Comment on “Anti‐Cancer Potential of Copper‐NTB Complex via Damaging Cellular Organelles and Apoptosis in Triple‐Negative Breast Cancer Therapy”

Adjuvant therapy of primary breast cancer. 4th International Conference on Adjuvant Therapy of Primary Breast Cancer St. Gallen, Switzerland.

In the article that accompanies this editorial, Mackey et al present the results of ROSE/TRIO-12, a randomized phase III trial comparing single agent docetaxel to the combination of docetaxel and ramucirumab in front-line metastatic breast cancer. This large, wellpowered, placebo-controlled international trial replaced bevacizumab (a vascular endothelial growth factor [VEGF] –A ligand blocking antibody used in numerous phase III trials) with ramucirumab (a human immunoglobulin G1 VEGF receptor [VEGFR] –2–binding monoclonal antibody recently approved for gastric cancer) as the anti-VEGF agent to be studied. The results are disappointing but familiar to those who have followed the story of anti-VEGF therapy in breast cancer—yet another failure. Bevacizumab, the first anti-VEGF therapy to enter the breast cancer arena, electrified the field in 2005 with the E2100 trial, which showed a doubling in progression-free survival (PFS) when combined with weekly paclitaxel. Two subsequent trials (AVADO [Phase III Trial of Avastin and Docetaxel] and RIBBON-1 [Regimens in Bevacizumab for Breast Oncology]) combined bevacizumab with docetaxel, and while neither demonstrated the same degree of PFS benefit as the initial trial, all three demonstrated statistically significant improvements in PFS. These trials were based on a substantial body of preclinical and clinical evidence suggesting the centrality of angiogenesis in general, and VEGF in particular, to breast cancer growth, invasion, and metastasis. Increased tumor VEGF was associated with impaired outcome in numerous clinical studies, and inhibition of VEGF in preclinical models (alone or in combination with other chemotherapeutics and biologics) was associated with improved outcome. Taxanes are imbued with their own antiangiogenic activity, and the combination of taxanes with bevacizumab in particular appeared to provide synergistic antitumor activity in preclinical models of breast cancer. Things went downhill from the initial presentation of the first three randomized trials. After the approval of bevacizumab for metastatic breast cancer by the US Food and Drug Administration (following a contentious ODAC meeting), mature survival results demonstrated that the three trials (individually and collectively) failed to demonstrate an overall survival advantage. Bevacizumab, the beneficiary of an accelerated approval based on initial results, lost its breast cancer label in the United States. Other failures followed. An ambitious adjuvant program was launched, based on the original disease-free survival results. The main results of these large adjuvant trials are now in, and like the metastatic trials, they disappoint. Whether the anti-VEGF hypothesis was tested in a general population (E5103), a human epidermal growth factor receptor 2 (HER2) –positive population (BETH [Treatment of HER2 Positive Breast Cancer With Chemotherapy Plus Trastuzumab vs Chemotherapy Plus Trastuzumab Plus Bevacizumab]) or in triplenegative breast cancer (BEATRICE [A Study of Avastin (Bevacizumab) Adjuvant Therapy in Triple Negative Breast Cancer]) the results were the same: no statistically significant improvement in disease-free survival was seen. Was this failure a failure of bevacizumab, or of the underlying anti-VEGF hypothesis for breast cancer? This is a reasonable question to ask: we do not always get it right with the first drug to target a malignant process. Sunitinib, a small molecule receptor tyrosine kinase inhibitor of VEGFR2 (and many, many other kinases) struck out in multiple phase III trials in metastatic breast cancer, despite interesting phase II monotherapy results. And now ramucirumab joins the list of failed attempts to use anti-VEGF therapy in metastatic breast cancer. Ramucirumab is a human immunoglobulin G1 monoclonal antibody that binds the extracellular domain of VEGFR-2, as opposed to bevacizumab’s ligand-binding qualities. While there was a numerically increased PFS resulting from the addition of ramucirumab to docetaxel (from 8.2 to 9.5 months), this did not reach statistical significance (P .077), and failed to prolong overall survival (27.3 v 27.3 months). The drug, in addition, added significantly more toxicity, in the form of increased rates of fatigue, hypertension, febrile neutropenia, hand-foot syndrome, and stomatitis. The US Food and Drug Administration approved ramucirumab for use in gastric cancer, where it (albeit modestly) improves both PFS and overall survival. So once again (as with bevacizumab and sunitunib) this seems a breast cancer failure rather than a general failure for the anti-VEGF hypothesis. Since ramucirumab, like bevacizumab and sunitunib, target essentially the same process (VEGF-driven angiogenesis) in the same disease, its failure is perhaps unsurprising. But why has VEGF-based therapy for breast cancer, which began with such promise, failed so completely? In particular, why has the improvement seen in PFS seen with bevacizumab (and at least hinted at with ramucirumab) not translated to an improvement in overall survival in the metastatic setting, or in disease-free survival in the adjuvant setting? JOURNAL OF CLINICAL ONCOLOGY E D I T O R I A L VOLUME 33 NUMBER 2 JANUARY 1

The role of radiation therapy in the management of primary breast cancer

Ninety-one assessable elderly women (greater than 65 years) with advanced breast cancer were treated with prednisolone 15 mg (or cortisone 75 mg) daily after primary endocrine treatment (estrogens, androgens or tamoxifen). Thirteen (14%) achieved an objective regression, and 19 (21%) others showed no change for greater than or equal to six months. Hence, 32 patients (35%) had control of disease for about one year. Responses were mainly in soft tissue and skeletal lesions and were independent of response to prior endocrine treatment. Toxicity was low. Low-dose corticosteroid treatment is of value in controlling advanced breast cancer in elderly women.

Section 1.- Role of Modeling in Pharmacotherapeutics.- Section 2.- PET and Nuclear Medicine Imaging of the Breast.- Functional Radiologic Imaging in Breast Cancer.- Section 3.- Prevention of Breast Cancer.- Section 4.- DCIS: Pathology and Molecular Markers.- Ductal Carcinoma In Situ: a Modern Approach to Patient Management.- Ductal Carcinoma In Situ: Systemic Treatment.- Section 5.- Tailored Surgery for Early Breast Cancer: Surgical Techniques.- Tailored Surgery for Early Breast Cancer: Biological Aspects.- Tailored Surgery for Early Breast Cancer: the Very Young Woman.- Tailored Surgery for Older Women with Breast Cancer.- Section 6.- Tailored Radiotherapy for Breast Cancer Stages I and II: Technical Aspects.- Breast Cancer Management in the Era of Molecular Medicine: Tailored Radiotherapy - Clinical and Biological Aspects.- Early Breast Cancer (Stage I and II): Tailored Radiotherapy for Very Young Women.- The Elderly and Breast Cancer Radiotherapy.- Section 7.- Early Breast Cancer (Stage I and Stage II): Tailored Systemic Therapy for Endocrine-Resistant Breast Cancer.- Early Breast Cancer (Stage I and Stage II): Tailored Systemic Therapy for Endocrine-Responsive Breast Cancer.- Tailored Therapy for Breast Cancer in Very Young Women.- Tailored Systemic Therapy for the Elderly Woman.- Section 8.- Locoregional Therapy Following Neoadjuvant Chemotherapy: an Evolving Paradigm of Treatment Individualization.- Medical Therapy of Locally Advanced Breast Cancer.- Section 9.- Metastatic Breast Cancer: Tailored Endocrine Therapy for Premenopausal Women.- Metastatic Breast Cancer: Tailored Endocrine Therapy for Postmenopausal Women.- Metastatic Breast Cancer: Tailored Chemotherapy for the Elderly Woman.- Section 10.- Treatment of Brain Metastases from Breast Cancer.- Surgical Management of Breast Cancer Liver Metastases.- Individualization of Bisphosphonate Therapy.- Breast Cancer Metastases to the Eye.- Organ-Specific Approaches: Pain Management.- Section 11.- Genomic and Molecular Classification of Breast Cancer.- Applications of Proteomics to Clinical Questions in Breast Cancer.- Section 12.- Targeting the HER Family of Receptors in the Treatment of Advanced Breast Cancer.- Biological Therapies for Metastatic Breast Cancer: Antiangiogenesis.- Breast Cancer Gene Therapy.- Innovative Rational-Derived, Target-Based and Cytotoxic Therapies for Breast Cancer and Other Malignancies.- Section 13.- Mechanisms of Breast Cancer Resistance to Chemotherapy.- Mechanisms of Resistance to Hormone Therapy.- Novel Signaling Pathways in Breast Cancer.- Mechanisms of Apoptosis Resistance In Breast Cancer.- Section 14.- Breast Cancer and Pregnancy.- Hormone Replacement Therapy After Breast Cancer.- Male Breast Cancer.- Patients' Preferences: What Makes Treatments Worthwhile?.- Breast Cancer: the Impact of Depression and its Treatment.- Molecular Profiling in Breast Cancer.- Clinical Trials in the Era of Treatment Tailoring.

BAY 1163877 is an orally available, highly potent and selective pan fibroblast growth factor receptor (FGFR) inhibitor. In an ongoing Phase 1 clinical trial (NCT01976741) BAY 1163877 showed clinical responses at exceptional tolerability in patients suffering from different tumor types including urothelial bladder carcinoma or lung tumors, which were selected based on elevated FGFR1-3 mRNA expression. In the preclinical phase, the compound demonstrated significant single agent anti-tumor activity in various tumor models with different FGFR alterations leading to FGFR overexpression (e.g. FGFR gene amplifications or mutations). Genetic alterations of FGFRs can also be found in breast cancer with 7.5 - 17% of all tumors harboring a FGFR1 gene amplification. Elevated FGFR1 mRNA levels can be found in up to 22% of breast cancer cell lines as well as clinical samples. Other FGFR alterations include FGFR2 or FGFR4 gene amplifications as well as elevated FGFR mRNA levels, which were reported in all breast cancer subtypes. We therefore investigated BAY1163877 monotherapy in various breast cancer models. Due to the favorable clinical safety profile of BAY1163877, we also examined a combination treatment with early line antihormonal therapies in hormone receptor positive breast cancer. In vitro profiling of BAY 1163877 in a number of breast cancer cell lines showed a clear association of efficacy with expression levels of different FGFR isoforms. The efficacy was further investigated in several patient- or cell line-derived breast cancer in vivo models. For instance, BAY 1163877 alone dosed 38mg/kg twice daily induced tumor growth inhibition of greater than 90% in a subcutaneous mouse syngeneic 4T1 breast cancer model expressing elevated levels of FGFR2. Resistance to endocrine therapy appears associated with FGFR1 gene amplification and may explain the poor prognosis of FGFR1 overexpressing tumors treated with adjuvant tamoxifen. We therefore investigated the combination of the panFGFR-inhibitor BAY 1163877 with the clinically used antihormonal compound fulvestrant in selected luminal breast cancer PDX models. Some of these models showed resistance to antihormonal treatment in monotherapy but improved in vivo efficacy in combined treatment using BAY 1163877 and fulvestrant. These data may warrant further clinical investigation of BAY1163877alone or in combination with antihormonal therapy in patients with FGFR overexpressing breast cancer. Citation Format: Oliver Politz, Peter Ellinghaus, Sebastian Bender, Sylvia Gruenewald, Franziska Siegel, Marie-Pierre Collin, Sabine Zitzmann-Kolbe, Dominik Mumberg, Karl Ziegelbauer. Preclinical activity of the FGFRinhibitor BAY 1163877 alone or in combination with antihormonal therapy in breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1079. doi:10.1158/1538-7445.AM2017-1079

Purpose: Somatic mutations in the tyrosine kinase domain of human epidermal growth factor receptor2 (HER2) have been reported to lead to resistance to HER2-targeted therapies in HER2-positive breast cancer, while activating mutations of HER2 have been described in HER2-negative breast cancer. The prevalence, clinicopathological characteristics, and phenotypes of HER2 mutations are not well established, thus we sought to describe the HER2 mutation profile of Chinese breast cancer patients. Methods: DNA samples were gathered from breast cancer patients undergoing neoadjuvant (N=102) or adjuvant therapy (N=498) at Fudan University Shanghai Cancer Center between January 1, 2006 and December 31, 2012. Sanger sequencing was performed to analyze all exons of HER2 to identify somatic mutations. To determine the phenotypes of novel HER2 mutations, in vitro kinase assays, protein structure analysis, cell culture, and xenograft experiments were conducted. Results: 10 HER2 somatic mutations were observed in 17 patients (17/600, 2.83%). 7 novel HER2 mutations were uncovered, 4 in the transmembrane domain and 3 in the kinase domain. Kinase domain mutations L768S and V773L were detected in HER2-negative tumors, while K753E was found in HER2-positive disease. In vitro kinase assays found that L768S and V773L exhibited a significant increase of tyrosine kinase-specific activity, while Western blots showed that L768S and V773L strongly increased phosphorylation of all signaling proteins in both MCF10A and MCF7cell lines, indicating that they were activating mutations. In Matrigel cultures, L768S and V773L formed acini when seeded in vehicle, but maintained spherical morphology when seeded in culture containing trastuzumab. The addition of lapatinib in Matrigel culture inhibited the growth of all except K753E, which was successfully inhibited by neratinib. Similarly, L768S, V773L and K753E increased the number of cell colonies formed in soft agar, trastuzumab and lapatinib treatment decreased the number of colonies formed by L768S and V773L, but only neratinib could inhibit the colony growth of K753E. Xenograft showed L768S and V773L displayed a more rapid growth, while K753E showed resistance to lapatinib in vivo. MCF10A cells bearing K753E mutation were found to be resistant to lapatinib (IC50>10,000 nmol/L), but could be inhibited by neratinib, though requiring a relatively higher dosage (IC50 of 32 nmol/L) than HER2 WT (IC50 of 480 nmol/L for lapatinib, <2 nmol/L for neratinib) and other HER2 mutations. Meanwhile, clinical follow-up showed that the 2 patients with K753E mutation who received adjuvant trastuzumab treatment presented with either brain or bone metastasis, in their 3rd and 5th year after initial cancer diagnosis, suggesting K753E mutation may have a role in trastuzumab resistance as well. Conclusions: HER2 somatic mutations were found in 2.83% of patients in this study. HER2-positive tumors harboring certain HER2 kinase domain resistance mutations may not benefit from trastuzumab or lapatinib treatment, and neratinib may offer an alternative treatment option for these patients. HER2-negative disease with activating mutations may benefit from HER2-targeted therapies, and may be of interest in prospective clinical trials. Citation Format: Wen-Jia Zuo, Yi-Zhou Jiang, Ke-Da Yu, Zhi-Ming Shao. Activating HER2 mutations promote oncogenesis and resistance to HER2-targeted therapies in breast cancer [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P1-04-04.

Background: The combination of CDK 4/6 inhibition and endocrine therapy has emerged as the new first line standard of care treatment for patients with hormone receptor (HR) +ve metastatic breast cancer (MBC)1. Ribociclib plus letrozole has been shown to improve PFS (25.3 vs 16.0 months; log-rank P=9.63x10-8) compared to letrozole alone2. More recently, this benefit has also been demonstrated in pre- and peri-menopausal women in combination with ovarian suppression and tamoxifen or an aromatase inhibitor (AI), with an improved overall survival (40.9 months vs OS not reached; HR = 0.712; p=0.00973) in the MONALEESA-7 study3. Approximately 800 patients in Australia participated in the ribociclib medicine access program (MAP) between May 2017 and June 2018, prior to government funding. Beyond eligibility criteria for the program and clinician name, no patient data was initially captured, consistent with usual practice for MAPs, due to the multiple challenges related to ethics, data ownership, security and patient privacy. We have previously demonstrated the feasibility of successful data collection alongside MAPs4 which can yield benefits for clinicians, industry and the broader medical community. Based on this we plan to retrospectively collect data for patients treated as part of the Australian ribociclib MAP. Trial Design: This is a secondary data use, non-interventional study of patients in Australia who received treatment with the combination of an AI and ribociclib, obtained via a MAP, for HR+ HER2- MBC. The target sample size is 250 patients from ~15 sites. De-identified patient data will be retrieved from the patient’s medical records and entered on to an electronic case report form. Data collection is anticipated to commence in July 2019 with the final treatment and survival outcomes collected in late 2020, thus allowing for a minimum of 24 month follow up for all patients from the start date of treatment with ribociclib and AI (May 2017 - June 2018). Study Aims: The primary aim of the study is to describe real world clinical and tumour characteristics of patients with HR+ HER2-ve MBC in Australia who are recommended and received ribociclib in combination with an aromatase inhibitor in the first line setting. Details of adjuvant therapy received and the tolerability of the treatment combination including dose interruptions, dose reductions and significant adverse events of interest related to ribociclib will be assessed. Secondary aims include time to treatment progression and progression free survival for the ribociclib and AI combination, and to explore the disease course post progression, including clinician choice of subsequent lines of therapy in routine clinical practice.

This presentation will review the topic of radiation-induced cardiac dysfunction in patients with breast cancer. Specific areas of discussion include the a review of the cardiac-sparing techniques available for radiation therapy in breast cancer treatment; guidelines for the prevention, diagnosis, and treatment of cardiac dysfunction after radiation exposure in patients with breast cancer; and new areas of research in the field of radiation-induced cardiac disease in breast cancer. Emerging knowledge of how concurrent systemic therapies may interact with radiation to affect heart function will also be discussed. In addition, future directions in the field of radiation-induced heart dysfunction will be reviewed. Citation Format: Carmen Bergom. Radiation therapy and cardiovascular disease in breast cancer [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 ED13-2.

Breast cancer is the most commonly diagnosed cancer in women, with many efforts aimed at reducing acute and late toxicity given the generally favorable clinical outcomes with the current standard of care. Carbon ion radiation therapy is an emerging technique that may reduce dose to adjacent organs at risk while allowing dose escalation to the target. Given the efficacy of the standard treatments for breast cancer, there have been few prospective studies to date investigating carbon ion radiation therapy in breast cancer. PubMed/Medline, Ebsco, Cochrane, and Scopus were systematically reviewed using the search terms "carbon ion" and "breast" in November 2019. Out of the 76 articles screened, 26 articles were included. This comprehensive review describes the physical and biological properties of carbon ion radiation therapy, with an emphasis on how these properties can be applied in the setting of breast cancer. Studies investigating the role of carbon ion radiation therapy in early stage breast cancers are reviewed. Additionally, the use of carbon ion radiation therapy in locally advanced disease, recurrent disease, and radiation-induced angiosarcoma are discussed. Although the data is limited, the early clinical results are promising. Further clinical trials are needed, especially in the setting of locally advanced and recurrent disease, to fully define the potential role of carbon ion radiation therapy in the treatment of breast cancer.

Background: The use of anti-estrogen (AE) therapies (selective estrogen receptor modulators [SERMs], aromatase inhibitors [AIs]) in breast cancer (BC) patients was recently associated with risk of developing rheumatoid arthritis (RA) (J Rheum 2015;42:55-9). We attempted to replicate and extend these results using electronic health record (EHR) enhanced cancer registry data that assessed specific AE therapies and also accounted for potential confounding by age, smoking status, and chemotherapy use. Methods: Using cancer registry and EHR data, we identified a cohort of BC patients who were newly diagnosed and treated at Mayo Clinic Rochester from 1998-2011 and had no previous diagnosis of RA. Smoking status at diagnosis, BC treatments and RA at diagnosis and during follow-up were identified using validated EHR-based algorithms. Hazard ratios (HRs) and 95% confidence intervals (CI) from a multivariate Cox model were used to estimate the association of AE use with risk of RA, controlling for age, smoking status at BC diagnosis, and BC chemotherapy use. Results: The analytic cohort of 9,244 newly diagnosed BC patients treated and followed at Mayo Clinic had a median age at diagnosis of 59 years (range 18-97); 32% were smokers; and 29% were treated with chemotherapy. During a median follow-up of 49 months (range 1-191), 19 patients developed RA. Compared to BC patients not receiving any AE therapy, those receiving AI monotherapy, but not SERM monotherapy or both SERMs and AIs, were at significantly increased risk of developing RA (Table). AE Therapy# of RA Cases / # patientsHR* (95% CI)P-valueNo AE therapy6/4,0711.00 (reference)SERMs only5/2,5371.20 (0.36 - 3.95)0.77AIs only5/7126.37 (1.77 - 22.92)0.005SERMs then AIs3/1,8750.90AI then SERMs0/490.91 (0.21 - 3.86)*Adjusted for age, smoking status and use of chemotherapy Conclusions: Our findings indicate that the use of AIs for BC therapy, but not SERMs or SERMs followed by AIs, is associated with increased risk for development of RA, when controlling for smoking status and use of chemotherapy. While needing replication, these findings suggest a specific role for AIs in RA development and suggest pathways that could be targeted to prevent this potential treatment complication. Citation Format: Matthew K. Breitenstein, Ming-Fen Ho, Richard M. Weinshilboum, James R. Cerhan, Jyotishman Pathak, Tim Bongartz, Liewei Wang, James N. Ingle. Association of anti-estrogen therapy in breast cancer patients and subsequent risk of rheumatoid arthritis: An electronic health record study. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-191. doi:10.1158/1538-7445.AM2015-LB-191

Recently, there is increased attention to neo-adjuvant endocrine therapy in breast cancer. Especially for selected tumour types and fragile elderly patients this might be a promising alternative to chemotherapy. Monitoring treatment effect during neo-adjuvant endocrine therapy is crucial to allow a timely switch to chemotherapy in case of a non-successful treatment. Most trials evaluating neo-adjuvant endocrine therapy use palpation as primary outcome and multiple radiological modalities as secondary outcomes. The aim of this study was to determine which evaluation corresponds best to pathological resection size after 6 months of neo-adjuvant endocrine therapy. This analysis was conducted in the TEAM-IIA trial in which 102 patients with early breast cancer (>2 cm and >50% ER expression) were treated with neo-adjuvant exemestane. In total, 83 patients were treated for 6 months and 19 for 3 months. Therapy response evaluation was performed using repeated palpation (mostly by the same clinician), mammography, ultrasound and MRI. Only measurements within 2 months before surgery were considered. After surgery, the size of the remaining tumour was reported and used as reference. In total, 93 resection size measurements were available. From the 93 patients for whom resection size was available, 69 patients were evaluated by palpation, 53 by ultrasound, 42 by mammography and 29 by MRI. Overall, palpation showed to be the most reliable predictor for resection size (correlation of 49%), followed by mammography (31%), ultrasound (14%) and MRI (1%). Mammography showed the smallest mean absolute error (MAE, 8.7 mm), followed by ultrasound (9.2 mm), palpation (11.4 mm) and MRI (12.3 mm). The low correlation of MRI with resection size was mostly due to a relative high number of radiological complete remissions (14%, n=4), of which only one was a true pathological complete response (pCR), while the other tumours were up to 80 mm at resection. Although of less influence on the correlation to resection size, false complete remissions were observed in all other modalities. Time to surgery was an important factor for all modalities. After correcting for non-predictive radiological complete responses and limiting the measurements to one month before surgery, all correlations increased significantly (mammography=72%, palpation=70%, ultrasound=58%, MRI=50%) with a concomitant decrease in mean absolute error. The low correlation of MRI with resection size was mostly due to non-visible measurements, interpreted as radiological complete remissions of which only one in four was a true pathological complete response (pCR) while the other tumours were 25, 65, and 80 mm at resection. This is the first study to report on the reliability of radiological evaluation during neo-adjuvant endocrine therapy. In this study, mammography was the most reliable radiological method, with stronger correlation and small mean absolute error. Non- visible observations in neo-adjuvant endocrine therapy did not always reflect pCR. Hence, in the neo-adjuvant endocrine therapy setting, radiological complete responses should be interpreted carefully, especially in MRI, and use of other modalities or improved image processing methods may be considered. Citation Format: Blok EJ, Charehbili A, Kroep JR, Seynaeve CM, van de Velde CJH, Kuppen PJK. Radiological evaluation of neo-adjuvant endocrine therapy in hormone-receptor positive early breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P6-01-05.

PEGylated hydrazided gold nanorods for pH-triggered chemo/photodynamic/photothermal triple therapy of breast cancer

Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: an overview of the randomised trials

Breast cancer targeted therapy: successes and challenges