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Mashup Score: 22
Pathologic response (PathR) by histopathological assessment of resected specimens, may be an early clinical endpoint associated with long-term outcomes with neoadjuvant therapy. Digital pathology may improve efficiency and precision of PathR assessment. LCMC3 (NCT02927301) evaluated neoadjuvant atezolizumab in patients with resectable non-small cell lung cancer (NSCLC) and reported 20% major pathologic response rate.
Source: www.jto.orgCategories: General Medicine News, Oncologists1Tweet
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Mashup Score: 41
Subcutaneous atezolizumab is approved for the treatment of various solid tumors. Previous results from the IMscin001 study (NCT03735121) demonstrated that the pharmacokinetics, efficacy, immunogenicity, and safety of subcutaneous and intravenous atezolizumab were consistent (data cutoff: April 26, 2022). We present updated data from this trial (data cut-off: 16 January 2023).
Source: www.jto.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 77
AbstractPurpose:. The classification of small cell lung cancer (SCLC) into distinct molecular subtypes defined by ASCL1, NEUROD1, POU2F3, or YAP1 (SCLC-A, -N, -P, or -Y) expression, paves the way for a personalized treatment approach. However, the existence of a distinct YAP1-expressing SCLC subtype remains controversial.Experimental Design:. To better understand YAP1-expressing SCLC, the mutational landscape of human SCLC cell lines was interrogated to identify pathogenic alterations unique to SCLC-Y. Xenograft tumors, generated from cell lines representing the four SCLC molecular subtypes, were evaluated by a panel of pathologists who routinely diagnose thoracic malignancies. Diagnoses were complemented by transcriptomic analysis of primary tumors and human cell line datasets. Protein expression profiles were validated in patient tumor tissue.Results:. Unexpectedly, pathogenic mutations in SMARCA4 were identified in six of eight SCLC-Y cell lines and correlated with reduced SMARCA4 m
Source: aacrjournals.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 19Clinical utility of circulating tumor DNA in patients with advanced KRASG12C-mutated non-small cell lung cancer treated with sotorasib. - 19 day(s) ago
For patients with KRASG12C-mutated NSCLC who are treated with sotorasib, there is a lack of biomarkers to guide treatment decisions. We therefore investigated the clinical utility of pre-treatment and on-treatment circulating tumor DNA (ctDNA), as well as treatment-emergent alterations upon disease progression.
Source: www.jto.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 73
We report long-term outcomes from a pooled analysis of patients with previously untreated metastatic non‒small-cell lung cancer (NSCLC) with programmed cell death ligand 1 (PD-L1) tumor proportion score (TPS) <1% enrolled in phase 3 studies of pembrolizumab plus chemotherapy versus placebo plus chemotherapy.
Source: www.jto.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 1
ESMO is Europe’s leading medical oncology society, providing a professional network for its members and working with national societies across Europe.
Source: www.esmo.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 72
We report long-term outcomes from a pooled analysis of patients with previously untreated metastatic non‒small-cell lung cancer (NSCLC) with programmed cell death ligand 1 (PD-L1) tumor proportion score (TPS) <1% enrolled in phase 3 studies of pembrolizumab plus chemotherapy versus placebo plus chemotherapy.
Source: www.jto.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 46Sotorasib Is a Pan-RASG12C Inhibitor Capable of Driving Clinical Response in NRASG12C Cancers - 1 month(s) ago
AbstractKRASG12C inhibitors, like sotorasib and adagrasib, potently and selectively inhibit KRASG12C through a covalent interaction with the mutant cysteine, driving clinical efficacy in KRASG12C tumors. Because amino acid sequences of the three main RAS isoforms—KRAS, NRAS, and HRAS—are highly similar, we hypothesized that some KRASG12C inhibitors might also target NRASG12C and/or HRASG12C, which are less common but critical oncogenic driver mutations in some tumors. Although some inhibitors, like adagrasib, were highly selective for KRASG12C, others also potently inhibited NRASG12C and/or HRASG12C. Notably, sotorasib was five-fold more potent against NRASG12C compared with KRASG12C or HRASG12C. Structural and reciprocal mutagenesis studies suggested that differences in isoform-specific binding are mediated by a single amino acid: Histidine-95 in KRAS (Leucine-95 in NRAS). A patient with NRASG12C colorectal cancer treated with sotorasib and the anti-EGFR antibody panitumumab achieved
Source: aacrjournals.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 46Sotorasib Is a Pan-RASG12C Inhibitor Capable of Driving Clinical Response in NRASG12C Cancers - 1 month(s) ago
AbstractKRASG12C inhibitors, like sotorasib and adagrasib, potently and selectively inhibit KRASG12C through a covalent interaction with the mutant cysteine, driving clinical efficacy in KRASG12C tumors. Because amino acid sequences of the three main RAS isoforms—KRAS, NRAS, and HRAS—are highly similar, we hypothesized that some KRASG12C inhibitors might also target NRASG12C and/or HRASG12C, which are less common but critical oncogenic driver mutations in some tumors. Although some inhibitors, like adagrasib, were highly selective for KRASG12C, others also potently inhibited NRASG12C and/or HRASG12C. Notably, sotorasib was five-fold more potent against NRASG12C compared with KRASG12C or HRASG12C. Structural and reciprocal mutagenesis studies suggested that differences in isoform-specific binding are mediated by a single amino acid: Histidine-95 in KRAS (Leucine-95 in NRAS). A patient with NRASG12C colorectal cancer treated with sotorasib and the anti-EGFR antibody panitumumab achieved
Source: aacrjournals.orgCategories: General Medicine News, Hem/OncsTweet
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Mashup Score: 46Sotorasib Is a Pan-RASG12C Inhibitor Capable of Driving Clinical Response in NRASG12C Cancers - 1 month(s) ago
AbstractKRASG12C inhibitors, like sotorasib and adagrasib, potently and selectively inhibit KRASG12C through a covalent interaction with the mutant cysteine, driving clinical efficacy in KRASG12C tumors. Because amino acid sequences of the three main RAS isoforms—KRAS, NRAS, and HRAS—are highly similar, we hypothesized that some KRASG12C inhibitors might also target NRASG12C and/or HRASG12C, which are less common but critical oncogenic driver mutations in some tumors. Although some inhibitors, like adagrasib, were highly selective for KRASG12C, others also potently inhibited NRASG12C and/or HRASG12C. Notably, sotorasib was five-fold more potent against NRASG12C compared with KRASG12C or HRASG12C. Structural and reciprocal mutagenesis studies suggested that differences in isoform-specific binding are mediated by a single amino acid: Histidine-95 in KRAS (Leucine-95 in NRAS). A patient with NRASG12C colorectal cancer treated with sotorasib and the anti-EGFR antibody panitumumab achieved
Source: aacrjournals.orgCategories: General Medicine News, Hem/OncsTweet
AI–based path response assessmt from neoadjuvant LCMC3 trial (atezo) @JTOonline: - digital MPR predicted visual MPR (AUC ROC 0.98) - digital %viable tumor correlated w visual (r=0.73) Laying the foundation for digital path in neoadj nsclc @IASLC #LCSM https://t.co/LwqL2z4Mtj