BJMO - volume 17, issue 7, november 2023
N. Willers MD, P. Enzlin PhD, P. Neven MD, PhD, S.N. Han MD, PhD
The improvements in breast cancer treatment have resulted in an increased survival rate and a growing number of breast cancer survivors. These survivors have to learn to cope with the side effects of breast cancer treatment. These side effects often have an important impact on patient’s general and sexual well-being. In clinical care, sexual side effects are often un(der)recognised because physicians and patients experience barriers to discussing sexuality-related issues. It is, nevertheless, important and relevant to discuss sexuality during the various stages of (breast) cancer treatment. For young women at the start of breast cancer treatment, fertility-related questions may arise. During the different phases of breast cancer treatment, sexual functioning and sexual experience may be altered by the physical, psychosocial, and relational impact of breast cancer diagnosis and treatment. This article aimed to highlight easy-to-use methods to discuss sexuality proactively for any healthcare provider involved in the care of the cancer patient. Mentioning sexuality in the early stages of (breast) cancer treatment and addressing sexual sequelae of breast cancer diagnosis and treatment can significantly improve patients’ quality of life.
(BELG J MED ONCOL 2023;17(7):252–8)
Read moreBJMO - volume 17, issue 6, october 2023
M. Piccart MD, PhD, J. Vansteenkiste MD, PhD, H. Prenen MD, PhD, F. Duhoux MD, PhD, A. Janssens MD, PhD, M. Delforge MD, PhD, A. Awada MD, PhD, P. Neven MD, PhD, A. Sibille MD, B. Neyns MD, PhD
The oncological treatment landscape is evolving at a very rapid pace with a continuous stream of novel treatment options. To fully leverage these therapeutic advances in clinical practice it is important to facilitate a rapid access to innovative anticancer drugs for patients. Specifically for Belgium, the delay from EMA approval to reimbursement for anticancer drugs is very long, with an average of almost 600 days, and a substantial proportion of innovative drugs never make it to the patient. The stringent focus of the Belgian Commission for Reimbursement of Medicines (CRM) on overall survival (OS) data in reimbursement decisions is believed to be an important contributor to this situation. However, the ever-increasing pace at which new anticancer therapies are being developed in combination with an earlier detection of cancer will make it increasingly difficult to present mature OS data at the time of regulatory approval in the years to come. As such, there is an urgent need for a debate with the regulators to consider more readily available endpoints in their reimbursement assessments. In fact, when a strong treatment effect is seen on an intermediate endpoint such as disease-free or progression-free survival, a benefit in OS is quite likely. As such, our reimbursement system needs to be adapted to better align with the scientific progress in oncology. In this, a temporary reimbursement decision based on intermediate endpoints could give Belgian patients earlier access to promising lifesaving medicines. In this, we as oncologists, including specialists in haematology, respiratory oncology, and gastrointestinal cancer, strongly encourage the CRM to use the grading provided by the ESMO magnitude of clinical benefit scale to evaluate the clinical added value of future cancer treatments. This will not only facilitate a faster patient access to innovative therapies, but will also help policy-makers in advancing ‘accountability for reasonableness’ in their resource allocation deliberations.
(BELG J MED ONCOL 2023;17(6):211–5)
Read moreBJMO - volume 17, issue 5, september 2023
A. Enguita PhD, T. Feys MBA, MSc, P. Neven MD, PhD, H. Wildiers MD, PhD
The 2023 ASCO meeting again featured several ground-breaking presentations in the field of breast cancer (BC). Early-stage highlights include the long-awaited data of the NATALEE trial assessing adjuvant ribociclib in combination with endocrine therapy (ET) and the PHERGain trial exploring chemotherapy de-escalation using 18F-FDF PET/CT metabolic response assessment. Other studies discussed new molecular biomarkers for recurrence and response, and the impact of ET timing intake on outcomes. Finally, flibanserin was shown to be effective in countering sexual dysfunction in BC patients receiving adjuvant ET. In the metastatic setting, the SONIA trial questioned the universal use of CDK4/6 inhibitors in the first line treatment of patients with hormone-receptor (HR) positive metastatic BC. Furthermore, a pooled analysis of the DESTINY-Breast01, -02, and -03 trials reaffirmed trastuzumab deruxtecan as an effective treatment option for patients across all age subgroups in HER2-positive BC. Finally, a less toxic capecitabine regimen emerged as an alternative to standard treatment in metastatic BC. These results, along with other important findings, are summarised in this report. We would like to acknowledge Prof. Hans Wildiers and Prof. Patrick Neven (University Hospitals Leuven) for their help in selecting the abstracts and adding a clinical interpretation to this overview.
(BELG J MED ONCOL 2021;15(5):193–201)
Read moreBJMO - volume 16, issue 1, february 2022
T. Geukens MD, M. De Schepper MD, F. Richard PhD, M. Maetens PhD, K. Van Baelen MD, S. Leduc MSc, E. Isnaldi MD, PhD, H.L. Nguyen MSc, I. Bachir MD, E. Vanden Berghe MSc, W. Van Den Bogaert MD, K. Punie MD, P. Neven MD, PhD, H. Wildiers MD, PhD, G. Floris MD, PhD, C. Desmedt PhD
The purpose of this review is to highlight the recent knowledge gathered on the genomics of metastatic breast cancer (BC), together with the clinical implications. Through large sequencing efforts, the genomic profile of BC is increasingly being deciphered, with a limited number of those findings having resulted in genomicmatched treatment options. The pace at which new discoveries are made is highest in the early setting, where large samples can easily be accessed through leftover tissue of resection specimens, and smaller diagnostic biopsies are also available. In the metastatic setting however, residual tissue from clinically indicated biopsies or resections are scarce. Some efforts have been undertaken through (inter)national, institutional, clinical trial- or patient-driven initiatives. They have highlighted important differences between the genomic landscape of metastatic versus primary tumour tissues. Especially in hormone receptor positive HER2 negative (HR+/HER2-) disease, driver mutations continue to accumulate after dissemination, most of them in the ESR1 or ERBB2 genes, or in genes involved in transcription regulation, MAPK- or PI3K-signaling pathways. Importantly, the genomic landscape is not homogeneous even within one patient, and significant heterogeneity is seen on an intra-patient, inter-lesion and intra-lesion level. This poses clinical challenges, with different subclones possibly harbouring differential sensitivity to systemic treatments and single biopsies not accurately reflecting the full molecular profile. Finally, through liquid biopsies, a more complete and less invasive insight into the tumour’s characteristic could theoretically be retrieved. However, it is unclear how well these profiles correlate with the actual diversity of the different lesions. Importantly, rapid autopsy programs have been shown to enhance research on the genomics of metastatic BC, and one such program was recently launched at UZ/KU Leuven.
(BELG J MED ONCOL 2022;16(1):18–28)
Read moreBJMO - volume 15, issue 6, october 2021
G. Broeckx MD, Ir A. Hébrant PhD, N. D’Haene MD, PhD, K. Van de Vijver MD, PhD, J. Van Huysse MD, I. Vanden Bempt MD, PhD, P. Aftimos MD, P. Neven MD, PhD, P. Pauwels MD, PhD
The PI3K/AKT pathway plays an important role in the oncogenesis of breast cancer. Activating mutations in PI3K, more specifically in the p110α catalytic unit of the class IA PI3K isoform (encoded by the PIK3CA gene), lead to an increased conversion of phosphatidylinositol-4,5-biphosphate (PIP2) to phosphatidylinositol-3,4,5-triphosphate (PIP3) inducing a cell signalling cascade for cell proliferation and cell survival. PIK3CA mutations are found in 20–32% of all breast cancers (BC), particularly in hormone sensitive (HR+) BC. In breast cancer, activation of the PI3K pathway coexists with the activation of the oestrogen receptor pathway. Inhibition of one of these pathways may lead to compensatory activation of the other pathway. Therefore, mono-therapy with PI3K inhibitors has limited activity in HR+ BC. On the other hand, this explains the efficacy of a PI3K/ER dual blockade. This dual blockade is researched in the phase III SOLAR-1 trial. In the PIK3CA-mutated cohort of this study, there is an improved outcome for patients with advanced or metastatic HR+ HER2- BC, harbouring activating hotspot mutations in PIK3CA and previously treated with an aromatase inhibitor and no more than one line of endocrine therapy for MBC, who received fulvestrant (a selective oestrogen receptor degrader) and alpelisib (a p110α-isoform specific inhibitor) in comparison to the patients that received fulvestrant and placebo. Based on these results, a medical need program for alpelisib in a heavily pre-treated setting and an amendment were approved by the EMA and the Belgian FAMHP. Supporting this data, we propose the mutational analysis of PIK3CA, preferably by next generation sequencing on FFPE tumour material, in advanced or metastatic HR+ HER2- BC, previously treated with three lines of systemic therapy.
(BELG J MED ONCOL 2021;15(6):304-14)
Read moreBJMO - volume 14, issue 6, october 2020
L. van Walle MD, J. Vandeven , C. Colpaert MD, PhD, FP. Duhoux MD, PhD, P. Neven MD, PhD, L. Van Eycken MD, N. van Damme PhD
The aim of this study is to provide a reference for the Belgian breast cancer population, offering detailed information on various patient and tumour characteristics for the breast cancer population as a whole, as well as for the different molecular subtypes. Incidence data for primary invasive breast cancer in females diagnosed in 2014 were selected in the Belgian cancer registration database and underwent individual manual reviewing of the pathology protocols. Subsequently, in 95% of the study population a surrogate molecular subtype was successfully derived, using the combined expression of oestrogen receptor, progesterone receptor, human epidermal growth factor receptor-2, and tumour differentiation grade as surrogate for the proliferation marker Ki67, in conformity with the 2011 St Gallen surrogate classification. Ultimately, differences between the molecular subtypes regarding initial presentation and histopathological features were evaluated by means of a Pearson Chi-squared test for independence. Furthermore, relative survival was calculated for the different molecular subtypes. Histologically, the large majority of the Belgian breast cancer population presents with invasive breast carcinoma of no special type (NST), formerly called invasive ductal carcinoma (75.2%), 14.5% with invasive lobular carcinoma and 5.8% with mixed ductal/lobular invasive carcinoma. Less than five percent of the population harbours less frequently occurring histological subtypes. The Belgian breast cancers are predominantly of the luminal A-like subtype (54.4%), followed by the luminal B-like HER2 negative (14.7%) and the luminal B-like HER2 positive subtype (12.2%). The mean age at diagnosis is 62 years, with almost a third of the patients being 70 years or older. One out of five patients is younger than 50 years, and in the triple negative population this group counts for 31.9%, compared to 16.6% in the luminal A-like breast carcinomas. Most patients (69.4%) are diagnosed with early stage breast cancer (clinical stage 0-II); six percent of the breast cancers are clinically metastasised at the time of diagnosis. For 19% of the patients, information on clinical stage was lacking or staging was not applicable. The unadjusted five-year relative survival proportion for the Belgian cohort is 91.4%. Luminal A-like breast cancer opposed to triple negative breast cancer have the best and worst relative survival, with respectively 96.8% and 77.4% five-year relative survival proportions.
(BELG J MED ONCOL 2020;14(6):263-73)
Read moreBJMO - volume 13, issue 7, november 2019
Ir A. Hébrant PhD, M. Lammens MD, PhD, C. Van den Broecke MD, N. D’Haene MD, PhD, J. Van den Oord MD, PhD, A. Vanderstichele MD, PhD, A. Dendooven MD, PhD, P. Neven MD, PhD, K. Punie MD, G. Floris MD, PhD, J. Van der Meulen MD, HA. Poirel MD, PhD, C. Dooms MD, PhD, S. Rottey MD, PhD, T. Boterberg MD, PhD, L. Brochez MD, PhD, M.C. Burlacu MD, G. Costante MD, D. Creytens MD, PhD, P. De Paepe MD, PhD, R. De Pauwn MD, B. Decallonne MD, PhD, F. Dedeurwaerdere MD, H. Denys MD, PhD, L. Ferdinande MD, PhD, R. Forsyth MD, PhD, M. Garmyn MD, PhD, T. Gevaert MD, PhD, J. De Grève MD, PhD, E. Govaerts MD, E. Hauben MD, PhD, J. Kerger MD, O. Kholmanskikh Van Criekingen MD, PhD, V. Kruse MD, PhD, Y. Lalami MD, L. Lapeire MD, PhD, P. Lefesvre MD, PhD, J.P. Machiels MD, PhD, B. Maes MD, PhD, G. Martens MD, PhD, M. Remmelink MD, PhD, I. Salmon MD, PhD, R. Sciot MD, PhD, S. Tejpar MD, PhD, K. Van de Vijver MD, PhD, L. Van de Voorde MD, I. Van den Berghe MD, A. Van den Bruel MD, K. Vandecasteele MD, PhD, L. Vanwalleghem MD, K. Vermaelen MD, PhD, R. Salgado MD, PhD, E. Wauters MD, PhD, B. Weynand MD, PhD, E. Van Valckenborgh PhD, G. Raicevic PhD, M. Van den Bulcke PhD, P. Pauwels MD, PhD
In order to advise the Federal Government on the reimbursement of molecular tests related to Personalised Medicine in Oncology, the Commission of Personalised Medicine (ComPerMed), represented by Belgian experts, has developed a methodology to classify molecular testing in oncology. The different molecular tests per cancer type are represented in algorithms and are annotated with a test level reflecting their relevance based on current guidelines, drug approvals and clinical data. The molecular tests are documented with recent literature, guidelines and a brief technical description. This methodology was applied on different solid tumours for which molecular testing is a clear clinical need.
(BELG J MED ONCOL 2019;13(7):286–95)
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