Human Papillomavirus 42 Drives Digital Papillary Adenocarcinoma and Elicits a Germ Cell–like Program Conserved in HPV-Positive Cancers

Leiendecker, Lukas; Neumann, Tobias; Jung, Pauline S.; Cronin, Shona M.; Steinacker, Thomas L.; Schleiffer, Alexander; Schutzbier, Michael; Mechtler, Karl; Kervarrec, Thibault; Laurent, Estelle; Bachiri, Kamel; Coyaud, Étienne; Murali, Rajmohan; Busam, Klaus J.; Itzinger-Monshi, Babak; Kirnbauer, Reinhard; Cerroni, Lorenzo; Calonje, Eduardo; Rütten, Arno; Stubenrauch, Frank; Griewank, Klaus G.; Wiesner, Thomas; Obenauf, Anna C.

doi:10.1158/2159-8290.cd-22-0489

Cited by 31 publications

(20 citation statements)

References 67 publications

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“…5 In their article, Bui et al 18 reported a series of eight acral sweat glands tumors diagnosed as "DPA." In contrast to prior observations with a larger set of tumors 5,14,16 they claim to have identified two "DPA" groups with distinct phenotypes, genetics, and outcomes. "Group A" (n = 4) included painless slow-growing nodules microscopically characterized by small, well defined dermal tumors forming independent glandular structures.…”

contrasting

confidence: 81%

“…Molecular analyses of sweat gland tumors have identified recurrent and mutually exclusive oncogenic drivers such as CRTC1/3::MAML2 in hidradenoma and their malignant counterparts 12 or BRAF mutations in tubular adenoma 13 . Recently, human papillomavirus 42 (HPV42) was discovered in DPA 5,14–17 . Indeed, DPA genome was found in 96%–100% of tested DPA tumors, 5,16 but not in any other sweat gland neoplasm or adenocarcinoma 5 …”

Section: Figurementioning

confidence: 99%

“…Recently, human papillomavirus 42 (HPV42) was discovered in DPA 5,14–17 . Indeed, DPA genome was found in 96%–100% of tested DPA tumors, 5,16 but not in any other sweat gland neoplasm or adenocarcinoma 5 …”

Section: Figurementioning

confidence: 99%

“…13 Recently, human papillomavirus 42 (HPV42) was discovered in DPA. 5,[14][15][16][17] Indeed, DPA genome was found in 96%-100% of tested DPA tumors, 5,16 but not in any other sweat gland neoplasm or adenocarcinoma. 5 In their article, Bui et al 18 reported a series of eight acral sweat glands tumors diagnosed as "DPA."…”

mentioning

confidence: 99%

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Acral BRAF‐mutated tubular adenoma should be distinguished from HPV42‐related digital papillary adenocarcinoma

Kervarrec

Busam

2023

J Cutan Pathol

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We read the article entitled "Two distinct pathogenic pathways of digital papillary adenocarcinoma -BRAF mutation or low-risk HPV infection," which was recently published in your journal, and would like to share our thoughts on the findings to avoid confusion in skin tumor nomenclature and prevent potential harm to patients from misdiagnosis.Digital papillary adenocarcinoma (DPA) is a rare sweat gland carcinoma capable of metastasis. It almost exclusively arises at acral sites. 1,2

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contrasting

confidence: 81%

Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

mentioning

confidence: 99%

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Acral BRAF‐mutated tubular adenoma should be distinguished from HPV42‐related digital papillary adenocarcinoma

Kervarrec

Busam

2023

J Cutan Pathol

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“…In 2008, MCPyV was linked to Merkel cell carcinoma (MCC) 22 , and has since been identified as an etiological agent in 80% of MCC tumors 23 . Recently, HPV42, previously classified as a "low-risk" HPV type, has been found in a majority of digital papillary adenocarcinomas 24 . It is suspected that viruses may play a causative role in the pathogenesis of other cancer types 25,26 , and there may be more oncoviruses that have yet to be discovered.…”

Section: Introductionmentioning

confidence: 99%

Genomic landscape of virus-associated cancers

Gómez

Schiavoni

Nam

et al. 2023

Preprint

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It has been estimated that 15%-20% of human cancers are attributable to infections, mostly by carcinogenic viruses. The incidence varies worldwide, with a majority affecting developing countries. Here, we present a comparative analysis of virus-positive and virus-negative tumors in nine cancers linked to five viruses. We find that virus-positive tumors occur more frequently in males and show geographical disparities in incidence. Genomic analysis of 1,658 tumors reveals virus-positive tumors exhibit distinct mutation signatures and driver gene mutations and possess a lower somatic mutation burden compared to virus-negative tumors of the same cancer type. For example, compared to the respective virus-negative counterparts, virus-positive cases across different cancer histologies had less often mutations of TP53 and deletions of 9p21.3/CDKN2A-CDKN1A; Epstein-Barr virus-positive (EBV+) gastric cancer had more frequent mutations of EIF4A1 and ARID1A and less marked mismatch repair deficiency signatures; and EBV-positive cHL had fewer somatic genetic lesions of JAK-STAT, NF-κB, PI3K-AKT and HLA-I genes and a less pronounced activity of the aberrant somatic hypermutation signature. In cHL, we also identify germline homozygosity in HLA class I as a potential risk factor for the development of EBV-positive Hodgkin lymphoma. Finally, an analysis of clinical trials of PD-(L)1 inhibitors in four virus-associated cancers suggested an association of viral infection with higher response rate in patients receiving such treatments, which was particularly evident in gastric cancer and head and neck squamous cell carcinoma. These results illustrate the epidemiological, genetic, prognostic, and therapeutic trends across virus-associated malignancies.

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Human papillomaviruses: Knowns, mysteries, and unchartered territories

Gelbard,

Munger

2023

Journal of Medical Virology

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There has been an explosion in the number of papillomaviruses that have been identified and fully sequenced. Yet only a minute fraction of these has been studied in any detail. Most of our molecular research efforts have focused on the E6 and E7 proteins of “high‐risk,” cancer‐associated human papillomaviruses (HPVs). Interactions of the high‐risk HPV E6 and E7 proteins with their respective cellular targets, the p53 and the retinoblastoma tumor suppressors, have been investigated in minute detail. Some have thus questioned if research on papillomaviruses remains an exciting and worthwhile area of investigation. However, fundamentally new insights on the biological activities and cellular targets of the high‐risk HPV E6 and E7 proteins have been discovered and previously unstudied HPVs have been newly associated with human diseases. HPV infections continue to be an important cause of human morbidity and mortality and since there are no antivirals to combat HPV infections, research on HPVs should remain attractive to new investigators and biomedical funding agencies, alike.

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Human Papillomavirus 42 Drives Digital Papillary Adenocarcinoma and Elicits a Germ Cell–like Program Conserved in HPV-Positive Cancers

Cited by 31 publications

References 67 publications

Acral BRAF‐mutated tubular adenoma should be distinguished from HPV42‐related digital papillary adenocarcinoma

Acral BRAF‐mutated tubular adenoma should be distinguished from HPV42‐related digital papillary adenocarcinoma

Genomic landscape of virus-associated cancers

Human papillomaviruses: Knowns, mysteries, and unchartered territories

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