J. Taipale

Multi-Omics Analysis Reveals the Attenuation of the Interferon Pathway as a Driver of Chemo-Refractory Ovarian Cancer

The paper identifies reduced IFN-I pathway activity as a driver of chemo-refractory ovarian cancer using multi-omics analysis in a clinical trial cohort.

Interfacial water confers transcription factors with dinucleotide specificity

The paper investigates how transcription factors recognize DNA dinucleotides through structural analysis, revealing water-mediated mechanisms that enhance specificity beyond mononucleotide recognition.

Shared requirement for MYC upstream super-enhancer region in tissue regeneration and cancer

The paper identifies a shared genomic region upstream of Myc that is critical for both intestinal regeneration and cancer, revealing a genetic link between tissue renewal and tumorigenesis.

Lineage-specific oncogenes drive growth of major forms of human cancer using common downstream mechanisms

The paper identifies common downstream mechanisms driven by lineage-specific oncogenes that regulate cell proliferation in various cancers.

Mutational inactivation of Apc in the intestinal epithelia compromises cellular organisation

This study identifies three distinct effector pathways regulated by Apc in murine intestinal epithelia, each contributing to normal tissue homeostasis and tumorigenesis when disrupted by oncogenic Apc mutations.

Myc-dependent cell competition and proliferative response requires induction of the ribosome biogenesis regulator Peter Pan

The paper identifies Peter Pan as a critical Myc target gene for cell growth in Drosophila, showing that its disruption blocks Myc-induced proliferation without affecting apoptosis.

Two distinct DNA sequences recognized by transcription factors represent enthalpy and entropy optima

The paper identifies two distinct DNA sequences recognized by transcription factors as enthalpy and entropy optima, revealing how thermodynamic factors influence binding affinity.

Mice deficient of Myc super-enhancer region reveal a differential control mechanism between normal and pathological growth

This study shows that deleting the Myc super-enhancer region in mice reduces Myc expression and tumor susceptibility without overt phenotypes, suggesting therapeutic potential for targeting this element in cancer.