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Appendix stained with Anti-L1CAM(CD171)
The L1 Cell Adhesion Molecule (L1CAM), also known as CD171, is a transmembrane glycoprotein protein crucial for neurogenesis and plays an essential role in neural cell adhesion and migration. Mutations in the X-linked L1CAM result in MASA syndrome; a neurological disorder causing mental retardation, aphasia, shuffling gait, and adducted thumbs. In addition to the brain, L1CAM expression is normally expressed in kidney tubular epithelium, intestinal crypt, and peripheral nerves. L1CAM has been investigated in various tumors, including colorectal, renal cell, ovarian, and thyroid carcinomas. Cytoplasmic and membrane expression of L1CAM were significantly correlated with poor clinical outcome, defined with aggressive tumor progression, invasion, and unfavorable prognosis. Mechanistic studies demonstrated the role of L1CAM in promoting cell proliferation and migration, conferring chemo-resistance and activation of the PI3K/Akt signaling pathway. In a large-scale evaluation of over a thousand early-stage endometrial cancers, 51% of L1CAM-positive tumors experienced recurrence versus 3% of L1CAM-negative tumors. Zeimet and colleagues recommended routine immunohistochemical L1CAM determination for all type I endometrial cancers due to its superiority over classical risk assessment, histopathological grading and FIGO stage I subdivision in predicting clinical outcome.
The L1 Cell Adhesion Molecule (L1CAM), also known as CD171, is a transmembrane glycoprotein protein crucial for neurogenesis and plays an essential role in neural cell adhesion and migration. Mutations in the X-linked L1CAM result in MASA syndrome; a neurological disorder causing mental retardation, aphasia, shuffling gait, and adducted thumbs. In addition to the brain, L1CAM expression is normally expressed in kidney tubular epithelium, intestinal crypt, and peripheral nerves. L1CAM has been investigated in various tumors, including colorectal, renal cell, ovarian, and thyroid carcinomas. Cytoplasmic and membrane expression of L1CAM were significantly correlated with poor clinical outcome, defined with aggressive tumor progression, invasion, and unfavorable prognosis. Mechanistic studies demonstrated the role of L1CAM in promoting cell proliferation and migration, conferring chemo-resistance and activation of the PI3K/Akt signaling pathway. In a large-scale evaluation of over a thousand early-stage endometrial cancers, 51% of L1CAM-positive tumors experienced recurrence versus 3% of L1CAM-negative tumors. Zeimet and colleagues recommended routine immunohistochemical L1CAM determination for all type I endometrial cancers due to its superiority over classical risk assessment, histopathological grading and FIGO stage I subdivision in predicting clinical outcome.
