Browsing 408 Presentations
Disclaimer Statement
- Javier Cortés (Barcelona, Spain)
190P - Phyllodes tumour of the breast: 10 years of experience in a Mexican oncology reference center
- Maria Ines Contreras Salcido (Monterrey, Mexico)
- Maria Ines Contreras Salcido (Monterrey, Mexico)
- José L. González Vela (Monterrey, Mexico)
- Jackeline G. Lara Campos (Monterrey, Mexico)
- Edio Llerena Hernandez (Monterrey, Mexico)
- David Hernández Barajas (Monterrey, Mexico)
- Oscar Vidal Gutiérrez (Monterrey, Mexico)
- Adriana Adriana González Gutiérrez (Monterrey, Mexico)
- Rolando J. Martínez Granados (Monterrey, Mexico)
- Marco A. Ponce Camacho (Monterrey, Mexico)
- Max Molina Ayala (Monterrey, Mexico)
Abstract
Background
Phyllodes tumor (PT) of the breast is a rare fibroepithelial neoplasm representing 1% of all breast tumors. The objective of this report is to describe the characteristics of patients in the Hispanic population with PT and describe the clinical and pathological variables of our population.
Methods
We performed a retrospective analysis of patients with PT treated at an Oncology referral center in North-East Mexico from the years 2013 to 2019.
Results
We registered 51 cases; 28 were excluded due to a lack of follow up. We included 23 cases in the final analysis. The mean age of diagnosis was 51 years, the diagnosis was made by self-detection in all cases, with a median time of evolution of 17.5 months and a median tumor size 12.8 cm, approximately 26% had a history of mammary resection with benign pathology. 39.1% were treated with radical mastectomy, simple mastectomy in 39.1% and 21.7% breast conservative surgery. PT were classified as benign 17.3%, borderline 13% and malignant 69.5%. Patients with malignant PT showed a heterologous component in 21.7%, 60% with mixed histology, (chondrosarcoma, liposarcoma, undifferentiated sarcoma, neural cystosarcoma, chondroid and bone), 20% fibromyxosarcoma and 20% osteosarcoma. 13% of the entire population had metastatic lung disease at the beginning of diagnosis; We observed 8 recurrences, 2 in borderline and 6 in malignant subtype. The recurrence-free interval in borderline subtype was 51 months and the main site of the recurrence were local; The recurrence-free interval was 5 months in malignant subtype, and the types of recurrence in order of frequency were in multiple sites 4 cases (lung, nervous central system, bone and liver), 1 case local and 1 case lung metastases. The treatments were chemotherapy (66.6%), radiotherapy (16.6%) and concurrent radiotherapy and chemotherapy (16.6%). The overall survival in the subgroup that developed distance disease was 6.9 months.
Conclusions
To our knowledge, this is one of the first studies, analyzing the clinical-pathological characteristics of phyllodes tumors in the North-East of Mexico. We found more cases with malignant subtype, bigger tumors and more heterologous component than other Hispanic reports.
Legal entity responsible for the study
María Inés Contreras Salcido.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
23P - Clinical, pathological and gene expression features of HER2-low breast cancer
- Francesco Schettini (Napoli, Italy)
- Francesco Schettini (Napoli, Italy)
- Nuria Chic (Barcelona, Spain)
- Fara Brasó-Maristany (Barcelona, Spain)
- Laia Paré (Barcelona, Spain)
- Tomás Pascual (Barcelona, Spain)
- Benedetta Conte (Genova, Italy)
- Olga Martinez Saez (Barcelona, Spain)
- Barbara Adamo (Barcelona, Spain)
- Maria Vidal (Barcelona, Spain)
- Aranzazu Fernandez-Martinez (Chapel Hill, United States of America)
- Blanca González-Farré (Barcelona, Spain)
- Esther Sanfeliu (Barcelona, Spain)
- Giuseppe Perrone (Rome, Italy)
- Patricia Villagrasa (Barcelona, Spain)
- Joaquin Gavila Gregori (Valencia, Spain)
- Carlos H. Barrios (Porto Alegre, Brazil)
- Ana Lluch (Valencia, Spain)
- Miguel Martin Jimenez (Madrid, Spain)
- Sabino De Placido (Naples, Italy)
- Aleix Prat (Barcelona, Spain)
Abstract
Background
Novel antibody-drug conjugates against HER2 are showing high activity in clinically HER2-negative (cHER2-) breast cancer (BC) with low HER2 expression. However, the clinical and molecular features of cHER2-/HER2-low BC are yet to be elucidated.
Methods
We collected retrospective data from 8 multicenter cHER2- BC datasets, including 4 clinical trials. HER2 status in each study was determined using standard FDA-approved antibodies and ISH-techniques and classified according to the ASCO/CAP guidelines. For this study, tumors were regrouped in HER2 0 (0 score) and HER2-low (1+ or 2+ with ISH-negativity). The following variables were compared between the 2 groups in all patients and according to hormone receptor (HR) status: age, grade, ki67, histotype, tumor size, HR, HER2 and nodal status. nCounter-based PAM50 subtypes distribution and the expression of the 50 PAM50 genes, including ERBB2, were also compared.
Results
A total of 3,136 patients with cHER2- disease (57.4% HER2-low and 42.6% HER2 0) were evaluated. Overall, 888 (28.3%) tumor samples came from metastatic sites. No statistically significant differences were found regarding clinicopathological variables between HER2-low and HER2 0. Within HR-positive (+) disease (n=2,497), 63.2% and 36.8% of tumors were HER2-low and HER2 0, respectively. Subtype distribution was similar across HR+/HER2-low and HR+/HER2 0. A total of 45/50 PAM50 genes were found differentially expressed between HR+/HER2-low and HR+/HER2 0 (False Discovery Rate [FDR]<5%). High expression of luminal (e.g. ESR1 and FOXA1) and ERBB2, and low expression of proliferation-related genes (e.g. MKI67) was found in HER2-low compared to HER2 0. Within triple negative BC (TNBC) (n=622), 34.2% were HER2-low and 65.8% were HER2 0. Subtype distribution was similar across TNBC/HER2-low and TNBC/HER2 0. No PAM50 gene was found differentially expressed between TNBC/HER2-low and TNBC/HER2 0 (FDR≥5%). Finally, ERBB2 mRNA levels were higher in HER2-low/HR+ tumors than HER2-low/TNBC (p<0.001).
Conclusions
HER2-low disease within clinically HER2- BC is frequent. However, significant differences exist according to HR status. Compared to HER2-low/TNBC, HER2-low/HR+ disease is a more distinct biological entity and has higher ERBB2 expression.
Legal entity responsible for the study
The authors.
Funding
Instituto de Salud Carlos III - PI16/00904, Pas a Pas, Save the Mama, Breast Cancer Now - 2018NOVPCC1294. Fundación Científica Asociación Española Contra el Cáncer - Ayuda Postdoctoral AECC 2017. Fundación SEOM, Becas FSEOM para Formación en Investigación en Centros de Referencia en el Extranjero 2016 and 2018.
Disclosure
C.H. Barrios: Honoraria (self), Advisory/Consultancy, Research grant/Funding (self): AstraZeneca, Novartis, Roche, GSK, Pfizer, Libbs, Daiichi Sankyo and MSD. A. Lluch: Research grant/Funding (self): Amgen, AstraZeneca, Boehringer-Ingelheim, GSK, Novartis, Pfizer, Roche/Genentech, Eisai, Celgene, Pierre Fabre; Advisory/Consultancy: Novartis, Pfizer, Roche/Genentech, Eisai, Celgene. M. Martin Jimenez: Research grant/Funding (self): Roche, PUMA and Novartis; Advisory/Consultancy: AstraZeneca, Amgen, Taiho Oncology, Roche/Genentech, Novartis, PharmaMar, Eli Lilly, PUMA, Taiho Oncology, Daiichi Sankyo and Pfizer; Speaker Bureau/Expert testimony: AstraZeneca, Amgen, Roche/Genentech, Novartis and Pfizer. A. Prat: Honoraria (self): Pfizer, Novartis, Roche, MSD Oncology, Lilly and Daiichi Sankyo; Research grant/Funding (self): Novartis and Roche; Travel/Accommodation/Expenses: Daiichi Sankyo; Advisory/Consultancy: NanoString Technologies, Amgen, Roche, Novartis, Pfizer and Bristol-Myers Squibb; Licensing/Royalties: patent PCT/EP2016/080056. All other authors have declared no conflicts of interest.
188P - Impact of HIV infection (HIV+) on baseline characteristics and survival of breast cancer (BC) patients (pts): A systematic review and meta-analysis
- Mariana D. Brandão (Brussels, Belgium)
- Mariana D. Brandão (Brussels, Belgium)
- Marco Bruzzone (Genova, Italy)
- Maria Alice Franzoi (Brussels, Belgium)
- Claudia De Angelis (Brussels, Belgium)
- Daniel Eiger (Brussels, São Paulo, Belgium)
- Rafael Caparica (Brussels, Belgium)
- Nicolas Dauby (Bruxelles, Belgium)
- Marcello Ceppi (Genova, Italy)
- Martine Piccart (Brussels, Belgium)
- Carla Carrilho (Maputo, Mozambique)
- Nuno Lunet (Porto, Portugal)
- Laurence Buisseret (Brussels, Belgium)
- Evandro De Azambuja (Brussels, Belgium)
- Matteo Lambertini (Genova, Italy)
Abstract
Background
The number of HIV+ women diagnosed with BC is increasing. Yet, data are conflicting regarding their stage at diagnosis, distribution of BC subtypes and prognosis. We aimed to assess differences in baseline characteristics and overall survival (OS) between HIV+ vs HIV-uninfected (HIV-) BC pts.
Methods
Systematic review using MEDLINE, Scielo and conference Abstract (hand search of studies presented in major meetings) up to 1 Jan 2020 with no language restrictions was performed. Cross-sectional or cohort studies comparing baseline characteristics (mean age, stage or BC subtypes) or OS of HIV+ vs HIV- BC pts were included. Main endpoints were age, late stage at diagnosis, proportion of subtypes and OS. Subgroup analyses were performed according to world region. Other endpoints were detailed stage and estrogen receptor (ER) status. Summary estimates (pooled mean age ratios [MR], odds ratios [OR] and hazard ratios [HR]) were calculated using random effects models.
Results
20 publications (5 from North America, 15 from Sub-Saharan Africa [SSA]) were included, with 3,174 HIV+ and 2,394,598 HIV- pts. Mean age was 18% lower among HIV+ pts vs HIV- pts (MR 0.82, 95% CI 0.76-0.89) and HIV+ pts had a 53% increased risk of presenting with late stage BC (OR 1.53, 95% CI 1.37-1.71). HIV+ pts had smaller odds of having ER+/HER2- BC, but there were no differences regarding other subtypes (Table). HIV+ pts had a 90% increased risk of dying compared to HIV- pts (adjusted HR 1.90, 95% CI 1.21-2.99), with similar results in North America and SSA.
HIV+ pts HIV- pts Pooled estimate (95% CI) P Age All 144 316 MR 0.82 (0.76-0.89) <.001 Late stage (III/IV) All 3014 2331751 OR 1.53 (1.37-1.71) <.001 SSA 1374 6107 OR 1.38 (1.22-1.57) <.001 North America 1640 2325643 OR 1.76 (1.58-1.95) <.001 ER+/HER2- All 498 1925 OR 0.81 (0.66-0.99) .043 HER2+ All 519 1969 OR 1.10 (0.80-1.52) .553 TNBC All 610 3147 OR 1.14 (0.90-1.43) .269 Luminal A All 326 1957 OR 0.65 (0.42-1.02) .059 Luminal B All 326 1957 OR 1.03 (0.79-1.35) .800 HER2-enriched All 326 1957 OR 1.08 (0.49-2.38) .842 OS (adjusted) All 1741 1561217 HR 1.90 (1.21-2.99) .005 SSA 291 890 HR 1.58 (1.25-1.98) <.001 North America 1426 1560131 HR 2.45 (1.11-5.41) .026 OS (unadjusted) All 291 890 HR 1.43 (1.06-1.92) .019
Conclusions
HIV+ pts are diagnosed with BC at a younger age and at a later stage. Even after adjusting for prognostic factors, HIV+ pts have a worse OS as compared to HIV- pts, both in SSA and North America. Further studies are needed to decipher the reasons behind these disparities that can be related to HIV infection, distinct BC biology and anti-cancer immune response and/or to a lower access to timely diagnosis and effective treatment.
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
M.D.R.A. Brandão: Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Roche/Genentech. D. Eiger: Research grant/Funding (institution): Novartis. R. Caparica: Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: AstraZeneca; Speaker Bureau/Expert testimony: Boehringer Ingelheim; Speaker Bureau/Expert testimony: Janssen; Travel/Accommodation/Expenses: Pfizer. M. Piccart: Honoraria (self), Officer/Board of Directors: Oncolytics; Research grant/Funding (institution), Officer/Board of Directors: Radius; Honoraria (self), Research grant/Funding (institution): AstraZeneca; Honoraria (self): Camel-IDS; Honoraria (self): Crescendo Biologics; Honoraria (self): Debiopharm; Honoraria (self): G1 Therapeutics; Honoraria (self), Research grant/Funding (institution): Roche/Genentech; Honoraria (self): Huya; Honoraria (self): Immunomedics; Honoraria (self), Research grant/Funding (institution): Lilly; Honoraria (self): Menarini; Honoraria (self), Research grant/Funding (institution): MSD; Honoraria (self), Research grant/Funding (institution): Novartis; Honoraria (self): Odonate; Honoraria (self): Periphagen; Honoraria (self), Research grant/Funding (institution): Pfizer; Honoraria (self): Seattle Genetics; Research grant/Funding (institution): Servier; Research grant/Funding (institution): Synthon. L. Buisseret: Travel/Accommodation/Expenses: Roche; Research grant/Funding (institution): AstraZeneca; Speaker Bureau/Expert testimony: BMS. E. de Azambuja: Advisory/Consultancy, Research grant/Funding (institution), Travel/Accommodation/Expenses: Roche/GNE; Advisory/Consultancy, Research grant/Funding (institution), Travel/Accommodation/Expenses: Novartis; Advisory/Consultancy: SeaGen; Research grant/Funding (institution): AstraZeneca; Research grant/Funding (institution): Servier. M. Lambertini: Advisory/Consultancy: Roche Diagnostics; Speaker Bureau/Expert testimony: Roche; Speaker Bureau/Expert testimony: Takeda; Speaker Bureau/Expert testimony: Theramex. All other authors have declared no conflicts of interest.
181TiP - Xentuzumab (Xe) in combination with everolimus (Ev) and exemestane (Ex) in patients with hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) metastatic breast cancer (mBC) and non-visceral involvement (XENERA™-1)
- Peter Schmid (London, United Kingdom)
- Peter Schmid (London, United Kingdom)
- Hope S. Rugo (San Francisco, CA, United States of America)
- Javier Cortés (Barcelona, Spain)
- Petra Blum (Biberach, Germany)
- Kate Crossley (Bracknell, United Kingdom)
- Dan Massey (Biberach, Germany)
- Howard A. Burris, III (Nashville, United States of America)
Abstract
Background
Ev, an mTOR inhibitor, plus Ex is a standard therapy for post-menopausal women with HR+/HER2- mBC. The activity of Ev in cancer cells is restricted by compensatory mechanisms, including reactivation of insulin-like growth factor (IGF)/mTOR signalling. Combining Ev with the IGF-1/-2 ligand-neutralising antibody Xe limits this feedback, thereby intensifying inhibition of tumour growth. These effects are more pronounced in patients with non-visceral metastases.
Trial design
This phase II, double-blind, placebo-controlled, randomised study will assess the efficacy and safety of Xe in combination with Ev and Ex, in up to 80 women with HR+/HER2- locally advanced/mBC and non-visceral disease. Eligibility criteria include being pre-menopausal and on ovarian suppression therapy, or post-menopausal; and having progressed on or within 12 months of completing adjuvant endocrine therapy, or on or within 1 month after endocrine therapy for advanced/mBC. Patients must have an Eastern Cooperative Oncology Group performance status ≤1, adequate organ function, and presence of only non-visceral disease (absence of brain, liver, lung, peritoneal or pleural metastases). Exclusion criteria include: >1 prior line of chemotherapy for mBC; >1 prior line with a CDK4/6 inhibitor; and prior therapy targeting IGF, AKT or mTOR. Patients are randomised (1:1) to Xe (1000 mg/week, iv) or placebo (weekly, iv), in combination with Ev (10 mg/day) and Ex (25 mg/day). Treatment will continue until disease progression, unacceptable toxicity or other reasons. The primary endpoint is progression-free survival. Secondary endpoints include overall survival, disease control, duration of disease control, objective response, and time to progression of pain/intensification of pain palliation. Safety, pharmacokinetics and exploratory biomarkers will also be evaluated. The first patient was enrolled in January 2019. Participating sites are in Australia, Belgium, Canada, France, Germany, Greece, Ireland, Italy, Portugal, Spain, the United Kingdom and the United States.
Clinical trial identification
2017-003131-11/NCT03659136.
Editorial acknowledgement
Medical writing assistance, supported financially by Boehringer Ingelheim, was provided by Jim Sinclair, PhD, of GeoMed, an Ashfield company, part of UDG Healthcare plc, during the development of this abstract.
Legal entity responsible for the study
Boehringer Ingelheim.
Funding
Boehringer Ingelheim.
Disclosure
P. Schmid: Advisory/Consultancy: Pfizer; Advisory/Consultancy, Research grant/Funding (self): AstraZeneca; Advisory/Consultancy, Research grant/Funding (self): Novartis; Advisory/Consultancy, Research grant/Funding (self), Consulting / spouse: Roche; Advisory/Consultancy: Merck; Advisory/Consultancy: Boehringer Ingelheim; Advisory/Consultancy: Bayer; Advisory/Consultancy: Eisai; Advisory/Consultancy: Celgene; Advisory/Consultancy: Puma; Research grant/Funding (self), Consulting / spouse: Genentech; Research grant/Funding (self): Oncogenex; Research grant/Funding (self): Astellas. H.S. Rugo: Research grant/Funding (self), Travel/Accommodation/Expenses: Pfizer; Research grant/Funding (self), Travel/Accommodation/Expenses: Merck; Research grant/Funding (self): Novartis; Research grant/Funding (self): Lilly; Research grant/Funding (self): Genentech; Research grant/Funding (self): OBI; Research grant/Funding (self): Odonate; Research grant/Funding (self), Travel/Accommodation/Expenses: Daiichi; Research grant/Funding (self): Eisai; Research grant/Funding (self): Seattle Genetics; Research grant/Funding (self), Travel/Accommodation/Expenses: Macrogenics; Research grant/Funding (self): Immunomedics; Travel/Accommodation/Expenses: Mylan; Travel/Accommodation/Expenses: Amgen; Travel/Accommodation/Expenses: AstraZeneca; Travel/Accommodation/Expenses: Puma. J. Cortés: Honoraria (self), Advisory/Consultancy, Research grant/Funding (institution): Roche; Honoraria (self), Advisory/Consultancy: Celgene; Daiichi Sankyo; Lilly; Advisory/Consultancy, Research grant/Funding (institution): AstraZeneca; Honoraria (self), Research grant/Funding (institution): Eisai; Pfizer; Advisory/Consultancy: Cellestia; Biothera Pharmaceutical; Merus; Seattle Genetics; Erytech; Athenex; Polyphor; Servier; Advisory/Consultancy: GSK; Leuko; Bioasis; Clovis Oncology; Honoraria (self): Novartis; Samsung Bioepis; Shareholder/Stockholder/Stock options: MedSIR; Research grant/Funding (institution): Ariad pharmaceuticals; Baxalta GMBH/Servier Affaires; Bayer healthcare; F.Hoffman-La Roche; Guardanth health; Piqur Therapeutics; Puma C; Queen Mary University of London; Seagen. P. Blum: Full/Part-time employment: Boehringer Ingelheim International GmbH. K. Crossley: Full/Part-time employment: Boehringer Ingelheim Ltd. D. Massey: Full/Part-time employment: Boehringer Ingelheim International GmbH. H.A. Burris, III: Shareholder/Stockholder/Stock options: HCA Healthcare/Sarah Cannon; Advisory/Consultancy, Research grant/Funding (institution): AstraZeneca; Incyte; Pfizer; Speaker Bureau/Expert testimony, Research grant/Funding (institution): Novartis; Advisory/Consultancy: Celgene; Daiichi Sankyo; FORMA Therapeutics; Research grant/Funding (institution): Agios; Arch; Array BioPharma; Arvinas; Bayer; BIND Therapeutics; BioAtla; BioMed Valley; Boehringer Ingelheim; Research grant/Funding (institution): Bristol-Myers Squibb; CicloMed; CytomX; eFFECTOR; Lilly; Roche/Genentech; Gilead Sciences; GlaxoSmithKline; Research grant/Funding (institution): Harpoon Therapeutics; Janssen; Jounce Therapeutics; Kymab; MacroGenics; MedImmune; Merck; Millennium Pharmaceuticals; Research grant/Funding (institution): Mirna Therapeutics; Moderna; Revolution Medicine; Seattle Genetics; Tesaro; TG Therapeutics; Verastem; Vertex Pharmaceutical.
146P - Safety and metabolic effects of fasting-mimicking diet in breast cancer patients
- Claudio Vernieri (Milan, Italy)
- Alessandra Raimondi (Milan, Italy)
- Francesca Ligorio (Milan, Italy)
- Emma Zattarin (Milan, Italy)
- Federico Nichetti (Milan, Italy)
- Sara Manglaviti (Milan, Italy)
- Giulia V. Bianchi (Milan, Italy)
- Giuseppe Capri (Milan, Italy)
- Licia Rivoltini (Milan, Italy)
- Filippo Guglielmo Maria De Braud (Milan, Italy)
Abstract
Background
Cycles of calorie-restricted, low-carbohydrate, low-protein diets, collectively referred to as fasting-mimicking diets (FMDs), have demonstrated synergistic antitumor activity in combination with cytotoxic chemotherapy (ChT) or endocrine therapies (ETs) in murine models of breast cancer (BC). These effects are mainly mediated through FMD-induced reduction of blood glucose, insulin and insulin-like growth factor 1 (IGF-1) levels. However, the safety and metabolic activity of the FMD in BC patients remain poorly investigated.
Methods
We concluded a first-in-human clinical trial to investigate the safety, feasibility and metabolic effects of triweekly cycles of a specific 5-day FMD regimen (day 1: 600 KCal; days 2-5: 300 KCal) in combination with standard antitumor therapies in 93 cancer patients (NCT03340935). FMD-related adverse events (AEs) were graded according to CTCAE v5.0. The concentration of relevant blood and urinary metabolites before and after the FMD in individual patients was compared through paired Wilcoxon test. Here we present results of a subgroup analysis in BC patients.
Results
Between February 2017 and February 2019 we enrolled 48 BC patients. Of them, 19 (39.6%) had limited-stage disease, whereas 29 (60.4%) had advanced BC. Most patients received the FMD in combination with ChT (72.9%) or ET (25%). The median number of completed FMD cycles was 5 (range: 1-8). Overall, the FMD was well tolerated, with an incidence of severe FMD-related AEs of 4.2% (G3 fatigue: 1 event; G3 hypoglycemia: 1 event). The FMD significantly reduced plasma glucose (median:-20.9%; range [-49.2%;+24%]), serum insulin (median:-52.8%; range [-91.3%;+200%]) and IGF-1 (median:-36.7%; range: [-72.3%;+24.5%]) concentration, while increasing urinary ketone bodies (median increase: 80 mg/dl; range [0;150]).
Conclusions
This is the first study to show that 5-day FMD is safe when combined with ChT or ETs in BC patients, and causes systemic metabolic changes that have been associated with promising antitumor effects in preclinical studies. Ongoing clinical trials are investigating if the FMD improves the anticancer activity of standard treatments in patients with different tumor types, including BC (NCT03700437; NCT03709147; NCT04248998).
Clinical trial identification
NCT03340935.
Legal entity responsible for the study
Fondazione IRCCS Istituto Nazionale dei Tumori (Milan, Italy).
Funding
Scientific Directorate of Fondazione IRCCS Istituto Nazionale dei Tumori (Milan, Italy).
Disclosure
F.G.M. De Braud: Advisory/Consultancy: Roche; Advisory/Consultancy: EMD Serono; Advisory/Consultancy: Nerviano Medical Msciences; Advisory/Consultancy: Sanofi. All other authors have declared no conflicts of interest.
35P - The role of interplay between microRNA-133a and Mre11 in breast cancer
- Li-chun Kao (Kaohsiung City, Taiwan)
- Li-chun Kao (Kaohsiung City, Taiwan)
- Fang-ming Chen (Kaohsiung City, Taiwan)
Abstract
Background
In Taiwan, breast cancer has been rapidly jumped to the first place in the incidence of women-specific malignancies. It will be urgent to discover some critical biomarkers predicting patient prognosis and outcome in Taiwan. Because Taiwanese breast cancer has a relatively lower incidence and earlier onset than Western population, the subset of clinical biomarkers and treatments applied in Western population may not be suitable for all Taiwanese population.
Methods
Recently microRNAs (miRNAs) were found to be frequently deregulated in breast cancer, and some specific miRNAs were found to be associated with the DNA damage response (DDR). We measured miR-133a, both circulating and intra-tumor levels, to identify the relationship among miR-133a, HER2, and sruvival. We also detected the protein level of Mre11, one of double-strand break repair protein complex, to fingure out the correlation with miR-133a.
Results
Our preliminary results showed that circulating miR-133a levels of breast cancer patients are significantly higher than those of health subjects by using the receiver operating characteristic (ROC) curve (p=0.001). Both circulating and intra-tumor miR-133a levels were inversely correlated with the HER2 status (p=0.015 and 0.011), suggesting that Her2 modulate the expression of miR-133a. The Kaplen-Meier survival curve further showed that high circulating miR-133a can increase the overall survival rate of patients who didn’t receive chemotherapy, implicating that miR-133a might also modulate the response of chemotherapy, which has been linking to DNA repair ability. We found that ectopic miR-133a overexpression suppressed the protein levels of Mre11 but did not impact its mRNA levels.
Conclusions
In this project, we aim to disclose the interplay of miR-133a with Her2 and Mre11 in breast cancer development. Furthermore, we will establish the minimally invasive screen platform to improve early detection, prognosis, and follow up of breast cancer. We believe that the accomplishment of this project will not only provide better understanding of the carcinogenesis of breast cancer but also a prescreening tool to facilitate decisions about which individuals to be recommended for further diagnostic tests or treatments.
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
143P - Quality of life (QoL) with palbociclib (PAL) plus endocrine therapy (ET) versus (vs) capecitabine (CAP) in luminal metastatic breast cancer (MBC) patients (pts) in the PEARL study
- Zsuzsanna Kahan (Szeged, Hungary)
- Zsuzsanna Kahan (Szeged, Hungary)
- Miguel Gil-Gil (L'Hospitalet de Llobregat, Spain)
- Manuel Ruiz-Borrego (Sevilla, Spain)
- Eva M. Carrasco (San Sebastian de los Reyes, Spain)
- Eva M. Ciruelos (Madrid, Spain)
- Montserrat Muñoz (Barcelona, Spain)
- Begona Bermejo De Las Heras (Valencia, Valencia, Spain)
- Mireia Margeli Vila (Badalona, Spain)
- Antonio Anton (Zaragoza, Spain)
- Maribel Casas (San Sebastian de los Reyes, Spain)
- Lourdes Calvo (A Coruña, Spain)
- Juan De la Haba (Cordoba, Spain)
- Manuel Ramos (A Coruña, Spain)
- Isabel Alvarez Lopez (San Sebastian, Spain)
- Einav Gal-Yam (Tel-Hashomer, Israel)
- Eric Gautier (San Francisco, United States of America)
- Massimo Corsaro (Milan, Italy)
- Graciela Rodrigálvarez (San Sebastian de los Reyes, Spain)
- Christoph Zielinski (Vienna, Austria)
- Miguel Martin Jimenez (Madrid, Spain)
Abstract
Background
PAL+ET was not superior to CAP in progression free survival in postmenopausal pts with luminal MBC resistant to aromatase inhibitors, but was better tolerated. Patient-reported outcomes (PROs) were a secondary objective.
Methods
601 pts were randomized to PAL (125 mg 3 weeks out of 4) + Exemestane/fulvestrant (standard doses) vs CAP (1250 mg/m2, or 1000 mg/m2 if >70 years, BID 2 weeks out of 3). Pts completed the European Organization for Research and Treatment of Cancer QoL C30 (EORTC QLQ-C30), the breast cancer specific module (EORTC QLQ-BR23) and the EuroQoL Health Utilities Index (EQ-5D-3L) questionnaires in the clinic prior to any test or discussion with healthcare personnel at baseline (BL), Day 1 every 2 (till cycle 7) or 3 cycles (thereafter) till end of treatment (EOT). High scores represent better level of functioning for functional and global QoL scales and more severe symptoms for symptom-oriented scales. Changes from BL and time to deterioration (TTD) were analyzed using linear mixed-effect and stratified Cox regression models, respectively.
Results
Questionnaire completion rate was >82% till cycle 13. Mean change of Global Health Status (GHS) scores from BL and cycle 3 was 2.9 for PAL+ET vs -2.07 for CAP (95% CI, 1.4-8.6; p=0.007). In certain timepoints between BL and EOT, significant differences were found for physical, role and social functioning and symptoms like nausea/vomiting, fatigue and diarrhea (favouring PAL+ET) and dyspnea, constipation and insomnia (favouring CAP). Significant differences in the Visual Analogue Scale of the EQ-5D-3L index score between BL and cycle 3 also favours PAL+ET. Median TTD in GHS was 8.6 months (m) for PAL+ET vs 6.2 m for CAP (HR 0.70, 95% CI, 0.56 to 0.89; p=0.003). Similar improvements for PAL+ET were also seen for other QLQ-C30 scales (physical, role, cognitive and social functioning, fatigue, nausea/vomiting, pain, loss of appetite and diahrrea) and for future perspective and systemic therapy side effects in the QLQ-BR23.
Conclusions
Pts with PAL+ET had better QoL compared to CAP in most items. TTD was significantly prolonged with PAL+ET vs CAP.
Clinical trial identification
NCT02028507; 2013-003170-27.
Legal entity responsible for the study
GEICAM Spanish Breast Cancer Group.
Funding
Pfizer and AstraZeneca.
Disclosure
Z. Kahan: Advisory/Consultancy: Pfizer. M. Gil-Gil: Advisory/Consultancy: Pfizer; Advisory/Consultancy: Kher; Advisory/Consultancy: Eisai; Advisory/Consultancy: Genomic Health; Advisory/Consultancy: Novartis. M. Ruiz-Borrego: Advisory/Consultancy, Speaker Bureau/Expert testimony: Pfizer; Advisory/Consultancy, Speaker Bureau/Expert testimony: Novartis; Advisory/Consultancy, Speaker Bureau/Expert testimony: Lilly. E.M. Carrasco: Shareholder/Stockholder/Stock options: Lilly; Research grant/Funding (institution), Travel/Accommodation/Expenses, Spouse/Financial dependant: Roche; Research grant/Funding (institution), Spouse/Financial dependant: Novartis; Research grant/Funding (institution), Spouse/Financial dependant: Pfizer; Research grant/Funding (institution), Spouse/Financial dependant: Celgene; Research grant/Funding (institution): AstraZeneca; Research grant/Funding (institution): MSD; Research grant/Funding (institution): Pierre-Fabre; Research grant/Funding (institution): Takeda; Spouse/Financial dependant: AbbVie; Spouse/Financial dependant: Amgen; Spouse/Financial dependant: Janssen; Spouse/Financial dependant: BMS; Spouse/Financial dependant: Incyte; Licensing/Royalties: PAM 50 taxane predictor. B. Bermejo De Las Heras: Advisory/Consultancy: Genentech; Advisory/Consultancy: Novartis. M. Margeli Vila: Advisory/Consultancy: Pfizer; Advisory/Consultancy: Roche; Advisory/Consultancy: Novartis. A. Anton: Research grant/Funding (self): AstraZeneca. M. Casas: Research grant/Funding (institution): AstraZeneca; Research grant/Funding (institution): Pfizer. J. de la Haba: Advisory/Consultancy, Speaker Bureau/Expert testimony: Pfizer; Advisory/Consultancy, Speaker Bureau/Expert testimony: Roche; Advisory/Consultancy, Speaker Bureau/Expert testimony: Lilly; Advisory/Consultancy, Speaker Bureau/Expert testimony: Novartis. M. Ramos: Speaker Bureau/Expert testimony: Pfizer; Speaker Bureau/Expert testimony: Roche; Speaker Bureau/Expert testimony: Novartis. I. Álvarez-López: Advisory/Consultancy, Research grant/Funding (self), Travel/Accommodation/Expenses: Roche; Advisory/Consultancy, Research grant/Funding (self), Travel/Accommodation/Expenses: Pfizer; Travel/Accommodation/Expenses: Eisai; Advisory/Consultancy: Novartis; Research grant/Funding (self): AstraZeneca; Advisory/Consultancy: Genomic Health. E. Gal-Yam: Advisory/Consultancy: Pfizer. E. Gautier: Shareholder/Stockholder/Stock options, Full/Part-time employment: Pfizer; Shareholder/Stockholder/Stock options: Pfizer; Full/Part-time employment: Pfizer. M. Corsaro: Full/Part-time employment: Pfizer. G. Rodrigálvarez: Research grant/Funding (institution): Pfizer; Research grant/Funding (institution): AstraZeneca. C. Zielinski: Advisory/Consultancy, Research grant/Funding (self): Roche; Advisory/Consultancy: Novartis; Advisory/Consultancy, Research grant/Funding (self): BMS; Advisory/Consultancy, Research grant/Funding (self): MSD; Advisory/Consultancy: Imugene; Advisory/Consultancy: Ariad; Advisory/Consultancy, Research grant/Funding (self): Pfizer; Advisory/Consultancy: Merrimack; Advisory/Consultancy, Research grant/Funding (self): Merck KGaA; Advisory/Consultancy: Fibrogen; Advisory/Consultancy, Research grant/Funding (self): AstraZeneca; Advisory/Consultancy: Tesaro; Advisory/Consultancy: Gilead; Advisory/Consultancy: Servier; Advisory/Consultancy: Shire; Advisory/Consultancy: Lilly; Advisory/Consultancy: Athenex. M. Martin Jimenez: Advisory/Consultancy, Speaker Bureau/Expert testimony: AstraZeneca; Advisory/Consultancy, Speaker Bureau/Expert testimony: Amgen; Advisory/Consultancy: Taiho Oncology; Advisory/Consultancy, Speaker Bureau/Expert testimony, Research grant/Funding (self): Roche/Genentech; Advisory/Consultancy, Speaker Bureau/Expert testimony, Research grant/Funding (self): Novartis; Advisory/Consultancy: PharmaMar; Advisory/Consultancy: Lilly; Advisory/Consultancy, Research grant/Funding (self): PUMA; Advisory/Consultancy, Speaker Bureau/Expert testimony: Pfizer; Speaker Bureau/Expert testimony: Daiichi Sankyo. All other authors have declared no conflicts of interest.
44P - Obesity is associated with a late-stage diagnosis in triple-negative breast cancer
- Alejandro Aranda Gutierrez (Monterrey, Mexico)
- Alejandro Aranda Gutierrez (Monterrey, Mexico)
- Ana S. Ferrigno (San Pedro Garza Garcia, Mexico)
- Mariana Moncada-Madrazo (San Pedro Garza Garcia, Mexico)
- Analy Gomez-Picos (San Pedro Garza Garcia, Mexico)
- Cynthia De la Garza-Ramos (San Pedro Garza Garcia, Mexico)
- Fernanda Mesa-Chavez (San Pedro Garza Garcia, Mexico)
- Hector Diaz-Perez (San Pedro Garza Garcia, Mexico)
- Servando Cardona (San Pedro Garza Garcia, Mexico)
- Rocio Ortiz-Lopez (Monterrey, Mexico)
- Cynthia Villarreal-Garza (San Pedro Garza Garcia, Tlalpan. D.F., Mexico)
Abstract
Background
Approximately one third of breast cancer (BC) patients are obese, a fact that has been associated with an increased frequency of aggressive clinicopathological features and worse disease outcomes. The aim of this study was to evaluate if obesity plays a selective role in disease stage according to molecular subtype.
Methods
Medical records of women diagnosed with BC between January 2013 and December 2015 in a center located in Monterrey, Mexico were retrospectively reviewed. The patients were grouped by body mass index (BMI; obese: ≥30 kg/m2 and non-obese: <30 kg/m2) and clinical stage (early-stage: 0-II and late-stage: III-IV). Associations between the variables were examined using Fisher's exact test of independence. The significance level was set at p < 0.05.
Results
A total of 821 patients were diagnosed with BC, of which 363 were excluded since information about disease stage was missing. Median age was 51 years (range: 29-88), with 14% classified as young. The predominant molecular subtype was luminal-A (55%), followed by triple-negative (23%), and luminal-B and HER2+ (11% each). Most patients presented with early-stage disease (56%). Overall, obesity was not associated with disease stage. However, when stratified by molecular subtype, obesity was associated with diagnosis at a late-stage among women with triple-negative disease (55% vs 35%, p=0.0495). None of the other molecular subtypes demonstrated an association between stage and BMI.
Conclusions
In this cohort, obesity was only associated with a late-stage diagnosis in women with triple-negative disease. Although obesity and related comorbidities have been associated with unfavorable characteristics in triple-negative tumors, the molecular factors involved have not been elucidated. Current evidence indicates that increased availability of steroid hormones, insulin-like growth factors, adipokines and inflammatory cytokines could all play an important role in the aggressiveness of these tumors. Major limitations are present in this study, mainly its retrospective nature, limited number of patients and lack of information regarding clinical outcomes. Future research is needed to confirm these findings and analyze their clinical relevance.
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
H. Diaz-Perez: Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Pfizer; Travel/Accommodation/Expenses: Roche; Travel/Accommodation/Expenses: Novartis; Travel/Accommodation/Expenses: Lilly; Travel/Accommodation/Expenses: Amgen; Travel/Accommodation/Expenses: Asofarma. C. Villarreal-Garza: Advisory/Consultancy, Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Roche Mexico; Advisory/Consultancy: Novartis; Advisory/Consultancy, Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Pfizer; Advisory/Consultancy: AstraZeneca; Speaker Bureau/Expert testimony: Myriad Genetics; Advisory/Consultancy: Lilly. All other authors have declared no conflicts of interest.
47P - Androgen receptor expression and survival in triple negative breast cancer
- Leonor Moyano (Santiago, Chile)
- Leonor Moyano (Santiago, Chile)
- José L. Soto (Santiago, Chile)
- María L. Garmendia (SANTIAGO, Chile)
Abstract
Background
Triple negative breast cancer (TNBC) is characterized by aggressive behaviour, with high morbimortality. Androgen Receptors (AR) have a role in the activation of cellular proliferation, migration and invasiveness. The AR are expressed in 7-75% of TNBC. This study evaluates the relationship between positive AR with clinical data, relapse and overall survival.
Methods
All TNBC cases from the Pathology Service of Instituto Nacional del Cáncer were studied between 2015 to 2019 (n=69). Eligible patients (n=32) had at least 18 months of follow-up, ending at the 31/01/2020 or death. From clinical files and biopsy reports, age, TNM, treatment, relapse and Ki67 were extracted. Date and cause of death were obtained from death certificates. AR status was determined by immunohistochemistry and defined as AR-positive (>1%) or AR-negative (0%). The Kaplan-Meier method was used to estimate survival rates. Crude and adjusted Hazards Ratios (HR) were estimated by proportional Cox regression model.
Results
At diagnosis the average age was 54.6 years (DE:14.7), tumor size 3.9 cm (DE:2.2), 59.4% had positive lymph nodes, positive skin 18.8% and 87.5% without metastasis. Stage I - II 53.1%, Stage III - IV 46.9%. 37.5% received lumpectomy, 50% mastectomy. Neoadjuvant chemotherapy 44%, 59.4% adjuvant or palliative, and 50% radiotherapy. Average follow-up was 38.9 months (DE:15.7). 50% relapsed in an average of 14.9 months (DE:10.9) and 28% died (months to death 32.1 (DE:7.9)). 56.3% had AR+. There was no difference between AR+ and AR- regarding size nor Ki67 expression. There was an increased rate of death with AR+ (33.3% vs 21.4%) and metastasis (16.7% vs 7.1%), but that was not significant. In adjusted Cox regression models, AR+ showed higher risk of relapse (HR:3.54 IC95%:0.65,19.3, p=0.144) and mortality (HR:3.85 IC95%:0.82,18.1, p=0.088).
Conclusions
This study confirmed a high mortality in TNBC. Expression of AR-positive appears to be correlated with increased recurrence and mortality. AR-positive could be a prognostic and predictive marker. TNBC AR-positive patients could potentially apply to anti-androgen targeted therapy. More prospective studies with larger samples size and longer follow-up are required.
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
101P - Predictors of 18F-fluorodeoxyglucose (F) positron-emission tomography (PET)-driven disease detection in patients (pts) with HER2[+] early breast cancer (EBC). A substudy of the PHERGain trial
- Antonio Llombart Cussac (Lleida, Spain)
- Aleix Prat (Barcelona, Spain)
- José Manuel Pérez-García (Madrid and Barcelona, Spain)
- José Mateos (Barcelona, Spain)
- Tomas Pascual (Barcelona, Spain)
- Santiago Escrivà-De-Romani (Barcelona, Spain)
- Agostina Stradella (Barcelona, Spain)
- Manuel Ruiz-Borrego (Sevilla, Spain)
- Begona Bermejo De Las Heras (Valencia, Valencia, Spain)
- Marleen Keyaerts (Brussels, Belgium)
- Miguel Sampayo-Cordero (Barcelona, Spain)
- Andrea Malfettone (Barcelona, Spain)
- Roldán Cortés (Barcelona, Spain and Ridgewood, New Jersey, Spain)
- Patricia Galván (Barcelona, Spain)
- Javier Cortés (Barcelona, Spain)
- Géraldine Gebhart (Brussels, Belgium)
Abstract
Background
PHERGain (NCT03161353) is assessing the early metabolic response by F-PET to neoadjuvant chemotherapy-free treatment with trastuzumab and pertuzumab and the opportunity of chemotherapy de-escalation with a response-adapted strategy in pts with HER2[+] EBC. In this substudy, clinical and molecular predictors of disease detection using F-PET were evaluated.
Methods
PHERGain inclusion criteria required a breast lesion with a SUVmax ≥1.5xSUVmean liver+2SD by F-PET (PERCIST). A total of 512 pts with HER2[+] EBC were screened and 75 (14.7%) were PET[-]. Association between SUVmax and clinicopathological features was analyzed in all screened pts. Moreover, evaluation of stromal tumor-infiltrating lymphocytes (TIL) and gene expression data by PAM50 classifier and Vantage 3D Cancer Metabolism Panel was conducted on a selected cohort of 21 PET[-] and 21 PET[+] matched pts.
Results
Median age of the entire screened population was 52 years, 41.8% had node[+] disease, and 68.4% had hormone receptor (HR)[+] status. Median tumor size by magnetic resonance imaging was 30 mm (range 9–157). Median SUVmax was 7.3 (range 1–39). In an unadjusted analysis of all screened pts, SUVmax was associated with tumor size, lymph node involvement, HR status, HER2 expression levels, Ki67 index, and histological grade (p<0.05). PET[-] tumors had lower tumor size, histological grade, and lymph node involvement than PET[+] tumors. Although no difference in TIL counts was found among selected PET[-]/[+] cases, PET[-] tumors showed a decreased risk of recurrence and lower proportion of HER2-enriched subtype by PAM50 than PET[+] tumors (p<0.05). In PET[-] pts genes involved in glucose metabolism (DLAT, IDH2, LDHA, PGK1, PGLS, and TPI1), hypoxia signaling (HIF1A), and carbon metabolism (SLC7A5, SLC16A3) resulted under expressed, whereas genes involved in the mTOR pathway (AKT2) and growth factor receptor (FLT3) were over expressed compared with PET[+] pts (false discovery rate q<0.05).
Conclusions
Taking into account the clinical and biological heterogeneity of HER2[+] disease, these results may need to be considered for an appropriate selection of PET[+] pts in HER2[+] EBC.
Legal entity responsible for the study
MedSIR.
Funding
Has not received any funding.
Disclosure
A. Llombart Cussac: Leadership role: Eisai; Leadership role: Celgene; Advisory/Consultancy, Speaker Bureau/Expert testimony, Leadership role, Travel/Accommodation/Expenses: Lilly; Advisory/Consultancy, Leadership role, Travel/Accommodation/Expenses: Pfizer; Advisory/Consultancy, Leadership role, Research grant/Funding (self), Travel/Accommodation/Expenses: Roche; Advisory/Consultancy, Leadership role, Travel/Accommodation/Expenses: Novartis; Speaker Bureau/Expert testimony, Leadership role: MSD; Shareholder/Stockholder/Stock options: MedSIR; Shareholder/Stockholder/Stock options: Initia-Research; Advisory/Consultancy, Research grant/Funding (self): Pierre-Fabre; Advisory/Consultancy: GenomicHealth; Advisory/Consultancy: GSK; Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: AstraZeneca; Research grant/Funding (self): Foundation Medicine; Research grant/Funding (self): Agendia. A. Prat: Honoraria (self), Advisory/Consultancy, Research grant/Funding (institution), Spouse/Financial dependant: Novartis; Honoraria (self), Advisory/Consultancy: Pfizer; Honoraria (self), Advisory/Consultancy, Research grant/Funding (institution): Roche; Honoraria (self): MSD; Honoraria (self): Lilly; Honoraria (self), Advisory/Consultancy, Travel/Accommodation/Expenses: Daiichi Sankyo; Honoraria (self), Advisory/Consultancy: Amgen; Advisory/Consultancy: Bristol-Myers Squibb; Advisory/Consultancy, Research grant/Funding (institution): PUMA Biotechnology; Advisory/Consultancy: Oncolytics Biotech; Advisory/Consultancy: AbbVie; Advisory/Consultancy: NanoString Technologies; Research grant/Funding (institution): INCYTE; Licensing/Royalties: PCT/EP2016/080056: HER2 as a Predictor of Response to Dual Her2 Blockade in the Absence of Cytotoxic Therapy; WO/2018/096191; Licensing/Royalties: Chemoendocrine score (CES) Based on PAM50 for breast cancer with positive hormone receptors with an intermediate risk of recurrence; Non-remunerated activity/ies, other: Peptomyc S.L. J.M. Pérez-García: Advisory/Consultancy, Travel/Accommodation/Expenses: Roche; Advisory/Consultancy: Lilly. S. Escrivà-De-Romani: Advisory/Consultancy, Speaker Bureau/Expert testimony, Research grant/Funding (institution), Travel/Accommodation/Expenses: Roche; Advisory/Consultancy, Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Pierre-Fabre; Speaker Bureau/Expert testimony: Eisai; Research grant/Funding (institution): Synthon; Travel/Accommodation/Expenses: Daiichi Sankyo. A. Stradella: Advisory/Consultancy, Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Roche; Speaker Bureau/Expert testimony: Eisai; Travel/Accommodation/Expenses: Pfizer. M. Ruiz-Borrego: Speaker Bureau/Expert testimony: Roche; Advisory/Consultancy, Speaker Bureau/Expert testimony: Novartis; Advisory/Consultancy, Speaker Bureau/Expert testimony: Pfizer; Advisory/Consultancy: MSD; Speaker Bureau/Expert testimony: Lilly; Speaker Bureau/Expert testimony: AstraZeneca. B. Bermejo De Las Heras: Advisory/Consultancy, Speaker Bureau/Expert testimony: Genentech; Advisory/Consultancy: MSD; Travel/Accommodation/Expenses: Pfizer. M. Keyaerts: Research grant/Funding (self): Camel-IDS; Research grant/Funding (self): Bayer; Licensing/Royalties: Nanobody imaging and therapy. M. Sampayo-Cordero: Honoraria (self), Advisory/Consultancy, Speaker Bureau/Expert testimony, Research grant/Funding (self), Travel/Accommodation/Expenses: MedSIR; Honoraria (self), Advisory/Consultancy, Speaker Bureau/Expert testimony, Research grant/Funding (self), Travel/Accommodation/Expenses: Syntax for Science; Honoraria (self), Advisory/Consultancy: Nestlé; Speaker Bureau/Expert testimony, Research grant/Funding (self), Travel/Accommodation/Expenses: Roche. A. Malfettone: Full/Part-time employment: MedSIR. R. Cortés: Full/Part-time employment: MedSIR. J. Cortés: Honoraria (institution), Advisory/Consultancy, Research grant/Funding (institution): Roche; Honoraria (institution), Advisory/Consultancy: Celgene; Advisory/Consultancy: Cellestia; Advisory/Consultancy, Research grant/Funding (institution): AstraZeneca; Advisory/Consultancy: Biothera Pharmaceutical; Advisory/Consultancy: Merus; Advisory/Consultancy: Seattle Genetics; Honoraria (self), Advisory/Consultancy: Daiichi Sankyo; Advisory/Consultancy: Erytech; Research grant/Funding (institution): Ariad pharmaceuticals/Baxalta GMBH/Servier Affaires/Bayer healthcare; Advisory/Consultancy: F.Hoffman-La Roche/Guardanth health/Pfizer/Piqur Therapeutics/Puma C/Queen Mary University of London; Honoraria (self), Advisory/Consultancy: Lilly; Honoraria (self), Advisory/Consultancy, Research grant/Funding (institution): Merck Sharp & Dohme; Advisory/Consultancy: Athenex/Polyphor/Servier/Bioasis/Clovis Oncology/Leuko/Gsk; Shareholder/Stockholder/Stock options: MedSIR; Honoraria (self): Novartis; Honoraria (self), Research grant/Funding (institution): Eisai. G. Gebhart: Spouse/Financial dependant, Martine Piccart received consultancy fees: Roche; Research grant/Funding (institution), Jules Bordet Institute received research funding: Roche. All other authors have declared no conflicts of interest.
94P - Integration of clinicopathological and genomic data and adjuvant treatment decisions in premenopausal women with recurrence scores between 16 and 25
- Maha E. Alsendi (Dublin, Ireland)
- Maha E. Alsendi (Dublin, Ireland)
- Mairi Lucas (Dublin, Ireland)
- Waseem M. Darwish (Letterkenny, Ireland)
- Michaela Higgins (Dublin, Ireland)
- Cathy Kelly (Dublin, Ireland)
Abstract
Background
Data from the TAILORx trial show a three way interaction between age, chemotherapy and recurrence score (RS). By integrating clinical risk and genomic information women under 50 years with high risk cancers and recurrence scores(RS) between 16 and 25 may derive an absolute benefit from chemotherapy (CT) of between 6-9%. This benefit may be due to CT-induced menopause. The addition of ovarian suppression (OS) to endocrine therapy (ET) in premenopausal women at high risk of breast cancer (BC) recurrence is better than ET alone (SOFT/TEXT). It is has been proposed that ET/OS may be a rational option for premenopausal patients with clinically high risk breast cancer BC and a RS between 16-25 or a clinically low risk BC with a RS between 21-25. The predicted risk of distant recurrence for these patients is 14.7% (+/-3.1%) and 11.4% (+/-3.9%) respectively. The objective of our study was to determine the proportion of premenopausal patients (pts) with a RS between16-25 and a clinically high or low risk BC.
Methods
We extracted the following on all pts with ER-positive, HER2-negative, node negative BC who had OncotypeDx testing as part of routine care between 2013-9; RS, age, menopausal status, tumour size, grade, adjuvant treatment. We classified pts as low or high clinical risk (CR) using the MINDACT criteria.
Results
325 patients had OncotypeDx testing between 2013-9. Of these 55 were < 50 years (17%) and were premenopausal at diagnosis. Of these 7 (13%) had a RS between 16-25 and a high CR BC and 3 (1%) had a RS between 21-25 and low CR BC. ET alone was given to 41 (73%) and 15 (27%) received CT and ET. Three (1%) patients received ET/OS.
Conclusions
Using integrated clinicopathological and genomic data, we found that almost 15% of our premenopausal pts had a RS between 16-25 and a high clinical risk BC or a RS between 21-25 and a low clinical risk BC. These patients have a predicted risk of distant recurrence of between 11-15% and therefore an additional therapy to reduce their risk is warranted. Most of these women received tamoxifen only, under a third received CT and only 1% received ET with OS. The recent data from TAILORx and the SOFT/TEXT trials would support a discussion about the addition of OS as a way to further reduce risk.
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.