UM‐SCC‐104: A New human papillomavirus‐16–positive cancer stem cell–containing head and neck squamous cell carcinoma cell line

Tang, Alice; Hauff, Samantha J.; Owen, Jennifer C.; Graham, Martin P.; Czerwinski, Michael; Park, Jung Je; Walline, Heather M.; Papagerakis, Silvana; Stoerker, Jay; McHugh, Jonathan B.; Chepeha, Douglas B.; Bradford, Carol R.; Carey, Thomas E.; Prince, Mark E.

doi:10.1002/hed.21962

Cited by 86 publications

(104 citation statements)

References 62 publications

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“…UM-SCC-47 (Lansford et al 1999) and UM-SCC-104 (Tang et al 2012) were kindly provided by Thomas Carey, University of Michigan; UPCI:SCC090 (White et al 2007) were from Susanne M. Gollin, University of Pittsburgh; UD-SCC-2 (Ballo et al 1999) were from Henning Bier, University of Dusseldorf; and HMS001 cells were from James Rocco, Harvard Medical School. Please see Table 1 and Supplemental Table 1. CAL 27, D562, SCC-25, SiHa, and CaSki cells were cultured as recommended by ATCC.…”

Section: Methods Human Cancer Cell Lines and Primary Tumorsmentioning

confidence: 99%

Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability

et al. 2013

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Genomic instability is a hallmark of human cancers, including the 5% caused by human papillomavirus (HPV). Here we report a striking association between HPV integration and adjacent host genomic structural variation in human cancer cell lines and primary tumors. Whole-genome sequencing revealed HPV integrants flanking and bridging extensive host genomic amplifications and rearrangements, including deletions, inversions, and chromosomal translocations. We present a model of ''looping'' by which HPV integrant-mediated DNA replication and recombination may result in viral-host DNA concatemers, frequently disrupting genes involved in oncogenesis and amplifying HPV oncogenes E6 and E7. Our high-resolution results shed new light on a catastrophic process, distinct from chromothripsis and other mutational processes, by which HPV directly promotes genomic instability.

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Section: Methods Human Cancer Cell Lines and Primary Tumorsmentioning

confidence: 99%

Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability

et al. 2013

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“…To date, the major hurdle for HPV/OPSCC screening is the paucity of relevant HPV/ OPSCC cell line models to be used for larger scale drug screening. Currently, there are only 5 HPV/HNC cell lines reported (UD-SCC-2 from hypopharynx, UPCI:SCC90 from the base of tongue, UM-SCC47 from lateral tongue, 93-VU-147T from the floor of the mouth and UM-SCC-104 from recurrent oral cavity [20]; and only one of these was derived from the oropharynx (UPCI:SCC90). Therefore, the development of additional HPV/OPSCC cell models will be of paramount importance to enhance the drug development process for HPV/OPSCC.…”

Section: Lack Of Preclinical Therapeutic Studies In Hpv/ Opscc Modelsmentioning

confidence: 99%

Primary Chemotherapy and Radiation as a Treatment Strategy for HPV-Positive Oropharyngeal Cancer

Lui

Grandis

2012

Head and Neck Pathol

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The incidence of human papillomaviruspositive oropharyngeal cancer (HPV/OPSCC) is rapidly increasing, which will represent a major public health burden for decades to come. Although HPV/OPSCC is generally associated with a better prognosis than HPV-negative OPS-CC, the survival rate of individuals with higher-risk clinical and pathologic features remains unchanged. Emerging evidence suggests that HPV/OPSCC is pathologically and molecularly distinct from HPV-negative OPSCC. This review focuses on summarizing treatment strategies for HPV/OPSCC by reviewing the peer-reviewed literature and noting ongoing and planned clinical trials in this disease. We also discuss the potential of designing targeted therapy based on the recent genomic findings of HPV/OPSCC.Keywords HPV/OPSCC Á Chemotherapy Á Radiation HPV-Related Head and Neck Cancer (HNC) and Related-Deaths on the RiseThe incidence of oropharyngeal squamous cell carcinoma (OPSCC), a site for head and neck cancer (HNC), is rising in developed countries including the US and Europe. In the past 2 decades, reports indicate that up to 70-80 % of OPSCC (the most common type of head and neck SCC in year 2010 [1]) in these developed countries are HPVpositive [2]. In fact, the number of HPV-positive OPSCC (hereafter named as HPV/OPSCC) is expected to continue to rise (due to oral sex, multiple sex partners, and premarital sex), while that of HPV-negative OPSCC has been decreasing since 1991 (which parallels the drop in smoking in the US). In fact, the total annual cases of HPV/OPSCC alone are predicted to outnumber that of all cervical cancer cases in the US by 2020 [1].HPV/OPSCC patients are treated with standard chemoradiation therapy or surgery with a generally high response rate [3]. However, treatment is often complicated by morbidities and the positive prognostic benefit of HPV can be mitigated by negative prognostic factors, such as smoking and lymph node metastases [4,5]. Recurrence, metastasis, and second primary cancer still account for the majority of deaths from HPV/OPSCC. The appreciable number of deaths from recurrence or treatment failure (*15 to 18/100, even with the most aggressive current treatment [6,7]), coupled with a dramatic surge in total number of HPV/OPSCC suggests that the total number of deaths from both HPV-positive and HPV-negative OPSCCs will be comparable. More strikingly, a recent study revealed that the highest-risk HPV/OPSCC patients had a 3-year overall survival of only 70.8 %, while the overall survival for the highest-risk HPV-negative OPSCC was 46 % [8] (original data can be found in Fig.

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“…Some studies have observed high expression of nuclear p53 in some human papillomavirus-containing tumors with wild-type p53 (Hafkamp et al, 2003), and other studies demonstrating low p53 expression (Wilczynski et al, 1998). Mechanism of overexpression of wild-type p53 in the presence of the virus is known (Tang et al, 2011).…”

Section: P16 Expressingmentioning

confidence: 99%

“…The variability of high risk human papillomavirus containing cell lines enhances our ability to study the role that human papillomavirus plays in head and neck squamous cell carcinoma development and response or resistance to therapy (Tang et al, 2011). Combination of several risk factors could explain this.…”

Section: P16 Expressingmentioning

confidence: 99%

“…Combination of several risk factors could explain this. A positive tobacco history in patients with human papillomavirus positive tumors may represent a distinct group of head and neck squamous cell carcinoma when all head and neck squamous cell carcinoma are divided by etiologic factors: human papillomavirus negative smokers, human papillomavirus positive never smokers, human papillomavirus positive ever smokers, etc… TPV status likely provided an additive and possibly synergistic effect with others risk factors (Tang et al, 2011).…”

Section: P16 Expressingmentioning

confidence: 99%

See 1 more Smart Citation

Human Papillomavirus Detection in Head and Neck Squamous Cell Carcinomas and Its Clinical Implications

Martı́n¹,

Carrillo²,

Tejada³

2012

Histopathology - Reviews and Recent Advances

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UM‐SCC‐104: A New human papillomavirus‐16–positive cancer stem cell–containing head and neck squamous cell carcinoma cell line

Cited by 86 publications

References 62 publications

Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability

Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability

Primary Chemotherapy and Radiation as a Treatment Strategy for HPV-Positive Oropharyngeal Cancer

Human Papillomavirus Detection in Head and Neck Squamous Cell Carcinomas and Its Clinical Implications

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