The Koebner Phenomenon in Immunosuppression-Related Kaposiʼs Sarcoma

Maral, Tuğrul

doi:10.1097/00000637-200044060-00012

Cited by 18 publications

(13 citation statements)

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“…33 The preferential migration of KSHV-infected cells to sites of inflammation and injury might, in part, provide a mechanistic explanation for the clinical observation that KS lesions sometimes arise precisely at the site of antecedent inflammation or injury, a property known as the Koebner phenomenon. 62 Thus, in addition to promoting the recruitment of inflammatory and dendritic cells into KS lesions, KSHV-and K13-induced CCL20 and CCR6 up-regulation may directly contribute to tumor initiation, proliferation, and metastases. Furthermore, because CCL20 is known to inhibit the proliferation of hematopoietic progenitor cells in response to multiple growth factors, 52 it may also contribute to the pathogenesis of bone marrow failure syndromes associated with KSHV infection.…”

Section: Discussionmentioning

confidence: 99%

Induction of CCL20 production by Kaposi sarcoma–associated herpesvirus: role of viral FLICE inhibitory protein K13-induced NF-κB activation

Punj¹,

Matta²,

Schamus³

et al. 2009

Blood

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Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvi-rus 8, is the etiologic agent of Kaposi sarcoma (KS), an angioproliferative le-sion characterized by dramatic angiogen-esis and inflammatory infiltration. In this study, we report that expression of chemo-kine CCL20, a potent chemoattractant of dendritic cells and lymphocytes, is strongly induced in cultured cells either by KSHV infection or on ectopic expression of viral FLICE inhibitory protein K13. This induction is caused by transcrip-tional activation of CCL20 gene, which is mediated by binding of the p65, p50, and c-Rel subunits of the transcription factor nuclear factor-B (NF-B) to an atypical NF-B-binding site present in the CCL20 gene promoter. The CCL20 gene induction is defective in K13 mutants that lack NF-B activity, and can be blocked by specific genetic and pharmacologic inhibi-tors of the NF-B pathway. CCR6, the specific receptor for CCL20, is also induced in cultured cells either by KSHV infection or on K13 expression. Finally, expression of CCL20 and CCR6 is increased in clinical samples of KS. These results suggest that KSHV and K13-mediated induction of CCL20 and CCR6 may contribute to the recruitment of den-dritic cells and lymphocytes into the KS lesions, and to tumor growth and metasta-ses. (Blood. 2009;113:5660-5668)

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Section: Discussionmentioning

confidence: 99%

Induction of CCL20 production by Kaposi sarcoma–associated herpesvirus: role of viral FLICE inhibitory protein K13-induced NF-κB activation

Punj¹,

Matta²,

Schamus³

et al. 2009

Blood

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“…Postirradiation primary KS occurring after radiotherapy has been described. 184 KS has been identified in association with other causes of tissue trauma, 185,186 probably best viewed as a manifestation covered under the term ''isotopic response,'' in which KS occurs at the site of other, unrelated skin diseases or trauma (Fig 10). 186 Recrudescent or new KS after HAART may be a sign of IRIS, as may a flare of cutaneous and/or visceral KS.…”

Section: Clinical Featuresmentioning

confidence: 99%

Kaposi sarcoma: A continuing conundrum

Schwartz

Micali

Nasca

et al. 2008

Journal of the American Academy of Dermatology

202

212

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“…Similar concerns may be evident on the vulva and conjuctiva [61,62]. Postirradiation primary KS of the head and neck occurring after radiotherapy of a brain tumor has been described by Pasquale, Nasca, and Micali [55], as it has in other areas of trauma, a manifestation covered under Prof. Vincenzo Ruocco's term, ''isotopic response,'' in which KS occurs at the site of other, unrelated skin disease or trauma [58,59].…”

Section: Clinical Featuresmentioning

confidence: 99%

Kaposi's sarcoma: An update

Schwartz

2004

Journal of Surgical Oncology

126

114

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While there have been many important advances in the study of Kaposi's sarcoma (KS), it remains both a challenge and an enigma in many ways. Kaposi's original description of "multiple idiopathic hemorrhagic sarcoma[s]" in patients who died within 2-3 years resembles KS in AIDS more than classic KS in elderly men of Italian, Jewish, or Mediterranean lineage, in whom the disease is usually benign. KS had been evident in about one-third of those with early AIDS, often as its presenting sign, a pattern markedly reduced in recent times since the introduction of highly active anti-retroviral therapy (HAART). The most important advance has been the convincing etiologic linkage of KS with human herpesvirus 8 (HHV-8), which is necessary but not sufficient. It has a low prevalence in the general population of the USA and UK, with an intermediate rate in Italy and Greece, and a high one in Uganda. KS risk may be significantly lower in AIDS patients with a history of anti-herpes therapy. Many aspects of HHV-8, including its transmission pattern and different genospecies, are being scrutinized. The diagnosis of KS may be difficult. One should be aware of KS clinical variants, including telangiectatic, eccymotic, and keloidal KS. One must consider a number of other disorders, including bacillary angiomatosis. HHV-8 DNA sequences in dermatofibromas and other tumors should probably not be viewed as representing a marker for KS. Therapeutic options vary for KS. Intralesional and low-dose outpatient intravenous vinblastine may be valuable, as immunosuppression with KS is not a good idea if it can be avoided. Anti-herpes virus therapy may have potential for wide use, especially in preventing the development of KS in at risk populations, such as HHV-8 seropositive individuals undergoing transplantation surgery.

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The Koebner Phenomenon in Immunosuppression-Related Kaposiʼs Sarcoma

Cited by 18 publications

References 0 publications

Induction of CCL20 production by Kaposi sarcoma–associated herpesvirus: role of viral FLICE inhibitory protein K13-induced NF-κB activation

Induction of CCL20 production by Kaposi sarcoma–associated herpesvirus: role of viral FLICE inhibitory protein K13-induced NF-κB activation

Kaposi sarcoma: A continuing conundrum

Kaposi's sarcoma: An update

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