HPV‐related oral dysplasia in a multiple myeloma patient after stem cell transplantation

Saleh, Wafaa; Cha, Seunghee; Bhattacharyya, Indraneel; Moreb, Jan S.; Katz, Joseph

doi:10.1111/scd.12344

Special Care in Dentistry

2018

DOI: 10.1111/scd.12344

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HPV‐related oral dysplasia in a multiple myeloma patient after stem cell transplantation

Wafaa Saleh

Seunghee Cha

Indraneel Bhattacharyya

et al.

Abstract: The development of dysplastic changes in oral epithelial lesions is a potential longterm complication after hematopoietic stem cell transplantation (HSCT). This may be related to mechanisms including radiation and chemotherapy regimens, chronic graftversus-host disease (cGVHD), inflammation, and prolonged immunosuppression. The current case describes a 54-year-old male with multiple myeloma treated by autologous and allogenic HSCT followed by development of cGVHD (mouth, skin and the eyes) with the complaint o… Show more

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Cited by 3 publications

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“…HPV infection does not necessarily lead to carcinoma. It is a multistep process that requires persistent infection of HPV and the presence of cofactors (12)(13)(14)(15)(16). In general, when HPV infects primitive basal keratinocytes, the viral genes E6 and E7, which encode the respective viral oncoproteins, are expressed.…”

mentioning

confidence: 99%

Human Papillomavirus 58 E7 T20I/G63S Variant Isolated from an East Asian Population Possesses High Oncogenicity

Boon

Xia

Lim

et al. 2020

J Virol

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Human papillomavirus (HPV) type 58 is the third most commonly detected HPV type in cervical cancer among Eastern Asians. Our previous international epidemiological studies revealed that HPV58 carrying an E7 natural variant, T20I/G63S (designated V1), was associated with a higher risk of cervical cancer. We recently showed that V1 possesses a greater ability to immortalize and transform primary cells, as well as degrading pRB more effectively, than the prototype and other common variants. In this study, we performed a series of phenotypic and molecular assays using physiologically relevant in vitro and in vivo models to compare the oncogenicity of V1 with that of the prototype and other common natural variants. Through activation of the AKT and K-Ras/extracellular signal-regulated kinase (ERK) signaling pathways, V1 consistently showed greater oncogenicity than the prototype and other variants, as demonstrated by increased cell proliferation, migration, and invasion, as well as induction of larger tumors in athymic nude mice. This study complements our previous epidemiological and molecular observations pinpointing the higher oncogenicity of V1 than that of the prototype and all other common variants. Since V1 is more commonly found in eastern Asia, our report provides insight into the design of HPV screening assays and selection of components for HPV vaccines in this region. IMPORTANCE Epidemiological studies have revealed that a wild-type variant of HPV58 carrying an E7 variation, T20I/G63S (V1), is associated with a higher risk of cervical cancer. We previously reported that this increased oncogenicity could be the result of the virus’s greater ability to degrade pRB, thereby leading to an increased ability to grow in an anchorage-independent manner. In addition to this, this report further showed that this HPV variant induced activation of the AKT and K-Ras/ERK signaling pathways, thereby explaining its genuine oncogenicity in promoting cell proliferation, migration, invasion, and formation of tumors, all to a greater extent than the prototype HPV58 and other common variants.

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mentioning

confidence: 99%

Human Papillomavirus 58 E7 T20I/G63S Variant Isolated from an East Asian Population Possesses High Oncogenicity

Boon

Xia

Lim

et al. 2020

J Virol

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Role of polycyclic aromatic hydrocarbons as a co-factor in human papillomavirus-mediated carcinogenesis

et al. 2019

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BackgroundHuman papillomavirus (HPV) is an etiological agent of cervical cancer. Yet co-factors are believed to be involved in HPV-mediated carcinogenesis. Polycyclic aromatic hydrocarbons (PAHs) are considered as one of these co-factors. Epidemiologic studies have associated high PAH exposure with increased risk for cancer development. To date, many studies focus on benzo[a]pyrene, however, the role of other PAHs should not be neglected. This study aimed to compare the potential of different PAHs as a co-factor in HPV-mediated carcinogenesis, and to investigate the possible mechanisms involved.MethodsThe effect of 17 PAHs on high-risk HPV (HPV16) were examined in this study. HPV16 E7 oncogene was expressed in primary cells extracted from baby rat kidney and treated with PAHs. The co-transforming ability of PAHs were measured by colony formation index according to the number and size of transformed colonies. Effects of PAHs on proliferation of HPV-null (C33A) and –infected (CaSki) were examined using CCK-8 assay. Wound healing assay and matrigel invasion chambers were used to investigate effects of PAHs on cell motility and invasivion of HPV-null (MCF7, C33A) and –infected (SiHa) cells.ResultsBenzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBA) and indeno[1,2,3-cd]pyrene (IDP) showed the greatest co-transforming potential in the baby rat kidney cell system. Short-term exposure to BaP, DBA, IDP and pyrene (PR) did not affect proliferation of C33A or CaSki cells, however, long-term exposure of these four PAHs led to dramatic increase in growth rate of CaSki cells by 120–140%. Besides, exposure of PAHs has an effect on cell motility and invasiveness of C33A and SiHa cells, but not for MCF7 cells. Exposure of BaP and DBA enhanced migration (1.26 to 1.40-fold) and invasion (1.68 to 1.94-fold) capacity of C33A cells. Intriguingly, exposure of all four types of PAHs boosted the migration (1.12 to 1.28-fold) and invasion (1.26 to 1.40-fold) capacity of SiHa cells.ConclusionsOur results indicate that exposure to PAHs can be a key co-factor in HPV-related cancer development. They could act on all three stages, namely initiation, promotion and progression. Further study is needed to unveil the mechanisms by which PAHs interact with HPV to cause malignancy.

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Oral HPV-associated dysplasia: is koilocytic dysplasia a separate entity?

Anaya-Saavedra,

Vázquez-Garduño

2024

Front. Oral. Health

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Oral epithelial dysplasia associated with high-risk HPV infection has received different names since its initial description, such as oral Bowenoid lesions, HPV-associated intraepithelial neoplasia, and oral koilocytic dysplasia. Some features, identified in more or less quantity in some of the descriptions, like apoptotic keratinocytes, karyorrhexis, and mitosoid figures, are intricately connected to viral transcriptional status and, consequently, viral load. Since the variety in terminology has introduced diagnostic confusion within medical and research communities, establishing a uniform and standardized approach to diagnosing HPV-oral epithelial dysplasia is crucial for accurate and early diagnoses and holds significant implications for patient outcomes, particularly in high-risk individuals.

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HPV‐related oral dysplasia in a multiple myeloma patient after stem cell transplantation

Cited by 3 publications

References 28 publications

Human Papillomavirus 58 E7 T20I/G63S Variant Isolated from an East Asian Population Possesses High Oncogenicity

Human Papillomavirus 58 E7 T20I/G63S Variant Isolated from an East Asian Population Possesses High Oncogenicity

Role of polycyclic aromatic hydrocarbons as a co-factor in human papillomavirus-mediated carcinogenesis

Oral HPV-associated dysplasia: is koilocytic dysplasia a separate entity?

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