Latest Research
All publications from the Cancer3.AI database, newest first.
Bilateral pheochromocytoma: differences in clinical and surgical outcomes with unilateral pheochromocytomas.
Donato S, et al
This study investigated differences in clinical presentation, surgical management, and outcomes between patients with bilateral pheochromocytoma — tumors affecting both adrenal glands simultaneously — and those with unilateral pheochromocytoma affecting only one gland. Bilateral pheochromocytoma is a rarer and more complex condition, often associated with hereditary syndromes such as multiple endocrine neoplasia type 2 or von Hippel-Lindau disease, and poses greater surgical risk due to the potential for permanent adrenal insufficiency. The research found notable differences in clinical features, genetic background, and perioperative outcomes between the two groups, with bilateral cases requiring more tailored surgical strategies to preserve residual adrenal cortical function. These findings are important for clinicians because they highlight the need for individualized surgical planning and long-term hormonal monitoring in patients with bilateral disease. The study contributes to improving patient safety and quality of life by refining guidelines for the management of this rare but serious endocrine tumor.
Endocrine
Source →Pituitary adenoma-induced IGF-I triggers increased proliferation and tumorigenic potential of thyroid cells by suppressing KLLN via MET/TP53 axis.
Guo X, et al
Researchers investigated how pituitary adenoma (PA), a chronic hormone-secreting tumor of the pituitary gland, leads to thyroid diseases such as goiter and thyroid cancer. The study focused on insulin-like growth factor I (IGF-I), a hormone elevated in PA patients, and its role in driving abnormal thyroid cell growth. Experiments in cell cultures and mouse models revealed that IGF-I promotes thyroid cell proliferation and tumor formation by reducing levels of a tumor-suppressing protein called Killin (KLLN). Mechanistically, IGF-I activates the MET receptor tyrosine kinase, which in turn suppresses the tumor protein TP53, and this chain of events leads to decreased KLLN expression and unchecked cell growth. These findings identify a previously unknown IGF-I/MET/TP53/KLLN signaling pathway linking pituitary adenoma to thyroid cancer development. For clinicians, this pathway presents several potential therapeutic targets that could be exploited to prevent or treat thyroid diseases arising in PA patients.
Experimental cell research
Source →S100A6 promotes liver metastasis by activating FGFR3 signaling in BAP1-deficient uveal melanoma.
Li Y, et al
Researchers investigated why uveal melanoma — a rare eye cancer — so frequently spreads to the liver and kills patients within a year, focusing on tumors that lack a tumor-suppressor protein called BAP1. The study found that BAP1 deficiency triggers epigenetic changes that switch on a gene called S100A6, causing it to be overproduced in cancer cells. Crucially, the team discovered that S100A6 acts as a previously unknown activator of a cell-surface receptor called FGFR3, setting off sustained inflammatory signals that remodel the tumor's surrounding environment in the liver and fuel metastasis. Blocking the S100A6–FGFR3 axis, either genetically or with experimental drugs, effectively halted liver metastasis in laboratory models. These findings reveal a targetable molecular pathway driving one of the most lethal and treatment-resistant forms of metastatic eye cancer, offering a potential new therapeutic strategy for patients with BAP1-deficient uveal melanoma.
Oncogene
Source →Impact of immunosuppressive therapy on non-melanoma skin cancer after solid organ transplantation: A critical systematic review.
Abulail JA, et al
A new systematic review published in Transplant Immunology examined how different immunosuppressive drugs used after solid organ transplantation affect the risk of developing non-melanoma skin cancer (NMSC), the most common malignancy in transplant recipients. Unlike previous studies that grouped all transplant patients together, the authors analyzed kidney, liver, lung, heart, and pancreas recipients as separate populations to better identify organ-specific patterns. Key findings showed that basiliximab, an induction agent, was generally linked to lower NMSC incidence compared to T-cell depleting therapies, while calcineurin inhibitors were consistently associated with higher skin cancer rates across multiple organ groups. Sirolimus- and mycophenolate-based maintenance regimens appeared to carry a lower NMSC risk in certain cohorts, though the evidence was not uniform across all organ types. Importantly, the review concluded that current data are insufficient to justify routine changes to immunosuppression solely to reduce skin cancer risk, and instead emphasized proactive prevention through regular structured skin examinations and dedicated post-transplant dermatology clinics.
Transplant immunology
Source →OLFM4 orchestrates the immunosuppressive microenvironment and drives gallbladder cancer progression.
Li W, et al
Researchers investigated the role of the protein OLFM4 (Olfactomedin-4) in gallbladder cancer (GBC), the most common and deadly malignancy of the bile ducts, using single-cell RNA sequencing to map the tumor microenvironment in detail. By comparing tumor tissues with adjacent healthy tissue from GBC patients, the study found that OLFM4-expressing cancer cells act as central communication hubs, reshaping the surrounding immune and structural environment to favor tumor growth through signaling pathways including SPP1-CD44, SPP1-Integrin, WNT/β-catenin, and TGF-β. OLFM4 expression was found to increase progressively with disease advancement, and its presence was linked to cancer cell proliferation, invasiveness, maintenance of stem-like properties, and resistance to the chemotherapy drug gemcitabine. When OLFM4 was experimentally silenced in cancer cells, tumor growth, migration, invasion, and chemoresistance were all significantly reduced in laboratory models. These findings establish OLFM4 as a promising biomarker for identifying aggressive gallbladder cancer and as a potential therapeutic target that could improve treatment outcomes for patients with this difficult-to-treat disease.
Journal of cancer research and clinical oncology
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