A phase Ib trial of an anti-idiotypic vaccine for Lewis Y (IGN 301) administered subcutaneously in patients with refractory solid tumors

Thakkar, Snehal Govind; Heeger, Peter S.; Wacker, B.; Roddy, Meagan; Waxenecker, Günter; Himmler, Gottfried; Loibner, Hans; Elson, Paul; Bukowski, Ronald

doi:10.1200/jco.2004.22.90140.2586

Cited by 3 publications

(1 citation statement)

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“…Thus, GD3 ganglioside vaccines and anti-idiotypic monoclonal antibodies, which mimic GD3 gangliosides, were carried out on melanoma patients with evidence of a low survival outcome [256]. Currently, some experimental vaccine therapeutics are approved, including GM2 KLH/QS-21 and MGV (GM2/GD2 KLH QS21) for malignant melanomas [257]; Theratope (sialyl-Tn Ag) for breast cancer [258]; IGN 301 (anti-idiotypic antibody) for LeY antigen associated with small cell lung cancer [259]. Moreover, the National Cancer Institute has declared MUC1 as a priority cancer antigen.…”

Section: Carbohydrate-based Cancer Drugsmentioning

confidence: 99%

GANAB and N-Glycans Substrates Are Relevant in Human Physiology, Polycystic Pathology and Multiple Sclerosis: A Review

Masi

Orlando

2022

IJMS

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Glycans are one of the four fundamental macromolecular components of living matter, and they are highly regulated in the cell. Their functions are metabolic, structural and modulatory. In particular, ER resident N-glycans participate with the Glc3Man9GlcNAc2 highly conserved sequence, in protein folding process, where the physiological balance between glycosylation/deglycosylation on the innermost glucose residue takes place, according GANAB/UGGT concentration ratio. However, under abnormal conditions, the cell adapts to the glucose availability by adopting an aerobic or anaerobic regimen of glycolysis, or to external stimuli through internal or external recognition patterns, so it responds to pathogenic noxa with unfolded protein response (UPR). UPR can affect Multiple Sclerosis (MS) and several neurological and metabolic diseases via the BiP stress sensor, resulting in ATF6, PERK and IRE1 activation. Furthermore, the abnormal GANAB expression has been observed in MS, systemic lupus erythematous, male germinal epithelium and predisposed highly replicating cells of the kidney tubules and bile ducts. The latter is the case of Polycystic Liver Disease (PCLD) and Polycystic Kidney Disease (PCKD), where genetically induced GANAB loss affects polycystin-1 (PC1) and polycystin-2 (PC2), resulting in altered protein quality control and cyst formation phenomenon. Our topics resume the role of glycans in cell physiology, highlighting the N-glycans one, as a substrate of GANAB, which is an emerging key molecule in MS and other human pathologies.

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