Cancer-related Molecular Pathways

The paper develops a mathematical model to study how DNA damage affects cell cycle progression, finding that polyploidisation is a key response in HepG2 cells.

The paper analyzes TP53 mutation patterns across 27 cancer types using data from 10,967 tumor samples, finding missense mutations are most common and mutation burdens vary by cancer type.

This study shows CDK11 is critical for cancer cell survival and identifies 1p36 deletions as a biomarker for CDK11 inhibitor sensitivity, but on-target toxicity limits therapeutic efficacy.

This study shows that reducing endogenous Myc levels in p53-deficient mice extends tumor-free survival and that tumors compensate by increasing Myc dosage or expression.

This study investigates whether consensus DNA sequences can regulate p53 aggregation in wild-type and mutant forms, finding that while consensus DNA inhibits wild-type p53 aggregation, oncogenic mutants evade this regulation and may even enhance aggregation.

This study identifies CKS proteins as multifaceted regulators of the cell cycle by modulating CDK activity and phosphorylation across diverse processes.

This study shows p53 inactivation is not universally linked to aneuploidy but is associated with increased chromosome loss in cancer.

The paper analyzes methylation and transcriptomic data to show that p53 R273H mutation in colon cancer is linked to partial or full EMT states and metastasis.

This study shows that sequential auto-processing of PIDD1 is essential for controlling ploidy in liver and heart development, with distinct roles for caspase-2 in different cell types.

This study shows CDKN1A stabilizes cyclin D3 by inhibiting its phosphorylation-dependent nuclear export after butyrate treatment, revealing a mechanism for butyrate-induced cell cycle arrest.

The paper uses single-cell RNA sequencing to show that cell-to-cell communication enhances p53 activation in response to chemotherapy, revealing a role for paracrine signaling in treatment response.

This study identifies ZMAT3 as a regulator of HKDC1 transcription through JUN, suppressing mitochondrial respiration in colorectal cancer cells.

This study shows that p53 deficiency causes hypertranscription and nucleotide insufficiency, leading to replication stress and genomic instability, including chromothripsis.

This paper develops a liposome-peptide formulation that enhances doxorubicin's effectiveness against p53R273H mutant tumors by disrupting PC4 interaction.

This study shows that Orientia tsutsugamushi downregulates TP53 to block DNA damage-induced apoptosis and promote bacterial replication.

This study identifies BTNL9 as a tumor suppressor in non-small cell lung cancer, showing it regulates cell cycle genes and enhances drug sensitivity through transcriptional control.

This study identifies shared cell cycle control mechanisms between CD8 T cells and embryonic stem cells, revealing similarities in cyclin expression and Emi1 function that support rapid proliferation.

This study identifies SUMOylation of HAdV E2A/DBP as a mechanism to inhibit p53 activity and apoptosis, revealing a novel pathway for viral oncogenic potential.

This study reveals that p21 continues to play a role in cell cycle re-entry after G0/G1 arrest, beyond its initial inhibitory function.

This study shows that combining MDM2 and PARP inhibitors synergistically inhibits p53 wild-type rhabdomyosarcoma growth in vitro and in vivo.

The paper shows copper induces p53 unfolding in cancer cells, leading to invasion and chemoresistance, with partial restoration by the chelator Trien.

The paper shows that E2F4DN, a non-phosphorylatable mutant of E2F4, reduces neuronal death by upregulating Cited2, suggesting its neuroprotective role in Alzheimer's disease.

This paper shows that mutant IDH disrupts p53 target gene regulation by altering chromatin states, disabling tumor suppression, and that this effect can be reversed with IDH inhibition.

The paper shows p53 maintains nuclear architecture to reduce carcinogen sensitivity and mutagenic potential by altering chromatin structure and UV lesion abundance.

The paper examines how different p53 mutations affect basal p53 activity and cellular response to genotoxicity in breast cancer cell lines.

This study shows that human P53 inhibits Escherichia coli cell viability when expressed, with effects observed under normal and stressful conditions, including phage infection and antibiotic treatment.

This study defines the murine basal p53 epigenome and transcriptional program in normal tissues, showing it regulates tumor suppressors distinct from the DNA damage response.

The paper investigates how p21 transcription variability arises through an incoherent feedforward loop involving p53 and MDM2, showing it enables rapid p21 induction and treatment-tolerant cell states.

This study shows p73 upregulates c-FLIP to suppress extrinsic apoptosis, and a compound degrades c-FLIP to enhance p73's antitumor effects in p53-mutant cancers.

This study shows that SARS-CoV-2 spike S2 subunit inhibits p53 activation of p21(WAF1), DR5, and MDM2 in cancer cells, potentially affecting tumorigenesis and chemotherapy response.