Similarly, an enlarged right supraclavicular lymph node tends to drain thoracic malignancies such as lung and esophageal cancer, as well as Hodgkins lymphoma. History
Virchows nodes are named after Rudolf Virchow (1821–1902), the German pathologist who first described the nodes and their association with gastric cancer in 1848. The French pathologist Charles Emile Troisier noted in 1889 that other abdominal cancers, too, could spread to the nodes. Additional images
References
This article incorporates text in the public domain from page 697 of the 20th edition of Grays Anatomy (1918)

Further reading
Cervin, J. R.; Silverman, J. F.; Loggie, B. W.; Geisinger, K. R. (1995). "Virchows node revisited. Analysis with clinicopathologic correlation of 152 fine-needle aspiration biopsies of supraclavicular lymph nodes". Archives of Pathology & Laboratory Medicine. 119 (8): 727–30. PMID 7646330. INIST:3670181 NAID 10026546830. Negus, D; Edwards, J M; Kinmonth, J B (7 December 2005). "Filling of cervical and mediastinal nodes from the thoracic duct and the physiology of virchows node—studies by lymphography". British Journal of Surgery. 57 (4): 267–271. doi:10.1002/bjs.1800570407. PMID 5437920. S2CID 19698597. Mizutani, Masaomi; Nawata, Shin-ichi; Hirai, Ichiro; Murakami, Gen; Kimura, Wataru (December 2005). "Anatomy and histology of Virchows node". Anatomical Science International. 80 (4): 193–198. doi:10.1111/j.1447-073x.2005.00114.x. PMID 16333915. S2CID 40130186. External links
synd/1222 at Who Named It? Image at umich.edu - must rollover
https://web.archive.org/web/20080216031919/http://www.med.mun.ca/anatomyts/head/hnl3a.htm
http://www.aafp.org/afp/20021201/2103.html
The separate subdivisions are categorized by the genes that they effect. The seven types are not evenly distributed amongst ethnic groups with OCA1 being the subtype most prominent in Caucasians - "accounting for approximately 50% of cases worldwide. "Previously, diagnosis was done from observation of hypopigmentation which is obvious at birth, but this is now insufficient early on to distinguish between the seven major types of OCA.Prenatal testing has been achieved through fetal skin biopsy followed by subsequent histologic and electron microscope examination for melanin levels. Clinical findings have established that molecular genetic testing of TYR, the gene encoding tyrosinase, can distinguish between 1A and 1B because the phenotypes can be identical during the first year of life. OCA1A results in complete loss of tyrosinase enzyme activity. Individuals with 1B will experience increased pigmentation with age because they have a very low level of melanin production that can increase. The histological approach for prenatal diagnosis is useful for all families at risk for OCA1 whereas the molecular genetic test is only helpful when at least one mutation is known. Management
There is currently no treatment for this disease. The extremely hypopigmented skin that is characteristic in OCA1 particularly leads to risk of skin damage and non-melanotic skin cancers due to increased sensitivity to UV rays. In OCA1B, because there is some presence of melanin, it grows with age and pigmentation can increase; the same cannot be said for OCA1A.