L. Bedard, Funda Meric-Bernstam, Mia Levy, Fabrice André, Charles L. Sawyers, Ben H. Park, Seth Sheffler-Collins, Jocelyn Lee, Stuart M. Gardos, Andrew Zarski, Nikolaus Schultz, JianJiong Gao, Shawn M. Sweeney, Ritika Kundra, Benjamin E. Gross, Jan Hudecek, Hugo Horlings, Chetna Wathoo, Christine M. Micheel, Semih Dogan, Natalie Blauvelt, Michele L. Lenoue-Newton, Michael J. Hasset, Monica Arnedos, Eva M. Lepisto, Celeste Yu, Bastien Nguyen, Qin Zhou, and Lillian M. Smyth

Abstract

Supplementary Tables and Figures

Published
2023
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8. Data from Characteristics and Outcome of AKT1E17K-Mutant Breast Cancer Defined through AACR Project GENIE, a Clinicogenomic Registry

Author

David M. Hyman, Deborah Schrag, Alexia Iasonos, Philippe L. Bedard, Funda Meric-Bernstam, Mia Levy, Fabrice André, Charles L. Sawyers, Ben H. Park, Seth Sheffler-Collins, Jocelyn Lee, Stuart M. Gardos, Andrew Zarski, Nikolaus Schultz, JianJiong Gao, Shawn M. Sweeney, Ritika Kundra, Benjamin E. Gross, Jan Hudecek, Hugo Horlings, Chetna Wathoo, Christine M. Micheel, Semih Dogan, Natalie Blauvelt, Michele L. Lenoue-Newton, Michael J. Hasset, Monica Arnedos, Eva M. Lepisto, Celeste Yu, Bastien Nguyen, Qin Zhou, and Lillian M. Smyth

Abstract

AKT inhibitors have promising activity in AKT1E17K-mutant estrogen receptor (ER)–positive metastatic breast cancer, but the natural history of this rare genomic subtype remains unknown. Utilizing AACR Project GENIE, an international clinicogenomic data-sharing consortium, we conducted a comparative analysis of clinical outcomes of patients with matched AKT1E17K-mutant (n = 153) and AKT1–wild-type (n = 302) metastatic breast cancer. AKT1-mutant cases had similar adjusted overall survival (OS) compared with AKT1–wild-type controls (median OS, 24.1 vs. 29.9, respectively; P = 0.98). AKT1-mutant cases enjoyed longer durations on mTOR inhibitor therapy, an observation previously unrecognized in pivotal clinical trials due to the rarity of this alteration. Other baseline clinicopathologic features, as well as durations on other classes of therapy, were broadly similar. In summary, we demonstrate the feasibility of using a novel and publicly accessible clincogenomic registry to define outcomes in a rare genomically defined cancer subtype, an approach with broad applicability to precision oncology.Significance:We delineate the natural history of a rare genomically distinct cancer, AKT1E17K-mutant ER-positive breast cancer, using a publicly accessible registry of real-world patient data, thereby illustrating the potential to inform drug registration through synthetic control data.See related commentary by Castellanos and Baxi, p. 490.

Published
2023
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9. Supplementary Tables 1-3 from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Author

Bryan T. Hennessy, Gordon B. Mills, René Bernards, Joe W. Gray, Vicente Valero, Marc J. van de Vijver, Mien-Chie Hung, Katrien Berns, Hugo Horlings, Laura K. Nolden, Lajos Pusztai, W. Fraser Symmans, Aysegul Sahin, Yinghui Guan, Zhi Hu, Mark Carey, Michael Davies, Wen-Lin Kuo, Richard M. Neve, Ana Lluch, Ana Maria Gonzalez-Angulo, and Katherine Stemke-Hale

Abstract

Supplementary Tables 1-3 from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Published
2023
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10. Supplementary Table Legends 1-3 from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Author

Bryan T. Hennessy, Gordon B. Mills, René Bernards, Joe W. Gray, Vicente Valero, Marc J. van de Vijver, Mien-Chie Hung, Katrien Berns, Hugo Horlings, Laura K. Nolden, Lajos Pusztai, W. Fraser Symmans, Aysegul Sahin, Yinghui Guan, Zhi Hu, Mark Carey, Michael Davies, Wen-Lin Kuo, Richard M. Neve, Ana Lluch, Ana Maria Gonzalez-Angulo, and Katherine Stemke-Hale

Abstract

Supplementary Table Legends 1-3 from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Published
2023
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11. Data from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Author

Bryan T. Hennessy, Gordon B. Mills, René Bernards, Joe W. Gray, Vicente Valero, Marc J. van de Vijver, Mien-Chie Hung, Katrien Berns, Hugo Horlings, Laura K. Nolden, Lajos Pusztai, W. Fraser Symmans, Aysegul Sahin, Yinghui Guan, Zhi Hu, Mark Carey, Michael Davies, Wen-Lin Kuo, Richard M. Neve, Ana Lluch, Ana Maria Gonzalez-Angulo, and Katherine Stemke-Hale

Abstract

Phosphatidylinositol 3-kinase (PI3K)/AKT pathway aberrations are common in cancer. By applying mass spectroscopy–based sequencing and reverse-phase protein arrays to 547 human breast cancers and 41 cell lines, we determined the subtype specificity and signaling effects of PIK3CA, AKT, and PTEN mutations and the effects of PIK3CA mutations on responsiveness to PI3K inhibition in vitro and on outcome after adjuvant tamoxifen. PIK3CA mutations were more common in hormone receptor–positive (34.5%) and HER2-positive (22.7%) than in basal-like tumors (8.3%). AKT1 (1.4%) and PTEN (2.3%) mutations were restricted to hormone receptor–positive cancers. Unlike AKT1 mutations that were absent from cell lines, PIK3CA (39%) and PTEN (20%) mutations were more common in cell lines than tumors, suggesting a selection for these but not AKT1 mutations during adaptation to culture. PIK3CA mutations did not have a significant effect on outcome after adjuvant tamoxifen therapy in 157 hormone receptor–positive breast cancer patients. PIK3CA mutations, in comparison with PTEN loss and AKT1 mutations, were associated with significantly less and inconsistent activation of AKT and of downstream PI3K/AKT signaling in tumors and cell lines. PTEN loss and PIK3CA mutation were frequently concordant, suggesting different contributions to pathophysiology. PTEN loss rendered cells significantly more sensitive to growth inhibition by the PI3K inhibitor LY294002 than did PIK3CA mutations. Thus, PI3K pathway aberrations likely play a distinct role in the pathogenesis of different breast cancer subtypes. The specific aberration present may have implications for the selection of PI3K-targeted therapies in hormone receptor–positive breast cancer. [Cancer Res 2008;68(15):6084–91]

Published
2023
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12. 45/#732 Homologous recombination deficiency and cyclin E1 amplification are correlated with immune cell infiltration and survival in high-grade serous ovarian cancer

Author

Lilian Van Wagensveld, Julliete Van Baal, Maite Timmermans, Duco Gaillard, Lauri Borghuis, Seth Coffelt, Effraim Rosenberg, Christianne Lok, Hans Nijman, Loes Kooreman, Annegien Broeks, Joyce Sanders, Marco De Bruijn, Rianne Van Der Wiel, Roy Kruitwagen, Maaike Van Der Aa, Gabe Sonke, Philip Schouten, Koen Van De Vijver, and Hugo Horlings

Published
2022
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14. External Quality Assessment 2.0

Author

Inne Nauwelaers, Nele Laudus, Dieter Peeters, Balazs Acs, Carsten Denkert, Stefan Michiels, Hugo Horlings, Kalliopi P. Siziopikou, Scott Ely, Dimitrios Zardavas, Roberts Mustimbo, John Bartlett, Giuseppe Floris, Johan Hartman, Carolien H. M. van Deurzen, Dorien Ceusters, Els Dequeker, Roberto Salgado, and Pathology

Subjects
Cancer Research, Oncology, SDG 3 - Good Health and Well-being
Abstract

New assays are developed regularly to improve health care for patients. It is important to ensure that assays are performed correctly. Therefore, it is advised to participate in training and proficiency (competence assessment) programs. Tumor infiltrating lymphocytes (TILs) might improve the estimates of response to therapy and prognosis. Herewith, we propose a new training and proficiency program in which each pathologist can train and test themselves regarding TILs (and PDL1) scoring.

Published
2022
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15. Characteristics and Outcome of

Author

Lillian M, Smyth, Qin, Zhou, Bastien, Nguyen, Celeste, Yu, Eva M, Lepisto, Monica, Arnedos, Michael J, Hasset, Michele L, Lenoue-Newton, Natalie, Blauvelt, Semih, Dogan, Christine M, Micheel, Chetna, Wathoo, Hugo, Horlings, Jan, Hudecek, Benjamin E, Gross, Ritika, Kundra, Shawn M, Sweeney, JianJiong, Gao, Nikolaus, Schultz, Andrew, Zarski, Stuart M, Gardos, Jocelyn, Lee, Seth, Sheffler-Collins, Ben H, Park, Charles L, Sawyers, Fabrice, André, Mia, Levy, Funda, Meric-Bernstam, Philippe L, Bedard, Alexia, Iasonos, Deborah, Schrag, and David M, Hyman

Subjects
Adult, Aged, 80 and over, Treatment Outcome, Mutation, Humans, Breast Neoplasms, Female, Registries, Middle Aged, Proto-Oncogene Proteins c-akt, Aged
Abstract

AKT inhibitors have promising activity in

Published
2019

16. In Reply

Author

Daphne de Jong, Hugo Horlings, Jelle Wesseling, and Laura van't Veer

Subjects
Cancer Research, Oncology
Published
2009
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