Gingival squamous cell carcinoma in a patient with chronic graft-versus-host disease

Otsubo, Hiroki; Yokoe, Hidetaka; Miya, Toshimichi; Atsuta, Fujio; Miura, Nobuyuki; Tanzawa, Hideki; Sato, Kenichi

doi:10.1016/s1079-2104(97)90065-2

Cited by 53 publications

(34 citation statements)

References 13 publications

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“…Oral mucosal GVHD resembles OLP both clinically and histologically (Fujii et al, 1988;Mattsson et al, 1992). As with OLP, SCC may develop in oral and cutaneous chronic GVHD (Otsubo et al, 1997;Gmeinhart et al, 1999). Although the antigen specificity of lichen planus and mucocutaneous GVHD is probably distinct, it is likely that they share similar immunological effector mechanisms, resulting in T-cell infiltration, basal keratinocyte apoptosis, epithelial basement membrane disruption, and clinical disease.…”

Section: Graft-vs-host Disease and Olpmentioning

confidence: 99%

The Pathogenesis of Oral Lichen Planus

Sugerman

Savage²,

Walsh³

et al. 2002

Critical Reviews in Oral Biology & Medicine

635

584

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Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8 + cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-␤1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-␣, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-␤1, TNF-␣, IFN-␥, IL-12) and promoters (MIF,. We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.

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Section: Graft-vs-host Disease and Olpmentioning

confidence: 99%

The Pathogenesis of Oral Lichen Planus

Sugerman

Savage²,

Walsh³

et al. 2002

Critical Reviews in Oral Biology & Medicine

635

584

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“…[5][6][7][8][9][10] Histological lesions in the oral mucosa are characterized by basal keratinocyte apoptosis, 11,12 and often evolve into chronic lichenoid lesions 10,13 that may, as idiopathic lichen, favor the development of spinocellular cancer. 14,15 Previous studies using several different murine models have suggested that the pathogenesis of GVHD lesions in the liver, skin and digestive tract might involve either death ligands from the tumor necrosis factor (TNF) family, such as the CD95 ligand (CD95L) or TNFa, expressed or released by allogeneic lymphocytes, 4,[16][17][18][19][20][21][22] or perforine/granzyme, released by allogeneic lymphocyte granules. 4,17,23 However, the potential contribution of these effector molecules to the pathogenesis of oral mucosa lesions remains unknown.…”

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confidence: 99%

CD95 ligand-dependant endothelial cell death initiates oral mucosa damage in a murine model of acute graft versus host disease

Deschaumes

Verneuil

Ertault-Daneshpouy

et al. 2007

Laboratory Investigation

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Oral mucosa lesions are one of the common pathological consequences of acute graft versus host disease (aGVHD), the major complication of allogeneic bone marrow transplantation caused by mature T lymphocytes of donor origin. Oral mucosa damage in aGVHD is characterized by apoptosis induction in the basal keratinocytes, associated with immune effector T-cell infiltration, but its pathogenesis remains unclear because these lesions might result from the patient conditioning therapy that includes radiation and/or chemotherapy. Here, using a murine model of aGVHD that does not involve any conditioning treatment, we show that the earliest detectable oral mucosa lesion is apoptosis of the endothelial cells from chorion capillaries, which precedes basal keratinocyte apoptosis induction. Neither vascular damage nor epithelial-cell death occurred in recipients of allogeneic lymphocytes from CD95 ligand (CD95L)-defective mice. Our findings indicate that oral mucosa lesions in aGVHD are initiated by endothelial-cell death and require CD95L expression by the allogeneic lymphocytes. This early vascular damage may contribute to the induction of further tissue damage in the oral mucosa, through the induction of hypoxia and vascular leakage of immune cells or soluble proapoptotic mediators.

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“…Most patients who develop malignancy after BMT also have chronic GVHD (5,13). Additionally, some authors have observed the development of such tumors on sites initially involved with GVHD-related inflammatory processes (7,14). The patient presented in this case report showed a white plaque on the tongue in addition to erosive areas with striated borders on other oral sites, which persisted for almost 4 years until SCC development.…”

Section: Discussionmentioning

confidence: 71%

Squamous cell carcinoma of the tongue after bone marrow transplantation in a patient with Fanconi anemia

Salum

Martins²,

Figueiredo

et al. 2006

Braz. Dent. J.

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Fanconi anemia (FA) is an autosomal recessive disorder that might cause a variety of congenital and developmental abnormalities. The most important features of FA are progressive bone marrow failure and development of malignancies, particularly acute myeloid leukemia and solid tumors. This paper reports the case of a 12-year-old patient with FA assisted at the Stomatology and Bucomaxillofacial Cancer Prevention Service of São Lucas Hospital, Brazil, who had been submitted to bone marrow transplantation (BMT) at the age of 5 and exhibited oral lesions characteristic of chronic graft versus host disease (GVHD). The patient was treated and followed-up for the oral lesions. Eleven years after the BMT, he developed squamous cell carcinoma of the tongue with an aggressive behavior, which was considered an untreatable condition. The patient died few months later from asphyxia at the age of 16. The reasons for development of these malignant conditions are unknown. However, chromosomal instability typically observed in FA cases, BMT factors and GVHD have been considered. Systematic follow-up of these patients allows early and less invasive therapeutic approaches.

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Gingival squamous cell carcinoma in a patient with chronic graft-versus-host disease

Cited by 53 publications

References 13 publications

The Pathogenesis of Oral Lichen Planus

The Pathogenesis of Oral Lichen Planus

CD95 ligand-dependant endothelial cell death initiates oral mucosa damage in a murine model of acute graft versus host disease

Squamous cell carcinoma of the tongue after bone marrow transplantation in a patient with Fanconi anemia

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