Latest Research
All publications from the Cancer3.AI database, newest first.
Poly r(C) binding protein (PCBP) 1 expression is regulated by the E3 ligase UBE4A in thyroid carcinoma.
Zhang M, et al
A new study published in Bioscience Reports investigated the molecular relationship between the RNA-binding protein PCBP1 (Poly r(C) binding protein 1) and the E3 ubiquitin ligase UBE4A in thyroid carcinoma, one of the most common endocrine cancers. The research focused on understanding how UBE4A controls the levels of PCBP1, a protein previously implicated in tumor suppression across several cancer types. The findings reveal that UBE4A regulates PCBP1 expression through the ubiquitin-proteasome degradation pathway, suggesting that elevated UBE4A activity may reduce PCBP1 levels and thereby promote cancer progression in the thyroid. This mechanistic insight identifies a potential new regulatory axis that could be exploited as a therapeutic target in thyroid carcinoma. For clinicians, understanding how tumor suppressor proteins are silenced at the post-translational level may open new avenues for targeted treatment strategies in patients with aggressive thyroid cancer.
Bioscience reports
Source →SPEN loss drives extra-follicular diffuse large B cell lymphoma with female-specific lethality and therapeutic vulnerabilities.
Pelzer B, et al
Researchers have identified a previously unrecognized biological pathway driving the BN2 subtype of diffuse large B-cell lymphoma (DLBCL), the most common aggressive blood cancer, by studying co-occurring mutations in two genes, SPEN and NOTCH2. Contrary to the longstanding view that all DLBCLs arise from B cells engaged in follicular immune responses inside lymph nodes, this study reveals that these mutations redirect cancer development along an extra-follicular trajectory involving marginal zone, memory, and autoimmune-like B cells. Critically, the research uncovered a striking sex disparity: female patients and female mice carrying these mutations experienced significantly worse survival compared to their male counterparts, a difference traced to enhanced X-chromosome-linked toll-like receptor (TLR) signaling. The team demonstrated in preclinical models that blocking IRAK, a key kinase in the TLR signaling pathway, represents a promising sex-specific therapeutic strategy for affected women. These findings redefine the developmental origins of BN2-DLBCL and identify a high-risk female population that may benefit from precision therapies targeting TLR-driven pathways.
Cancer discovery
Source →Changes in the Surgical Management of Pheochromocytoma.
Thibeault F, et al
A comprehensive review published in the Journal of Laparoendoscopic & Advanced Surgical Techniques examines how the surgical management of pheochromocytoma, a rare and potentially life-threatening tumor of the adrenal gland, has transformed over recent decades. The review concludes that minimally invasive adrenalectomy—performed laparoscopically or robotically via transabdominal or retroperitoneal approaches—has replaced open surgery as the standard of care for localized tumors, achieving comparable cancer control outcomes with reduced patient risk. A critical genomic finding is that approximately 40% of pheochromocytoma cases carry hereditary germline mutations, which now directly shapes surgical planning, including the use of cortical-sparing adrenalectomy in hereditary cases to preserve adrenal cortical function and avoid lifelong steroid dependence. Preoperative alpha-adrenergic blockade remains the guideline-backed standard to prevent dangerous cardiovascular crises during surgery, though its routine use in low-risk patients is an area of ongoing clinical debate. Even in metastatic disease, surgery continues to play a meaningful role within a multimodal treatment framework, providing symptom control and potential survival benefit in carefully selected patients. These advances collectively signal a move toward individualized, genomically informed surgical care that aims to improve both long-term oncologic and functional outcomes for patients with this complex disease.
Journal of laparoendoscopic & advanced surgical techniques. Part A
Source →Impact of diagnosis and targeted interventions on the quality of life and neuropsychiatric outcomes of patients with adrenal tumours: a systematic review.
Ruggiero B, et al
A comprehensive systematic review published in the European Journal of Endocrinology examined how diagnosis and targeted treatments affect health-related quality of life and neuropsychiatric outcomes in patients with adrenal tumours across six subtypes. Analysing 117 studies involving 35,361 patients, researchers found that all adrenal tumour subtypes were consistently associated with impaired wellbeing, with a clear gradient of severity ranging from mild impairment in non-functioning tumours to the most pronounced and persistent deficits in adrenal Cushing's syndrome, phaeochromocytoma/paraganglioma, and adrenocortical carcinoma. While targeted interventions generally improved patient-reported outcomes, recovery was frequently incomplete and residual symptoms remained common even after treatment. Critically, the review identified a major gap in the field: no disease-specific neuropsychiatric assessment tools exist for adrenal tumour patients, limiting the precision with which clinicians can monitor psychological recovery. The authors conclude that long-term, patient-centred care is essential for this population and call for the development of adrenal tumour-specific outcome measures to better capture the full burden of these conditions.
European journal of endocrinology
Source →BUB1 as a candidate non-oncogene addiction vulnerability in metastatic phaeochromocytoma/paraganglioma.
Ahmadi M, et al
Phaeochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors with very limited treatment options once they spread to distant organs. Researchers mined large gene expression datasets (TCGA and COMETE) to identify molecular dependencies in metastatic PPGLs and discovered that BUB1, a kinase that guards chromosomal stability during cell division, is significantly overexpressed in metastatic compared to non-metastatic tumors. Experiments in a human phaeochromocytoma cell line confirmed that silencing BUB1 genetically, or blocking it pharmacologically with the compound BAY1816032, substantially reduced cancer cell viability, colony formation, migration, and invasion. BUB1 inhibition also suppressed markers of epithelial-to-mesenchymal transition, a key biological process that enables cancer cells to escape and spread through the body. This is the first study to demonstrate BUB1 overexpression in metastatic PPGL tissue, establishing the kinase as a promising therapeutic target and potential biomarker, pending validation in larger multi-institutional patient cohorts.
Scientific reports
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