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At present, many countries worldwide are interested in HPV detection from anal among HPV infected patients.
In Thailand, the HPV infection and cervical cancer screening with thin pap liquid based cytology is also used as a new approach in the Royal Charity Project during the auspicious birthday anniversary of Prof. Regarding the methods of study, 40 patients with positive result of cervical high risk (hr) HPV (mean age 39.5 years, range 2261 years). Oncogenic viruses Key Concepts Normal cells infected with certain viruses can be transformed into cancer cells due to expression or activation of viral. EBV- Epstein Barr Virus most potent transforming agent, widespread in all human populations usually carried as an asymptomatic persistent infection (latent). Burkitts lymphoma Nasopharyngeal carcinoma Hodgkins lymphoma 40-50% of patients are EBV seropositive NPC tissue stained for the presence of EBV late antigens. E6 and E7 proteins inactivate tumour suppressor proteins p53 and pRB Transforming activity of HPV16 is associated with mainly E6 and E7proteins E6 and E7 are multifunctional proteins that can increase cell proliferation and survival by interfering with tumour suppressor activity.
To prevent cervical cancers in children aged 9–15 years and women from 16-26 years expected to prevent up to 70% of nearly 100 percent effective in preventing precancerous cervical lesions, precancerous vaginal and vulvar lesions and genital warts caused by infection with the HPV types 6, 11, 16 or 18 in women between the ages of 16 and 26.
Antiretroviral or anti HIV therapy All approved anti-HIV drugs attempt to block viral replication within cells by inhibiting either RT or HIV protease. Human Herpes Virus 8 (HHV8) or Kaposis sarcoma associated virus KSHV Herpes virus family Type 1 - causes cold sores on lips (~90% of population) Type 2 - sexually transmitted disease that causes "cold sores" on the genitals (~ 25% of US adults).
Head and neck squamous cell carcinoma (HNSCC) and its associated morbidities remain a worldwide public health concern. For example, p16 is an important tumor suppressor and cell cycle regulator commonly lost in HPV-negative HNSCC [2, 11].
Clinical specimensThirty-one frozen tumors from patients with newly diagnosed primary HNSCC and four normal mucosa samples (routine tonsillectomy) were collected with written informed consent under an Institutional Review Board (IRB) Health Sciences Committee (HSC)-approved protocol at Vanderbilt University Medical Center. RNA isolation, RT-PCR, and DNA microarray analysesEach tumor was examined by H&E staining to ensure presence of tumor and enriched by macro-dissection to achieve at least 70% tumor cellularity in each preparation. HPV detection and DNA sequencingTumor DNA was isolated and HPV DNA was detected using a previously established PCR-based method [14].
Western blot analysismiR-205 transiently transfected cells were seeded at equivalent densities in full serum (10% FBS), allowed to proliferate for 24 hrs, and processed for SDS-PAGE and Western blot analysis as previously described [15]. Growth assaysTransiently transfected cells were seeded in 96-well plates for Matrigel colony formation and proliferation assays in 1% serum as previously described [15]. Thirty-one tumors from newly diagnosed HNSCC patients were assayed for HPV status by PCR detection of HPV viral DNA. To determine whether specific miRNA profiles were associated with HPV status, HPV-positive miRNA expression was compared to the HPV-negative transcript levels. To further explore these findings in other dataset, HPV-specific differential expression of these miRNAs was evaluated within the HNSCC samples available in The Cancer Genome Atlas (TCGA) [23]. Consequently, miR-205 is a potential HNSCC oncogene capable of enhancing proliferation in an HPV-independent manner. To assess miRNA deregulation in HNSCC, we catalogued the differentially expressed miRNAs between malignant tumors and normal mucosa. In the first instance, a closer investigation of the families significantly upregulated within our analysis could yield some insight.
In the second case, recent sequencing projects have suggested tumor suppressor loss is a major contributing factor to the development of HNSCC, despite the heterogeneity of the disease [3, 4].
The sheer number of miRNAs deregulated in our tumor versus normal analysis is substantial and the power of this analysis is admittedly hampered by a statistical limitation. Although the aforementioned statistical considerations hampered the power of tumor versus normal analyses, this was not a concern when comparing miRNA expression between HPV-positive (n=14) and HPV-negative (n=15) tumors which were randomized across three separate microarray plates. While the function of miR-129-3p itself is largely unknown, its precursor transcript, miR-129-2, is a well-studied tumor suppressor and frequently hypermethylated in a number of different cancers [29, 50-52]. Prior work in our laboratory elucidated the deregulation of cell cycle pathways in HNSCC and we wanted to extend these findings within our differential miRNA transcripts.
Using two-dimensional and three-dimensional growth assays, we have demonstrated that miR-205 overexpression increases the proliferation of HNSCC cell lines independent of HPV status.
We have determined that miRNAs are globally upregulated in human HNSCCs and only modest differences exist in the miRNA profile defining HPV-positive and HPV-negative disease.
AcknowledgementsThe project was funded in part by Damon Runyon Clinical Investigator Award (CL-28-05) and NIH NIDCR R01 (DE017982) to CHC. DisclosureThe authors declare they have no competing interests as defined by Journal of Cancer Research and Therapy, or other interests that might be perceived to influence the results and discussion reported in this paper. Nuttavut Kantathavorn, a gynecology specialized physician of Chulabhorn Hospitaland principal investigator of the Royal Charity Project on “New approach of cervical cancer prevention and surveillance” during the auspicious birthday anniversary of Prof. Just as in England, the numbers of patients with HPV infection are very much decreased due to higher coverage of cervical cancer screening of more than 80%, leading to quite little finding of  cervical cancer.
Nuttavut shared his experience joining the annual academic conference of the British Gynecological Cancer Society in London, England during July 5-6, 2012, saying that the conference provided him great knowledge on cervical cancer screening in British females which would focus on the HPV infection and cervical cancer screening with thin pap liquid based cytology that could provide high efficiency of almost 100%. Nuttavut presented a result of “New approach of cervical cancer prevention and surveillance” in 5,000 Thai females aged 20-70 years to assess the testing technique for cervical and anal HPV as well as association of cervical and anal HPV infection.
These patients were recruited for Linear array HPV testing (Roche, USA) during December 13, 2011-February 24, 2012. The spatula was used to collected cells from anus by rotating one time along anus wall, and endobrush with K-Y jelly into anus to dentate line (above 2 cm from anal verge). Nuttavut mentioned that Thailand still faces with the lack of complete coverage examination, which requires support from other concerned units, both private and public sectors, to provide adequate knowledge to Thai females on the most appropriate way of prevention. Viral genomes show the presence of several human gene homologues (cellular proto-oncogenes) Infective viruses kidnap proto-oncogenes which are then transformed into oncogenes e.g.
Traditionally, the development of HNSCC has been linked to long-term tobacco and alcohol consumption, resulting in an older patient population [1]. In the present investigation, we examined the global deregulation of miRNAs that occur in HNSCC compared to normal mucosa.
Clinical data were obtained from Vanderbilt University Head and Neck Cancer Tissue and Clinical Database as previously described [5]. Antibodies for E2F1, cleaved and total caspase-3, cyclin D1, Bim, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA).
To achieve optimal colony detection and due to the different growth rates of the cell lines, SCC15 was incubated on Matrigel (BD Biosciences, San Jose, CA) for 4 days, while 93VU147T was cultured for 6 days. When the differential transcripts were organized in this fashion, seven families of miRNAs were significantly upregulated while two were downregulated (Table 2, Supplementary Table 3). Cells were seeded in 96-well format and changes in proliferation were estimated by MTS metabolism (Figure 2A). This observation is consistent with the fact this transcript was upregulated in both HPV-positive and HPV-negative tumors in our miRNA analysis. Additionally, we also determined the HPV-specific differential miRNA expression within our tumor cohort. For example, the let-7 family (MIPF0000002) is widely considered to exert tumor suppressive functions through its negative regulation of Ras and HMGA2 [35-37]. These mutations are more common in HPV-negative disease, simply because HPV viral proteins actively disable the p53 and pRb pathways to similar effect, rendering the requirement for additional tumor suppressor mutation redundant. Differential expression analysis between a large number of tumors (n=29) and a small number of normal samples (n=4) increases the probably a given transcript will experience a statistically significant modulation.
A major consequence of miR-129-2 silencing is SOX4 upregulation [29], a feature that has not yet been described in the HPV-positive HNSCC proteome. Consequently, we evaluated miR-205 as a putative regulator of E2F1 expression and associated pathway signaling. To begin characterizing miRNAs of interest within our screen, we functionally evaluated miR-205 in an HPV-positive and HPV-negative cell line. This work was also supported in part by the Radiation Therapy Oncology Group Translational Research Program, funded through RTOG U10 CA21661 and CCOP U10 CA37422 from the National Cancer Institute (NCI). Roll in the coconut and store in the fridge on a tray lined with greaseproof paper until eaten.

In contrast, most females in Thailand have never received the most appropriate cervical cancer screening.
Her Royal Highness Princess Chulabhorn, July 4, 2012 on “New approach of cervical cancer prevention and surveillance”, to screen HPV infection in Thai females just like in other developing countries through high technology methods such as mRNA detection or new markers namely P16 or Ki-67 to increase the specificity and accuracy of screening. The cervical cancer care team of Chulabhorn Hospital investigated HPV infection of cervix at other genital organs including vagina, vulva, perineum and anus. Further study to determine clinical significance of cervical and positive anal HPV should be thus recommended. Also, public relation activities should be conducted among Thai females to promote annual check-up and cervical cancer screening. Zidovudine (AZT), ddI, ddC, Stavudine Non nucleoside RT inhibitors (NNRTI) e.g Delavirdine and Nevirapine Protease inhibitors block active, catalytic site of HIV protease Multidrug therapy HAART (highly active antiretroviral therapy) usually consists of triple therapy including –2 nucleoside analogues + 1 protease inhibitor –1 non nucleoside RT inhibitor + 1(2) prot. HBV integrates into genome and produces a protein Hbx, involved in HCC HCV does not integrate into the genome but can interact with host proteins and cause an inflammatory response, which can transform cells e.g. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
In the current investigation, we determined whether cancer- or human papillomavirus (HPV)-specific miRNA deregulation could further elucidate signal transduction events unique to head and neck squamous cell carcinoma (HNSCC). Recently, high-risk human papillomavirus (HPV) infection has also been described as a causal agent for HNSCC development, although this subtype affects a younger population [2]. These short, non-coding RNAs inhibit target protein expression through complimentary base-pairing with mature mRNA transcripts which blocks translation.
Quality and quantity of RNA was determined using the Agilent RNA 6000 NanoLabChip kit and Agilent 2100 bioanalyzer (Agilent Technologies, Santa Clara, CA). Samples determined to be HPV-positive by this method were further confirmed using HPV16-specific PCR for E7 as previously described [5].
Steenbergen, Vrije University, The Netherlands) and SCC15 (ATCC) HNSCC cell lines were cultured as previously described [15].
Cells proliferated for 48 hrs, were snap frozen, then lysed and analyzed for luminescence using the Dual Luciferase Reporter Assay System (Promega, Madison, WI) with the GloMax Multi Detection System (Promega, Madison, WI). Matrigel colonies were stained by MTT metabolism [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium] and quantified for colony number and average colony size using GelCount™ (Oxford Optronix, Oxford, UK) per manufacturer’s instructions. In the remaining samples, transcripts determined not detectable were replaced with a maximum Ct value of 40 prior to calculating ?Ct values.
When the differential expression of specific miRNA transcripts was analyzed, 154 miRNAs were significantly upregulated while 103 were concomitantly downregulated in the tumor versus normal analysis (Benjamini-Hotchberg adj. Once again, the magnitude and sum total of miRNA deregulation favored an upregulation of critical miRNA families.
216 HPV-negative, Illumina HiSeq), miR-449a was confirmed as a transcript upregulated in HPV-positive HNSCCs (p=0.02, Supplemental Figure S4). Cells were passively lysed and analyzed (A) for E2F1 3’UTR activity by chemiluminescent detection of luciferase and renilla transfection control. Additionally, cleaved caspase-3, Bim, and p16 were not detected in this cell line, common consequences of HPV-negative HNSCC development. These cells were also seeded in Matrigel colony formation assays (B) to determine changes in clonigenicity and proliferation during anchorage-independent growth. Thus, miR-205 upregulation can alter proliferation in both cell lines, but the specific phenotypic modulations may depend on the degree of E2F1 modulation and its function within its associated molecular landscape. The subsequent analysis has determined that HNSCCs experience a net gain of transcripts compared to normal mucosa, with a few interesting exceptions. However, let-7b is specifically downregulated in acute lymphoblastic leukemia [38], melanoma [39], and ovarian cancer [40], but upregulated in gastric cancer [41] and our current analysis. Previous studies have also established that HNSCC is associated with a hypomethylated genome compared to normal mucosa [47]. Thus, it is possible the sum total of significant transcripts is artificially inflated due to a lack of statistical power or batch effects. However, the modulations that occur downstream may be functionally dependent on HPV status despite sharing a similar phenotypic outcome. We determined miR-205 is capable of regulating E2F1 protein expression in HNSCC and this transcript classically studied as a tumor suppressor provides a growth advantage to both cell lines. The contents of this article are the sole responsibility of the authors and do not necessarily represent the official views of the NCI or the Commonwealth of Pennsylvania. Roll balls from 1 tsp of the mixture and space out on a lined baking tray to store in the fridge. The 44% of women with ASCUS who tested negative for high-risk HPV were able to avoid colposcopy. Particularly, anus may be the reservoir site of cervical HPV, leading to recurrent infection.
While mutation and gene expression studies have uncovered molecular heterogeneity among HNSCCs [3-6], a decisive role for microRNAs (miRNAs) in HNSCC development is currently unclear. Recent studies from several laboratories have demonstrated that miRNAs represent a critical component of human cancer development, with evidence suggesting that miRNAs regulate key proteins involved in pro-survival pathways [7].
Consequently, p16 has served as a prognostic and histologic surrogate marker for HPV infection.
As expected, all 14 HPV-positive tumors were associated with the oropharynx (p=0.002, Fisher’s Exact test, oropharynx versus non-oropharynx) [25]. To further validate miR-205 is upregulated in HNSCC, this transcript was analyzed for differential expression within the Illumina HiSeq dataset containing 28 HPV-positive and 216 HPV-negative HNSCCs as well as 39 adjacent normal samples (Supplemental Figure S5).
Consequently, the loss of these proteins could affect the regulation and functional role of E2F1 in this context. To determine how miR-205 modulation affects three-dimensional cell growth, transiently transfected cells were seeded on Matrigel and allowed to proliferate 4-6 days in an anchorage-independent manner. Similar miRNA investigations in HNSCC have also observed a net gain in miRNAs rather than a loss [31-34].
Let-7f is also downregulated in sarcoma [42], lung [43], ovarian [44], and prostate cancer [45], while it is upregulated in breast cancer [46] and our current study.
Thus, it could be expected that hypomethylation may drive the net gain of miRNA expression observed in HNSCC. This was a surprising result given the myriad ways HPV-positive and -negative tumors differ in gene and protein expression [5, 10], genomic mutational profiles [3, 4], and clinical outcome [2]. Future investigations will be required to determine whether HPV-specific miR-129-3p silencing involves epigenetic mechanisms or more traditional means of gene expression regulation.
A recent proteomic screen of HPV-positive and HPV-negative tumors determined an E2F1 gene signature is associated with the protein expression profile of HPV-positive tumors [10]. Yet, the specific mechanisms inherent to miR-205 HNSCC oncogenic signaling may depend on the molecular context.
Minor cytologic abnormalities of the cervix, such as atypical squamous cells of undetermined significance (ASCUS), are vastly more common than high-grade squamous. Differential miRNA expression analysis concluded HNSCC is characterized by a general upregulation of miRNAs compared to normal mucosa. Thus, we wanted to determine the degree of miRNA deregulation in newly diagnosed HNSCC tumor samples compared to normal mucosa. In addition, miRNA function is extremely important for defining response to radiation therapy, chemotherapy, and can predict patient outcome in certain cancers. This subset of HNSCC is associated with the oropharynx and better overall survival [2, 12, 13]. A reaction was also run using the ABI miRNA Reverse Transcription kit (#4366596) and Megaplex RT Human Pool A primers (#4399966). Cells were incubated in antibiotic-free medium overnight and harvested for assay or Western blot analysis the following day. For 96-well proliferation assays, MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, Promega, Madison, WI] was diluted in DPBS (Dulbecco’s phosphate buffered saline, Invitrogen, Carlsbad, CA) per manufacturer’s instructions. To determine differential miRNA expression, empirical Bayes moderated t-statistics were used to assess differential expression of miRNAs associated with HNSCC or HPV status. Additionally, the number of samples representing different clinical stages of HNSCC was equivalent between the HPV-positive and HPV-negative patient populations.
While these upregulated families have been studied intensively, the function of the downregulated families remains poorly understood and may represent novel tumor suppressors regulating HNSCC-specific oncogenes. The average expression of both miRNAs was more similar to normal tissue in HPV-negative samples suggesting the mechanisms for the differential expression are specific to HPV infection.

Once again, miR-205 was overexpressed in HPV-positive and –negative HNSCC with respect to normal control (p-value=1.2 x 10-5). SCC15 recapitulated the more aggressive phenotype reflective of an HPV-negative cell line lacking p16 and pro-apoptotic pathway members (Figure 2B). Although the degree to which individual transcripts are upregulated differs widely between these studies, the general trends in miRNA deregulation are concordant. Furthermore, let-7i was upregulated in a previous HNSCC screen [31], however this transcript was not statistically significant within our analysis.
In other cancers, the hypothesis that miRNA downregulation leads to tumorigenesis hinges on the likelihood that repression of candidate oncogenes is relieved during deregulation.
Based on previous investigations, there are known mechanistic consequences of miR-449a and miR-129-3p deregulation. More importantly, differential miRNA expression is not a likely explanation for the vast differences observed between these subtypes of disease. This transcript has also been utilized as an exquisitely sensitive diagnostic marker for HNSCC detection in lymph node metastases [55], however our current analysis represents the first time this gene had been functionally evaluated in the context of this specific disease.
Consequently, HPV-positive cells may have a unique sensitivity to modulations in E2F1 protein expression not inherent to HPV-negative cells. Consequently, our functional evaluation has determined that cancer-specific miRNA deregulation can have similar phenotypic outcomes despite relying on HPV context dependent mechanisms.
Provides objective results and enables HPV-negative women to be returned to routine screening with a high degree of confidence that they are at little to no risk of. Finally, residual liquid base cytology was performed for DNA extraction using QIAamp DNA Mini kit. Additionally, our tumor cohort contained equivalent numbers of HPV-positive and –negative tumors, thus we could also accurately detect miRNA deregulation specific to HPV-related disease. Despite this well-studied mechanism, 4-37% of p16-negative HNSCC is HPV-positive and 0-57% of p16-positive HNSCC is HPV-negative. The Benjamini-Hotchberg correction [18] was applied to the resulting p-values to account for multiple hypothesis testing.
This miRNA is an important tumor suppressor which is silenced by hypermethylation in a number of different cancers [26-28].
Unfortunately, the miRNA sequencing reads in this dataset were not aligned to miR-129-3p in the level 3 data.
This cell line was more clonigenic and produced larger colonies than the HPV-positive counterpart (93VU147T). These results imply two possibilities: (1) miRNAs classically studied as tumor suppressors mediate oncogenic events in HNSCC, or (2) HNSCC development is uniquely reliant on tumor suppressor loss and a net gain of miRNAs could exacerbate this process. However, active targeting of tumor suppressor pathways by miRNA overexpression may also represent a viable means of deregulating growth and cell cycle checkpoints. Notch1 is a validated target of miR-449a and a putative tumor suppressor in HNSCC [3, 4, 48]. Consequently, we sought to investigate shared putative genes between these subtypes that may yield more clinically relevant mechanisms for general HNSCC deregulation.
In a manner analogous to HNSCC let-7 upregulation, this gene set represents a miRNA family classically studied as a tumor suppressor which is paradoxically upregulated in this disease [56]. Thus, future investigations of the miRNAs reported within this analysis will serve as excellent examples of context dependent signaling in HNSCC and potentially reveal critical signaling interactions targetable by pharmacological intervention. In older women, ASCUS results are more often because of vaginal infection or cervical inflammation, not an infection of HPV. The upregulation of miR-449a was also validated within an independent dataset obtained from TCGA containing 279 HNSCCs and 39 normal adjacent mucosa samples.
High-risk HPV is a sexually-transmitted virus long established as the primary factor in cervical cancer tumorigenesis. The discrepancies in reporting depend on the modality utilized to detect HPV and the proportion of oropharynx vs.
After 2-4 hrs of incubation at 37°C, 100µl of reactant was removed from the wells and absorbance was analyzed at 450nm using the GloMax Multi Detection System plate reader. In light of recent genomic sequencing projects and the mounting clinical evidence that these subtypes of HNSCC represent very different diseases [2-4], the degree of similarity they share on a miRNA level is unexpected. The equilibrium of hundreds of target transcripts unique to different tissue types defines the pathological consequences of miRNA modulation.
Although miRNAs can regulate innumerable targets, the probability of tumor suppressor loss increases as the number of upregulated miRNAs accumulate.
Additionally, Notch2 and two Notch ligands (DLL1 and JAG1) have been computationally defined as targets of miR-449a [30].
While putative targets of the miR-200 family have received much more attention, little is known concerning miR-205-mediated HNSCC signaling. However, similar functional changes occurred in SCC15 following miR-205 modulation without consistent changes in E2F1 protein.
Previous work from our laboratory has shown that HPV-positivity results in a distinct global gene expression pattern apart from HPV-negative head and neck cancer patients [5]. TLDAs were analyzed on ABI7900HT real-time PCR machine and run with the ABI default TLDA protocol. Although samples were spread across five arrays, a batch effect was not incorporated in our statistical model because all four normal samples were analyzed on the same array.
Thus, the three-dimensional growth characteristics recapitulated the two-dimensional growth modulation previously observed. Thus, it is imperative that the function of these families is rigorously evaluated in future HNSCC investigations to determine their decisive role in contributing to this specific disease. Thus, overexpression of this transcript could serve to suppress Notch signaling by simultaneously downregulating the receptors and ligands associated with the activity of this critical pathway. Previous studies have demonstrated that miR-205 can be an oncogene or a tumor suppressor depending on the genetic context. Aside from a lack of apoptotic pathway and p16 expression, SCC15 is also characterized by high levels of EGFR and AKT activation [61].
Thus, we sought to determine whether these observations extend to miRNA expression as well, potentially explaining some of the notable proteomic differences between these two HNSCC subtypes [10]. For example, miR-205 is overexpressed in cervical cancer and functionally serves to increase the proliferation and migration of these cells [57]. This study demonstrates miRNA expression is highly deregulated in HNSCC and functional evaluations of these miRNAs may reveal novel HPV context dependent mechanisms in this disease. Consequently, we were interested in determining whether candidate microRNAs could be identified within our screen that could further resolve the discrepancies observed in HNSCC cell cycle deregulation. Thus, miR-205 modulation of E2F1 in SCC15 may be tangential to its oncogenic effects due to additional targets unique to its molecular context. It was already well-established that miRNAs can have differential functions depending on the disease-state in question, and our current investigation has determined that the same miRNA can have differential signaling consequences within the same disease.
Additionally, high expression of E2F1 in malignant melanoma has been shown to downregulate miR-205 and lead to anticancer drug resistance [60]. However, the paths utilized depend on the subtype and genetic context available, yet ultimately these changes result in similar phenotypic modulations. Consequently, the function of miR-205 needs to be evaluated within each specific genetic context.
Consequently, our miRNA screen and functional studies suggest miR-205 can enhance the HNSCC oncogenic phenotype regardless by multiple molecular mechanisms independent of HPV status. We also analyzed independent HNSCC miRNA expression determined with high throughput sequencing from the Cancer Genome Atlas (TCGA) for additional transcript validation [23]. HPV status was established using a combination of p16 staining and confirmation with next generation sequencing. Read per megabase mapped (RPPM) expression values were log transformed for normality [24], and differential expression was assessed using univariate, one-sided t-statistics.
Reflex HPV testing had a sensitivity of 96% for detecting HSIL and a negative predictive value of 98%. To avoid platform bias, analyses were performed separately for samples measured with the Illumina Genome Analyzer (7 HPV-positive and 28 HPV-negative) and Illumina HiSeq (39 normal, 28 HPV-positive, 216 HPV-negative).

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