Kaposi Sarcoma
Prognosis
This section is being prepared by our editorial process.
🔬 Histological Types
📚 Latest Research
KSHV promotes leukocyte adhesion and transendothelial migration via induction of VCAM1.
Zhang Z, et al
Researchers have identified a novel mechanistic link in Kaposi's sarcoma (KS): KSHV-infected endothelial cells in latency constitutively express vascular cell adhesion molecule 1 (VCAM1), which drives leukocyte adhesion and transendothelial migration (TEM) — hallmark processes of KS tumor lesions — independently of exogenous inflammatory cytokine stimulation. Using siRNA knockdown and antibody blockade, the team confirmed that VCAM1 is the essential mediator of these processes, and further traced its induction to the non-canonical NF-κB (NF-κB2) pathway, demonstrating that depletion of NIK, IKKα, RelB, or NF-κB p52 significantly reduces VCAM1 levels and impairs leukocyte recruitment. Crucially, the viral latency protein vFLIP was pinpointed as the direct driver of VCAM1 upregulation, as endothelial cells infected with a vFLIP-deleted KSHV mutant showed markedly reduced VCAM1 expression and leukocyte TEM. These findings reveal vFLIP and the VCAM1 axis as potential therapeutic targets to disrupt the inflammatory microenvironment that fuels KS tumor progression.
mBio
Source →HMGB1 as a convergent host factor in virus-induced carcinogenesis.
Kim SW, et al
A new conceptual review proposes that the chromatin-associated protein HMGB1 acts as a convergent host factor exploited by multiple human oncogenic viruses — most notably Kaposi's sarcoma-associated herpesvirus (KSHV) — to promote cancer progression through two sequential functional nodes. At the first node, intracellular HMGB1 supports viral replication by acting on viral chromatin or structured viral RNA, while at the second node, viral oncoproteins trigger HMGB1 secretion that sustains infected-cell survival and remodels the tumor microenvironment. KSHV is currently the only virus with experimental evidence supporting both nodes in matched systems, making the two-node model a hypothesis rather than an established principle. The authors also flag the absence of HMGB1 data for Merkel cell polyomavirus as a tractable gap and identify HMGB1- and RAGE-directed agents as realistic candidates for clinical evaluation in virus-associated cancers.
Biochemical and biophysical research communications
Source →The TRAF6-Akt axis is required for efficient lytic replication of KSHV.
Liu Z, et al
A new study demonstrates that TRAF6, long regarded solely as an antiviral defense protein, paradoxically promotes lytic replication of Kaposi's sarcoma-associated herpesvirus (KSHV) by mediating K63-linked polyubiquitination and activation of the kinase Akt. CRISPR-mediated knockout or small-molecule inhibition of either TRAF6 or Akt reduced KSHV replication efficiency, while introduction of constitutively active Akt fully rescued viral replication in TRAF6-deficient cells. The same TRAF6-Akt axis was found essential for lytic replication of Epstein-Barr virus but dispensable for Human cytomegalovirus, revealing a shared mechanism selectively exploited by oncogenic herpesviruses. These findings identify the TRAF6-Akt signaling axis as a promising therapeutic target for KSHV-associated diseases, including Kaposi sarcoma.
PLoS pathogens
Source →💊 Therapies
This section is being prepared by our editorial process.
🥗 Diet
🫙 Supplements
🧪 Tumor markers
This section is being prepared by our editorial process.