Lymphoepithelioma
From Wikipedia, the free encyclopedia
| Lymphoepithelioma | |
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| Classification and external resources | |
Nasopharyngeal lymphoepithelioma in a lymph node. Note the small, blue lymphocytes between the larger cancer cells.
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| ICD-O: | M8082/3 |
Lymphoepithelioma is a type of poorly differentiated nasopharyngeal carcinoma characterized by prominent infiltration of lymphocytes in the area involved by tumor. Lymphoepithelioma is also known as "class III nasopharyngeal carcinoma" in the WHO classification system. It has a high tendency to metastasize and is responsive to radiotherapy. Most cases are associated with Epstein-Barr virus infection.[1]
Lymphoepithelioma may also be referred to as Schmincke-Regaud tumor, after the German pathologist Alexander Schminke and French radiologist Claude Regaud.
Lymphoepithelioma-like carcinomas are carcinomas that arise outside of the nasopharynx, but resemble a lymphoepithelioma histologically. Lymphoepithelioma-like carcinomas may be found in almost any epithelial organ, including the lung, thymus, breast, colon, endometrium, prostate, and skin,[1] as well as urinary bladder, trachea, esophagus, stomach, salivary glands, vulva.[2]wikipedia
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These tumors are of interest because of their
1. possible viral induction or association: leading to believe that genes associated with the Virus are either imbedded in the normal tissue pathways inducing the transformation and therefore specific targets will be those that can block such incorporation. That indeed a different vaccine can be tried for the EBV virus in endemic regions once drivers of incorporation can be identified. Is it the DNA-ase, RNA-ase or CDK or just the cyclins...Here it appears that epigenetic events involving splicing molecules will be important. There got to be splicing and reconnection of Nuclear materiat, juxta-position to promoters and regulator factors for this disease to progress. Is there a Core binding factor like molecule driving this condition? I believe a genetic study is in order here to tell us!
What is the status of the NF-kB and what are the specific Cytokine (interon1, IL-2,4,6, 11,12,23) TNF and TGF-Beta. Role of some Known integrins (avB) and prominent Metaloproteases.
2. The response to concurrent Radiation and chemotherapy tends to suggest DNA breakdown is critical in this disease
emphasizing that P53 must be amplified (mostly secondarily), that DNA repair potential will have prognosis significance and Microsatellite instability will also have prognosis significance. MDM2, E, Rb genes would be important. Begin a question, can Velcade and the Aurora add something in Maintenance settings in this disease...Certainly an interesting approach!
can Vincristine and others Methotrexate like agents targeting the lymphoid component be given in maintenance setting, have a value in terms of prolonging survival or progression free survival?
A good study should include both the endemic and the non endemic portion to clearly see the importance of viral impact !
CRBCM is still alive!
We can go on
combining Cisplatin, Velcade and Aurora B as a new Induction therapy in Endemic Nasopharyngeal cancer....
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