The Nature of Hyaline (Eosinophilic) Globules and Vascular Slits of Kaposiʼs Sarcoma

Kao, Grace F.; Johnson, Frank B.; Sulica, Virginia I.

doi:10.1097/00000372-199006000-00006

Cited by 65 publications

(22 citation statements)

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“…Intracellular junctions between neoplastic endothelial cells are frequently defective allowing the extravasation of large numbers of erythrocytes from vessel lumens into the surrounding tissue. [50][51][52][53] These renegade cells become more numerous as the disease progresses and abnormal networks of slitlike vascular spaces expand. Erythrophagocytosis by KS cells is also a common feature.…”

Section: Discussionmentioning

confidence: 99%

“…by guest www.bloodjournal.org From described the presence of hyaline globules in plaque-and nodularstage KS, and histologic staining has revealed that these are the remnants of degenerated erythrocytes. 51 In light of these histologic findings, it is conceivable that up-regulation of HO-1 by KSHV infection could confer a selective advantage to KS cells within the high heme lesional microenvironment compared with neighboring uninfected cells. The availability of potent inhibitors of HO-1 in clinical use elsewhere 55,56 makes this enzyme a potentially important treatment target in KS.…”

Section: Discussionmentioning

confidence: 99%

“…Because of the potential for increased exposure of KS cells to free heme and heme-containing proteins in KS tissue, [50][51][52][53][54] we investigated the possibility that HO-1 up-regulation might affect the response of KSHV-infected cells to heme. Overexpression of HO-1 A indicates apoptosis; TNFR1, tumor necrosis factor receptor 1; absent, protein present in mock-infected cells but not in KSHV-infected cells (fold change cannot be called); CA, cell adhesion; CD, cell division; FK506, tacrolimus; GAP, GTPase-activating protein; T-LAK, lymphokine-activated killer cells with T-cell phenotype; MAPKK, mitogen-activated protein kinase kinase; CS, cell shape; DR, DNA repair; M, metabolism; GTP, guanosine 5Ј-triphosphate; O, other; IFN, interferon; PS, protein sorting; T, transcription; TGFB, transforming growth factor beta; TG, tumorigenesis; and U, unknown.…”

Section: Ho-1 Up-regulation Increases Proliferation Of Kshv-infected mentioning

confidence: 99%

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Kaposi sarcoma-associated herpesvirus (KSHV) induces heme oxygenase-1 expression and activity in KSHV-infected endothelial cells

McAllister

Hansen

Ruhl

et al. 2004

Blood

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IntroductionKaposi sarcoma-associated herpesvirus (KSHV; also human herpesvirus-8) is implicated in all clinical forms of KS 1,2 as well as the lymphoproliferative disorders primary effusion lymphoma (PEL) 3,4 and multicentric Castleman disease (MCD). 5 Endothelial cells harbor the KSHV genome in vivo, 1,6,7 are permissive for virus infection in vitro, [8][9][10][11] and are thought to be the precursors of spindle cells. [12][13][14][15] We and others have shown that in vitro infection of human dermal microvascular endothelial cells (DMVECs) with KSHV induces a spindle cell morphology and characteristics of a transformed phenotype, including loss of contact inhibition and growth in soft agar. [8][9][10][11] Because explanted KS cells fail to maintain the KSHV genome following serial passage, 16,17 in vitro infection of DMVECs has proved to be an invaluable tool for the study of KSHV pathogenic mechanisms. 18,19 KSHV, like other herpesviruses, has a substantial coding capacity that includes viral genes unique to this human pathogen, genes that share homology with other members of the herpesviridae, as well as genes that appear to have originated in the host genome. 20,21 Of note, at least 3 of these gene products, vFLIP (viral Fas-associating protein with death domain-like interleukin-1␤ [IL-1␤]-converting enzyme [FLICE]-inhibitory protein), viral cyclin (vCYC), and latency-associated nuclear antigen (LANA), are believed to comprise the viral latency expression program and are consistently expressed in all virally infected cells in KS, PEL, and MCD. [22][23][24] The gene product of open reading frame 71 (ORF 71), vFLIP, is thought to play an important role in prevention of apoptotic cell death. 25 The activity of a homolog of cellular cyclin D, vCYC (ORF 72), 26 together with the modulation of cellular transcription wrought by LANA (ORF 73) 27 is thought to be involved in KSHV-induced host cell transformation. Additionally, LANA is indispensable for maintenance of the viral genome. 28 Other gene products, such as viral G-protein-coupled receptor (vGCR) 29,31 are classified as lytic gene products and are expressed in only a minority of cells in vivo. [32][33][34] Although reactivation of KSHV from the latent state and subsequent completion of the viral lytic expression cascade is incompatible with survival of a host cell, lytic gene products are thought to have paracrine influences on both latently infected and uninfected cells and are thus considered vital for lesion development. 35 We have used our previously described in vitro KS model to dissect viral mechanisms of pathogenesis. 18,19 The salient features of our model include recapitulation of KS cell physiology, including spindle cell formation, loss of contact inhibition, and anchoragedependent growth restriction; long-term propagation of predominantly latently infected cells; and the ability to generate ageand passage-matched KSHV-infected and uninfected cultures. 11 This system has been amenable to gene expression profiling by cDNA microarrays and has ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Ho-1 Up-regulation Increases Proliferation Of Kshv-infected mentioning

confidence: 99%

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Kaposi sarcoma-associated herpesvirus (KSHV) induces heme oxygenase-1 expression and activity in KSHV-infected endothelial cells

McAllister

Hansen

Ruhl

et al. 2004

Blood

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“…The clinical presentation was quite unusual; the endoscopy revealed numerous polypoid mucosal nodules ®lling the lumen of the rectum and sigmoid colon. Microscopically, besides the classical pattern of KS as seen elsewhere, the striking histologic feature was the presence of eosinophilic intracytoplasmic globules, thought to be phagocized sequestrated red blood cells, in the neoplastic cells [18], and Cowdry type A nuclear inclusions caused by HHV-8 infection, which ®ndings have not been described except skin KS [19].…”

Section: Discussionmentioning

confidence: 80%

Primary Kaposi sarcoma of the bowel in a HIV‐negative patient

Insabato

Vizio

Terracciano

et al. 2001

Journal of Surgical Oncology

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A case of Kaposi sarcoma with HIV-negative and sequence of HHV-8 positive and exclusive rectosigmoid and descending colon involvement without immunodeficiency is reported. Histologically, in addition to typical features of Kaposi sarcoma, Cowdry type A inclusions were seen. PCR analysis of the tumor showed positivity for human herpesvirus 8. Two of the six reported cases of Kaposi sarcoma limited to the bowel were from African men before the AIDS epidemic. J. Surg. Oncol. 2001;76:197-200.

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“…These structures are thought to represent digested erythrocytes as the neoplastic cells seem to have phagocytic activity. 21 Based on immunolabeling studies, KS is best regarded as a lesion of lymphatic endothelial cells, as it expresses CD34, CD31, Fli-1, VEGFR-3, and podoplanin (D2-40). [22][23][24][25] Virtually all examples show nuclear labeling with HHV-8 antibodies (Figure 3c).…”

Section: Kaposi Sarcomamentioning

confidence: 99%

Gastrointestinal tract spindle cell lesions—just like real estate, it's all about location

Voltaggio

Montgomery

2015

Modern Pathology

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Interpretation of gastrointestinal tract mesenchymal lesions is simplified merely by knowing in which anatomic layer they are usually found. For example, Kaposi sarcoma is detected on mucosal biopsies, whereas inflammatory fibroid polyp is nearly always in the submucosa. Gastrointestinal stromal tumors (GISTs) are generally centered in the muscularis propria. Schwannomas are essentially always in the muscularis propria. Mesenteric lesions are usually found in the small bowel mesentery. Knowledge of the favored layer is even most important in interpreting colon biopsies, as many mesenschymal polyps are encountered in the colon. Although GISTs are among the most common mesenchymal lesions, we will concentrate our discussion on other mesenchymal lesions, some of which are in the differential diagnosis of GIST, and point out some diagnostic pitfalls, particularly in immunolabeling.

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The Nature of Hyaline (Eosinophilic) Globules and Vascular Slits of Kaposiʼs Sarcoma

Cited by 65 publications

References 0 publications

Kaposi sarcoma-associated herpesvirus (KSHV) induces heme oxygenase-1 expression and activity in KSHV-infected endothelial cells

Kaposi sarcoma-associated herpesvirus (KSHV) induces heme oxygenase-1 expression and activity in KSHV-infected endothelial cells

Primary Kaposi sarcoma of the bowel in a HIV‐negative patient

Gastrointestinal tract spindle cell lesions—just like real estate, it's all about location

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