Latest Research
All publications from the Cancer3.AI database, newest first.
A case of small bowel obstruction caused by konjac.
Ooya Y, et al
This case report documents an exceptionally rare instance of small bowel obstruction (SBO) caused by konjac, a gelatinous food product derived from the Amorphophallus konjac plant that is widely consumed across Asia and increasingly popular in Western countries. A man in his 50s presented with acute abdominal pain after eating konjac at breakfast, and after conservative treatment at a local clinic failed to resolve his symptoms, he was transferred to a surgical center for further evaluation. Abdominal computed tomography revealed signs of SBO without a clear cause, and emergency laparotomy ultimately uncovered four connected pieces of konjac physically blocking the small intestine, which were successfully removed. The patient recovered without complications and was discharged on postoperative day 8. Although most cases of SBO result from postoperative adhesions, hernias, or tumors, this case highlights konjac ingestion as a rare but real dietary cause that clinicians should consider, particularly as global consumption of konjac-based products continues to rise.
Journal of surgical case reports
Source →Targeting keratin 6 A overcomes gemcitabine resistance by restoring equilibrative nucleoside transporter 1 and TAM-mediated metabolic compensation in pancreatic cancer.
Zhang J, et al
Researchers investigated the molecular mechanisms driving gemcitabine resistance in pancreatic cancer, a disease where chemotherapy routinely fails due to intrinsic or acquired drug resistance. Using integrated public genomic datasets, spatial transcriptomics, single-cell sequencing, and clinical tissue microarrays, the team identified keratin 6A (KRT6A) as a key driver of resistance that is overexpressed in pancreatic tumors and linked to poor patient survival. In a cohort of 90 gemcitabine-treated patients, high KRT6A protein levels were associated with significantly lower disease control and objective response rates, confirming its clinical relevance. Mechanistically, KRT6A was shown to suppress ENT1, the membrane transporter responsible for importing gemcitabine into cancer cells, while simultaneously triggering MIF signaling that recruits immunosuppressive M2 tumor-associated macrophages and creates a cytidine-rich metabolic environment that competes with drug uptake. To therapeutically exploit this vulnerability, the researchers engineered a tumor-targeted lipid nanoparticle (c-Lip@siKRT6A) that silences KRT6A, and demonstrated in mouse xenograft models that combining this nanocarrier with gemcitabine markedly suppressed tumor growth. These findings establish KRT6A as a clinically actionable target and present a viable nanomedicine strategy to restore chemosensitivity in one of the deadliest and most treatment-resistant cancers.
Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
Source →Molecular biologic and Epstein-Barr virologic advances in extranodal natural killer/T cell lymphoma over the past four decades.
Harabuchi Y
A comprehensive forty-year review published in Auris, nasus, larynx examines the molecular biology and Epstein-Barr virus (EBV) mechanisms underlying extranodal natural killer/T-cell lymphoma (ENKTL), a rare and aggressive cancer that causes destructive lesions of the nasal cavity and midline facial structures, historically misidentified as 'lethal midline granuloma.' The review traces the disease's reclassification in the 1980s and 1990s as an NK/T-cell malignancy definitively linked to EBV, whose oncoprotein LMP1 activates key oncogenic signaling pathways — JAK/STAT, NF-κB, PI3K/Akt, and RAS/MAPK — while epigenetic regulators such as EZH2 and HDAC, and chromosomal deletions affecting tumor suppressors PRDM1 and FOXO3, further drive disease progression. Laboratory studies identified autocrine and paracrine feedback loops involving multiple cytokines and chemokines — including IL-9, IL-10, IL-15, HGF, CCL17, and CXCL10 — that amplify tumor proliferation, and diagnostic accuracy has improved through measurement of serum EBV DNA copy numbers, viral microRNA miR-BART2-5p, and the novel biomarker soluble CD27. On the treatment front, modern concurrent chemoradiotherapy using multidrug-resistance-independent agents has raised five-year overall survival rates to over 80% for localized disease, a dramatic improvement over early anthracycline-based regimens that failed due to multidrug resistance. The field is now transitioning toward combining chemoradiotherapy with immune checkpoint inhibitors and molecularly targeted small-molecule drugs, underscoring the need for continued research to improve outcomes in patients with advanced or relapsed disease, where prognosis remains poor.
Auris, nasus, larynx
Source →GHRH and insulin hypersecretion from a pancreatic neuroendocrine tumor in multiple endocrine neoplasia type 1.
Lamback E, et al
Researchers report a rare case of a female patient with genetically confirmed multiple endocrine neoplasia type 1 (MEN1) who harbored a pancreatic neuroendocrine tumor that simultaneously secreted both growth hormone-releasing hormone (GHRH) and insulin. The GHRH hypersecretion drove ectopic acromegaly and caused somatotroph hyperplasia in the pituitary gland, which was initially misidentified as a primary pituitary tumor and surgically removed. Only after that surgery triggered severe hypoglycemia was the underlying GHRH- and insulin-cosecreting pancreatic tumor identified and excised, with histopathology confirming dual hormone production. The authors propose that in MEN1 patients, the expected hypoglycemia from an insulin-secreting tumor may be concealed by the opposing effects of elevated growth hormone on blood glucose, creating a diagnostically misleading clinical picture. This case underscores the need for thorough ectopic hormone screening in MEN1 patients and highlights that multihormonal co-secretion from pancreatic neuroendocrine tumors can produce overlapping, mutually masking symptoms that significantly delay correct diagnosis.
JCEM case reports
Source →Systematic Review of the Molecular Basis for Cavernous Sinus Invasion in Somatotropinomas.
Ovenden CD, et al
Somatotropinomas are growth hormone-secreting pituitary tumors that frequently invade the cavernous sinus, a critical anatomical structure at the base of the skull, complicating surgical removal and worsening patient outcomes. This systematic review, conducted according to PRISMA 2020 guidelines, pooled data from 43 studies encompassing 1,824 patients — including 724 with invasive tumors — to map the molecular drivers of this aggressive behavior. Researchers identified key molecules across four biological domains: epithelial-mesenchymal transition (including E-cadherin, Fascin 1, and MMP-9), cellular proliferation (including PTTG, AIP, STAT3, and E2F1), hormonal signaling (including GNAS, SSTR2, and DRD5), and tumor angiogenesis (including VEGF and Drp1), all of which were significantly altered in invasive compared to non-invasive tumors. These molecular changes provide a coherent scientific explanation for why somatotropinomas preferentially target the cavernous sinus and represent promising candidates for novel targeted therapies or prognostic biomarkers. The authors note that most existing studies rely on older analytical techniques and call for larger datasets analyzed with modern proteomic and transcriptomic methods to fully elucidate the responsible pathways. Ultimately, these findings pave the way for more personalized treatment strategies and improved risk stratification for patients with this challenging tumor type.
Endocrine-related cancer
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