Background: Osteonecrosis of the jaw is a very delicate side effect of Denosumab.
BackgroundDespite the deleterious consequences of iron deficiency (ID) in patients with cancer, underdiagnosis is frequent. The CARENFER study aimed to assess the prevalence of ID using both serum ferritin concentration and transferrin coefficient saturation (iron-saturation of transferrin, TSAT) index, as well as ID anaemia in patients with cancer.MethodsThis prospective cross-sectional study was conducted in 15 oncology units in France in 2019. All patients present in the medical unit during the 2-week study period, regardless of the type of tumour (solid or haematological) and treatment, were eligible. Serum ferritin concentration, TSAT index and haemoglobin level were determined. ID and ID-associated anaemia were defined according to European Society of Medical Oncology 2018 Guidelines: ID was defined either as ferritin <100 µg/L (absolute ID) or as ferritin ≥100 µg/L and TSAT <20% (functional ID).ResultsA total of 1221 patients with different types of solid malignant tumours were analysed: median age 64 years; 89.4% under treatment for their cancer, mainly by chemotherapy (75.4%). Overall, ID was found in 57.9% (55.1–60.6) of patients. Among them, functional ID accounted for 64% of cases. ID anaemia was reported in 21.8% (19.6–24.2) of all patients with cancer. ID was highly prevalent in untreated (75/130, 57.4%) and non-anaemic (419/775, 54.1%) patients.ConclusionThis study highlights the high prevalence of ID in patients with cancer, whether or not associated with anaemia or treatment. These results emphasise the need to a better detection and management of ID in cancer, thereby optimising overall patient care.Trial registration numberClinicalTrials.gov Identifier: NCT03924271.
BackgroundCell-free DNA detection is becoming a surrogate assay for tumor genotyping. Biological fluids often content a very low amount of cell-free tumor DNA and assays able to detect very low allele frequency mutant with a few quantities of DNA are required. We evaluated the ability of the fully-automated molecular diagnostics platform Idylla for the detection of KRAS, NRAS and BRAF hotspot mutations in plasma from patients with metastatic colorectal cancer (mCRC). Materials and methodsFirst, we evaluated the limit of detection of the system using two set of laboratory made samples that mimic mCRC patient plasma, then plasma samples from patients with mCRC were assessed using Idylla system and BEAMing digital PCR technology. ResultsLimits of detection of 0.1%, 0.4% and 0.01% for KRAS, NRAS and BRAF respectively have been reached. With our laboratory made samples, sensitivity up to 0.008% has been reached. Among 15 patients' samples tested for KRAS mutation, 2 discrepant results were found between Idylla and BEAMing dPCR. A 100% concordance between the two assays has been found for the detection of NRAS and BRAF mutations in plasma samples.
Background: Pathogenic BRCA1/2 mutations currently serve as the main biomarker of homologous recombination deficiency (HRD) for PARP inhibitor (PARPi) selection, which have also been reported to correlate with the efficacy of platinum (Pt) chemotherapy. However, patients without BRCA1/2 alterations can also present HRD phenotype through other mechanisms and might benefit from PARPi or Pt chemotherapy.Methods: HRD score of tumor samples from 199 patients (Cohort I: ovarian, breast, pancreatic, prostate, and uterine cancers) were evaluated by targeted next-generation sequencing (NGS) (GeneseeqPrimeÒ HRD). A cohort of 416 independent solid tumor patients (Cohort II) were further analyzed for exploring HRD score distribution, while another cohort of 84 high-grade serous ovarian cancer patients (Cohort III) who received Pt chemotherapy were analyzed for investigating the predictive value of HRD score in treatment efficacy.Results: HRD score, combining loss of heterozygosity (LOH), telomeric allelic imbalance (TAI), and large-scale station transitions (LST), of Cohort I ranges from 0 to 107, 32% of which harbor BRCA1/2-deficiency (pathogenic mutations with LOH, 2 pathogenic mutations, or homozygous deletion). HRD score 38 was defined as HRDpositive that accounts for approximately 95% of the BRCA1/2-deficient cases. In Cohort II, 14% of them were BRCA1/2-deficient with a median HRD score of 67 which was significantly higher than that of the BRCA1/2-sufficient ones (28; p<0.001). In BRCA1/2-wildtype subgroup, 37% of patients have HRD scores38 (51%, 42%, and 8% for ovarian, breast, and pancreatic cancers). In Cohort III, patients with a platinumfree interval (PFI) of over 6 months (Pt-sensitive) have significantly higher HRD scores than Pt-resistant patients (median: 55 vs 34, p¼0.04). In BRCA1/2-wildtype patients, a significantly longer PFS was observed when HRD38 than those with HRD<38 (median: 17.8 vs 11.8 months, p¼0.04).Conclusions: Our study reported an HRD evaluation pipeline based on targeted NGS in diverse cancer types, and HRD38 was chosen to define HRD-positive status, which correlates with better clinical outcomes of Pt-chemotherapy.
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