Although sentinel lymph node biopsy (SLNB) has proved to be able to diagnose axillary lymph node status safely and reliably, there is still not enough evidence to suggest that it can be used in patients who have undergone neoadjuvant chemotherapy (NAC) for lymph node-sparing surgery. The present study used molecular approaches to determine whether SLNB can be reliably used in patients who have been treated with NAC before SLN surgery, and whether the total tumor load of the SLN can be used as a predictive factor in axillary lymphadenectomy (ALD). We used one-step nucleic acid amplification (OSNA) to analyze a total of 111 consecutive patients who presented operable invasive breast carcinomas and who had been treated with NAC. SLN was positive in 55 patients and the identification rate was 100%. In 9 of these 55 patients, ALD showed that other lymph nodes were also involved. In all of the other 46 patients, the only lymph node to be identified as positive was SLN. Metastasis was not found in any of the axillary lymph nodes in the isolated tumor cell group. The total tumor load, defined as the amount of cytokeratin 19 mRNA copy numbers in all positives SLN (copies/µL), showed three risk groups related to the possibility of positive non-sentinel nodes. OSNA is a diagnostic technique that is highly sensitive, specific, and reproducible and it can be used to analyze sentinel lymph nodes after NAC. Total tumor load may be able to help predict additional metastases in axillary lymphadenectomy.

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4152 Background: Despite huge efforts patients (pts) with advanced PDAC, still have a dismal long-term prognosis. The lack of available good-quality tissue samples for next generation sequencing (NGS) prevents from finding actionable alterations that could guide personalized treatments. Circulating tumor DNA (ctDNA) provides a non-invasive method for obtaining molecular information with therapeutic potential. Here, we present prospective data of ctDNA sequencing in pts with PDAC. Methods: We collected a single blood sample from advanced PDAC pts at any line of treatment (Tx) and at least 10 days apart from their last therapy. The samples were analyzed by Guardant360 plasma-based NGS, a standardized assay which covers microsatellite instability [MSI] evaluation and analysis of all four types of somatic alterations in 74 genes. Alterations were reported either as pathogenic or non-pathogenic. We classified each gene alteration according to the different OncoKB therapeutic levels of evidence [LE]. Additionally, we gathered the dates of both blood collection and molecular report. In case the molecular report showed no tumor-related alterations, it was interpreted as either absence of detectable mutations or low ctDNA levels, which would translate low disease burden or pts responding to therapy. Demographic and clinical data have been accessed from the medical records. Results: From 08/2019 to 09/2021 we collected blood samples from 94 PDAC pts. 56% of them were male and 53% were >65 years old. At the time of sample collection, nearly all pts were metastatic (98%). Regarding previous lines of Tx, 57% pts were Tx naïve; 10% were receiving active systemic Tx and 33% had experienced disease progression. Molecular reports were available in an average of 9.1 days. A total of 243 gene alterations were detected, having 94% of pts at least 1 genomic alteration, which was pathogenic in 69% of the cases (see Table). There were no pathogenic alterations ranked as OncoKB LE 1-2 ( MSI or NTRK). Seventy alterations (30%) were ranked as OncoKB LE 3A and 4 ( ARID1A, BRAC2, CDKN2A, KRAS). Three of these pts were treated with PARP inhibitors due to the presence of BRCA2 mutations. No ctDNA was detected in 15 pts (16%), despite being the sample collected >10 days from receiving their last Tx. Of these, 11 had low tumor burden (only peritoneal or lung metastases) and 4 had documented response to the Tx by the time the samples were collected. Conclusions: Real-time and prospective genomic profiling of pts with advanced PDAC using ctDNA is feasible and conveniently fast, which would allow its role in identifying and developing therapeutic targets for approved Tx or clinical trial treatments. [Table: see text]

To describe the clinical outcomes and risk factors for 90‐day mortality in patients with solid tumours (ST) and coronavirus disease 2019 (COVID‐19) during the first outbreak in Catalonia. This is a multicentre retrospective study including adults with ST and COVID‐19 confirmed by real time reverse transcription polymerase chain reaction between 13 March and 30 April 2020. Clinical and survival data were collected. Follow‐up ended on 30 July 2020. Multivariate and survival analysis were performed. A hundred and fifteen patients were included. In all, 42.6% had advanced disease and were receiving anticancer treatment; 7% were admitted to the ICU and 22.6% died during hospitalisation. Thirty‐day mortality was 27.8%, which increased to 33.9% at 90 days. Ninety‐day mortality was associated with current smoker status (hazard ratio [HR]: 2.91, 95% CI [confidence interval]: 1.03‐8.33, P = .044), baseline ECOG‐PS 2 to 3 (HR: 3.88, 95% CI: 1.77‐8.46, P < .001]), dyspnoea (HR: 3.02, 95% CI: 1.31‐6.96, P = .009), a respiratory rate ≥ 24 (HR: 2.24, 95% CI: 1.02‐4.92, P = .046) and sepsis (HR: 3.97, 95% CI: 1.78‐8.88, P < .001). Of the 76 survivors, 73.6% had a follow‐up visit. Of those, 33.9% had their cancer controlled and 23.2% had progressed. Thirty‐five survivors were receiving anticancer treatment before COVID‐19 diagnosis though 14 had to discontinue the treatment. Eight survivors without previous anticancer therapy started therapy. The median time to start anticancer therapy after COVID‐19 was 45 days (interquartile range: 28‐61). In conclusion, 90‐day mortality in patients with ST and COVID‐19 was 33.9%; current smoker status, poor ECOG‐PS, dyspnoea, respiratory rate ≥24 and sepsis were independent risk factors for mortality; and survivors did not restart their anticancer treatment until 1.5 months after COVID‐19 diagnosis.