Lőrinc Sándor Pongor

This study shows that folate metabolism remodels epithelial states in colorectal cancer cells, affecting their response to fluoropyrimidine chemotherapy.

This study shows that HDAC inhibition with entinostat enhances immunotherapy response in SCLC by reprogramming tumor immunology and neuroendocrine status.

This study identifies key cellular programs and pathways driving metastatic organotropism in small cell lung cancer using preclinical models and multiomic profiling.

This study shows that LMNA deficiency in SCLC increases R-loop accumulation, leading to genomic instability and poor patient survival.

This study compares genomic alterations and transcriptional phenotypes in circulating tumor DNA and matched metastatic tumors in SCLC patients, finding cfDNA reflects tumor mutations, identifies resistance mechanisms, and tracks tumor evolution.

The paper maps genome-wide topoisomerase binding sites to identify TOP3A as a sensor of transcription-replication conflicts.

This study maps the SCLC tumor microenvironment and identifies cancer-associated fibroblasts as key drivers of neuroendocrine state plasticity and poor prognosis.

This study shows D-type cyclins inhibit mismatch repair (MMR) in G1 phase by shielding p21, while their degradation in S phase enables proper MMR function, maintaining genome stability.

This study identifies higher-order coordination of DNA repair proteins in single cells by analyzing their genome-wide localization using DamID and ChIC sequencing.

This study identifies Matrin3's role in regulating CDC14B alternative splicing, which affects cell proliferation and mitotic spindle dynamics in colorectal cancer cells.

The paper investigates replication origin over-activation in cancer cells and finds two distinct pools of origins are activated under different conditions.

BAMscale processes DNA sequencing datasets to generate normalized peak scores and scaled coverage tracks for visualization.