Jesika Agarwala
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jesika Agarwala has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Argyrios Tzouvelekis
Department of Respiratory Medicine, Medical School, University of Patras, 26504 Patras, Greece
1 shared publication - Dimitrios Ampazis
Department of Respiratory Medicine, Cavan & Monaghan Hospital, Lisdarn, H12Y7W1 Cavan, Ireland
1 shared publication - Eleni Pavli
Department of Pathology, General Hospital of Patras, 26504 Patras, Greece
1 shared publication - Fotios Sampsonas
Department of Respiratory Medicine, University Hospital of Patras, 26504 Patras, Greece
1 shared publication - Maria Malvina Eleftheriou
Department of Surgery, General & Upper Gastrointestinal Surgical Unit, Royal Infirmary of Edinburgh, 51 Little France Crescent, Old Dalkeith Road, Edinburgh EH16 4SA, UK
1 shared publication - Pinelopi Bosgana
Department of Pathology, General Hospital of Patras, 26504 Patras, Greece
1 shared publication
Latest Publications
- Open Access
EGFR-Mutated Small Cell Lung Cancer: Molecular Characterization and Clinical Implications of EGFR-TKIs
Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy defined by a number of genetic and molecular features, including near-universal TP53 and RB1 inactivation, MYC amplifications, Notch pathway disruption, and hyperactivated PI3K/AKT/mTOR signaling. The subtypes of SCLC, SCLC-A/N/P/I, are primarily based on four transcription regulators (ASCL1, NeuroD1, YAP1, POU). This review provides a concise overview of the molecular landscape of SCLC and then focuses on the subset displaying epidermal growth factor receptor (EGFR) alterations. EGFR-positive SCLC presents either as rare primary (de novo) disease (2.6–19.3%) or as transformed SCLC originating from EGFR-mutant non-small cell lung cancer (NSCLC) in 3–14% of cases following EGFR tyrosine kinase inhibitor (TKI) therapy. In both cases, the tumors harbor EGFR mutations with the most frequent one being exon 19 deletions. A number of pathways have been identified regarding the lineage transformation with the co-occurring TP53 and RB1 loss predominating, while a number of other molecular mechanisms have been explored, including activation of epithelial-to-mesenchymal transition factors (ZEB1, SLUG), MDM4 or BCL2L2/NFKBIA co-amplifications, and newly postulated genetic variants such as FBN1 and PALLD, alongside emergent surface expression of DLL3, B7-H3, and PTK7. Once SCLC transformation occurs, tumors tend to drop EGFR dependence and display profound resistance to EGFR-TKIs, necessitating a shift to standard platinum–etoposide chemotherapy, with or without immunotherapy. The value of EGFR-TKIs has been explored, as an add-on treatment, in several cases and its efficacy has not so far provided satisfactory outcomes. An update of the literature, within this particular field, is being provided along with the value for routine serial re-biopsy (tissue or liquid) upon disease progression, especially when EGFR-TKIs have been used. Early identification of neuroendocrine transformation can prevent futile EGFR-TKI monotherapy, capture mixed histologies, and recognize potential re-transformation back to adenocarcinoma.
Open AccessEGFR-Mutated Small Cell Lung Cancer: Molecular Characterization and Clinical Implications of EGFR-TKIs
Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy defined by a number of genetic and molecular features, including near-universal TP53 and RB1 inactivation, MYC amplifications, Notch pathway disruption, and hyperactivated PI3K/AKT/mTOR signaling. The subtypes of SCLC, SCLC-A/N/P/I, are primarily based on four transcription regulators (ASCL1, NeuroD1, YAP1, POU). This review provides a concise overview of the molecular landscape of SCLC and then focuses on the subset displaying epidermal growth factor receptor (EGFR) alterations. EGFR-positive SCLC presents either as rare primary (de novo) disease (2.6–19.3%) or as transformed SCLC originating from EGFR-mutant non-small cell lung cancer (NSCLC) in 3–14% of cases following EGFR tyrosine kinase inhibitor (TKI) therapy. In both cases, the tumors harbor EGFR mutations with the most frequent one being exon 19 deletions. A number of pathways have been identified regarding the lineage transformation with the co-occurring TP53 and RB1 loss predominating, while a number of other molecular mechanisms have been explored, including activation of epithelial-to-mesenchymal transition factors (ZEB1, SLUG), MDM4 or BCL2L2/NFKBIA co-amplifications, and newly postulated genetic variants such as FBN1 and PALLD, alongside emergent surface expression of DLL3, B7-H3, and PTK7. Once SCLC transformation occurs, tumors tend to drop EGFR dependence and display profound resistance to EGFR-TKIs, necessitating a shift to standard platinum–etoposide chemotherapy, with or without immunotherapy. The value of EGFR-TKIs has been explored, as an add-on treatment, in several cases and its efficacy has not so far provided satisfactory outcomes. An update of the literature, within this particular field, is being provided along with the value for routine serial re-biopsy (tissue or liquid) upon disease progression, especially when EGFR-TKIs have been used. Early identification of neuroendocrine transformation can prevent futile EGFR-TKI monotherapy, capture mixed histologies, and recognize potential re-transformation back to adenocarcinoma.