Latest Research
All publications from the Cancer3.AI database, newest first.
Isolated levator palpebrae superioris enlargement as the sole harbinger of primary orbital lymphoma.
Agarwal A, et al
Researchers describe a rare case of a 59-year-old man who developed a gradually worsening, painless drooping of the right eyelid caused by an unusual presentation of primary orbital lymphoma. Unlike typical orbital lymphomas that affect multiple eye muscles, this tumor was confined exclusively to the levator palpebrae superioris — the muscle responsible for lifting the upper eyelid — while neighboring muscles remained completely unaffected. Advanced MRI imaging, including diffusion-weighted sequences that measure water movement in tissues, provided critical clues pointing to a malignant process before the biopsy was performed. Tissue sampling confirmed a low-grade B-cell non-Hodgkin lymphoma of the extranodal marginal zone type, and thorough systemic evaluation showed the disease had not spread beyond the orbit. The patient was successfully treated with localized radiotherapy, achieving full resolution within three months. This case alerts clinicians that isolated enlargement of a single eyelid-lifting muscle, even without pain, should raise suspicion for lymphoma and underscores the diagnostic value of diffusion-weighted MRI in such atypical presentations.
Orbit (Amsterdam, Netherlands)
Source →Unraveling the inflammatory bridge: genomic evidence identifies TNFRSF9 as a potential biomarker linking Sjögren's syndrome to total risk non-Hodgkin lymphoma.
Wang H, et al
Researchers investigated the biological mechanisms linking Sjögren's syndrome (SS), a chronic autoimmune disease, to an elevated risk of non-Hodgkin lymphoma (NHL), using a genetic analysis method called Mendelian randomization applied to large-scale genome-wide association study data. The study confirmed that SS is a genuine causal risk factor for NHL, with affected patients carrying a 40% higher odds of developing lymphoma compared to those without the condition. Among 91 circulating inflammatory proteins examined, only TNFRSF9 — a member of the tumor necrosis factor receptor family involved in immune regulation — was both significantly elevated by SS and independently capable of increasing lymphoma risk, with mediation analysis showing it accounts for approximately 18% of the total SS-to-NHL causal effect. These findings position circulating TNFRSF9 as a promising blood-based biomarker that could help clinicians identify which SS patients are at greatest risk of progressing to lymphoma. The study also raises the possibility that TNFRSF9 may serve as a therapeutic target to interrupt the inflammatory pathway driving lymphoma development in autoimmune patients.
Clinical rheumatology
Source →Inducing TRIB2-targeted protein degradation to reverse chemoresistance in acute myeloid leukaemia.
Rigby E, et al
Researchers investigated TRIB2, a protein that drives acute myeloid leukaemia (AML) and helps cancer cells resist chemotherapy, exploring new strategies to eliminate it as a therapeutic target. Using a combination of CRISPR gene editing, mutational analysis, and novel drug compounds, the team found that the approved cancer drug afatinib can rapidly trigger the destruction of TRIB2 protein and kill AML cells through mechanisms that may be independent of its known targets. A newly designed PROTAC molecule (compound 5K) was also shown to effectively degrade TRIB2 and kill leukaemia cells at low concentrations, while combining TRIB2 degradation with the standard AML chemotherapy drug cytarabine produced enhanced cancer-cell killing. The study also identified a specific site on TRIB2 (lysine-63) that is critical for its natural breakdown, and showed that blocking this site made leukaemia cells more resistant to treatment and more aggressive in animal models. These findings provide strong preclinical evidence that targeting TRIB2 for destruction — using drugs like afatinib or purpose-built PROTAC degraders — represents a promising new strategy to overcome chemotherapy resistance in AML patients.
The Biochemical journal
Source →A Rare Primary Adrenal Malignancy Manifesting as a Hemorrhagic Mass: Case Report and Literature Review.
Ghaithi SA, et al
Researchers report an exceptionally rare case of primary adrenal extranodal natural killer/T-cell lymphoma (ENKTL), a highly aggressive blood cancer with fewer than ten documented cases worldwide affecting the adrenal gland. A 55-year-old man presented with worsening left-sided abdominal pain and significant weight loss, and initial imaging suggested the adrenal mass was simply a hemorrhage, delaying the correct diagnosis. Surgery was required to remove the mass, but complications involving a major abdominal vein necessitated conversion from minimally invasive to open surgery, and subsequent tissue analysis confirmed the rare lymphoma through specific immune markers and Epstein-Barr virus detection. Following surgery, residual cancer was found on PET/CT imaging, but six cycles of SMILE chemotherapy achieved a complete metabolic response, representing one of the most successful treatment outcomes ever reported for this cancer type. This case underscores the importance of obtaining tissue biopsies for unusual adrenal masses, especially when patients present with systemic symptoms such as dramatic weight loss, and of considering blood cancers in the differential diagnosis of adrenal lesions.
Case reports in endocrinology
Source →RB loss modulates chromatin organization by regulating cohesin-dependent loops and enhancer-promoter interactions.
Lee H, et al
Researchers investigated the role of the retinoblastoma protein (RB), a well-known tumor suppressor, in controlling how DNA is physically organized within the cell nucleus. The study reveals a previously unknown function of RB: beyond its classical role of blocking cell division genes, RB also regulates cohesin, a protein complex that shapes the three-dimensional architecture of chromosomes. Specifically, RB promotes the removal of cohesin from insulator regions called CTCF sites during cell division, which alters the formation of DNA loops and the boundaries between chromosomal domains known as topologically associating domains (TADs). As a result of these structural changes, RB enhances physical contacts between gene enhancers and promoters, activating the expression of hundreds of additional genes that were not previously linked to RB function. These findings significantly expand our understanding of how RB acts as a tumor suppressor and suggest that its loss in cancer may disrupt gene regulation far more broadly than previously appreciated, with potential implications for understanding cancer progression and identifying new therapeutic targets.
Nature communications
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