Latest Research
All publications from the Cancer3.AI database, newest first.
Leveraging Configuration Interaction Singles for Qualitative Descriptions of Ground and Excited States: State-Averaging, Linear-Response, and Spin-Projection.
Tsuchimochi T, et al
This study addresses a longstanding challenge in quantum chemistry: accurately describing the electronic excited states of molecules using configuration interaction singles (CIS), a computationally efficient but systematically flawed method. Researchers developed a unified variational framework that extends CIS through orbital optimization in both state-specific and state-averaged forms, a double-CIS scheme for linear-response orbital relaxation, and techniques for breaking and restoring spin symmetry. Benchmark calculations revealed that spin projection alone worsens the known overestimation of excitation energies in weakly correlated systems, but combining spin projection with state averaging or double-CIS corrections substantially reduces errors, especially for Rydberg excited states. The framework was further validated on strongly correlated systems, such as the bond dissociation of hydrogen fluoride and nitrogen, demonstrating complementary benefits of state averaging and spin projection. Although not directly a medical study, improved computational methods for describing molecular electronic structure underpin drug discovery, photochemistry, and materials design relevant to biomedical applications.
Journal of chemical theory and computation
Source →Invasive breast carcinoma with a DCIS-like growth pattern: Clinicopathological features and diagnostic pitfalls.
Xu X, et al
Researchers conducted a retrospective study to characterize a rare and poorly understood form of breast cancer known as DCIS-like invasive carcinoma, which closely mimics ductal carcinoma in situ (DCIS) under the microscope and is frequently misdiagnosed as a non-invasive lesion. Among 319 breast carcinoma cases reviewed, 11 were identified as DCIS-like invasive carcinoma, displaying growth patterns such as cribriform, papillary, solid, and comedo forms, and all lacked the myoepithelial cell markers that normally distinguish true DCIS from invasive cancer. A key finding was that four of the eleven patients developed axillary lymph node metastases that paradoxically retained the DCIS-like morphology, definitively confirming the invasive nature of these tumors despite their deceptive appearance. The study also found high interobserver agreement among pathologists when using specific markers such as CK5/6 and CK14, and one patient developed cervical lymph node metastasis 51 months after surgery, highlighting the long-term risk these tumors can pose. These findings underscore that accurate diagnosis requires combining careful microscopic evaluation with a panel of myoepithelial and basement membrane markers to avoid misclassifying an invasive cancer as a non-invasive one, which could lead to inadequate treatment.
Pathology, research and practice
Source →Apelin inhibits cyst growth and improves kidney function in mice with polycystic kidney disease.
Nyimanu D, et al
Researchers investigated whether a naturally occurring signaling molecule called apelin plays a role in autosomal dominant polycystic kidney disease (ADPKD), a common inherited condition in which fluid-filled cysts progressively destroy kidney tissue and lead to kidney failure in roughly half of patients by midlife. The study found that circulating levels of apelin were significantly reduced in ADPKD patients compared to healthy controls, even before measurable decline in kidney function, suggesting that loss of apelin signaling may contribute to disease progression. In laboratory experiments, treating human ADPKD kidney cells grown as 3D cysts with apelin or a synthetic apelin receptor activator called Azelaprag slowed cyst growth, while in a mouse model of ADPKD, apelin treatment reduced kidney weight, cyst burden, blood urea nitrogen levels, and renal cAMP — a key driver of cyst expansion — as effectively as the approved drug Mozavaptan. Apelin also suppressed the expression of genes linked to cyst progression, including markers of kidney injury such as NGAL and KIM-1, pointing to a broader protective effect on the kidney. These findings identify the apelin receptor as a promising new therapeutic target for ADPKD, offering a potentially complementary or alternative treatment strategy to existing therapies.
bioRxiv : the preprint server for biology
Source →A Rare Case of Cutaneous Crystal-Storing Histiocytosis With Kappa Light Chain Restriction and Unusual BCL6 Expression.
Wang L, et al
Crystal-storing histiocytosis (CSH) is an exceptionally rare condition in which crystalline proteins accumulate inside immune cells called histiocytes, and its appearance in the skin is particularly uncommon and diagnostically challenging. Researchers report the case of a 63-year-old woman who developed firm, thickened plaques on her face, chest, and upper arms, which on biopsy revealed clusters of histiocytes packed with crystalline material alongside a lymphoplasmacytic infiltrate. Laboratory and molecular testing identified an IgG kappa monoclonal gammopathy and a clonal immunoglobulin gene rearrangement, leading to a diagnosis of cutaneous involvement by a B-cell lymphoma with plasmacytic differentiation causing localized CSH. The case also uncovered important diagnostic pitfalls: a BRAF V600E antibody test appeared falsely positive but was refuted by next-generation sequencing, and an unusual BCL6 expression in histiocytes was noted but its significance remains unclear. These findings underscore the critical need for clinicians and pathologists to recognize cutaneous CSH as a potential sign of an underlying blood cancer, and to apply confirmatory molecular testing before drawing conclusions from immunohistochemical staining alone.
Journal of cutaneous pathology
Source →PITPβ Drives JAK2 V617F-Mediated Myeloproliferative Neoplasms by Promoting PtdIns(3,4)P ₂ -Dependent AKT Hyperactivation.
Vantsev NA, et al
Researchers investigated how a protein called PITPβ contributes to the development of myeloproliferative neoplasms (MPNs), a group of blood cancers driven by a common mutation in the JAK2 gene known as JAK2 V617F. The study found that deleting PITPβ specifically in blood-forming cells dramatically improved survival in mouse models of JAK2 V617F-driven MPN, raising 25-week survival rates from just 10% to 85%, while also reducing abnormal spleen enlargement and the overproduction of red blood cell precursors. Mechanistically, PITPβ was shown to fuel a lipid signaling molecule called PtdIns(3,4)P₂, which in turn sustains hyperactivation of the AKT protein kinase — a key driver of uncontrolled cell growth in MPN — without affecting other signaling pathways such as STAT5 or ERK. Importantly, treating MPN mice with capivasertib, an FDA-approved AKT inhibitor, replicated the beneficial effects seen when PITPβ was genetically deleted, validating AKT as a therapeutic target downstream of this newly identified pathway. These findings reveal a previously unknown PITPβ–PtdIns(3,4)P₂–AKT signaling axis that selectively sustains pathological signaling in JAK2-mutant blood cancers, opening the door to new treatment strategies for MPN patients.
bioRxiv : the preprint server for biology
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