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FDA approves HPV vaccine for people up to 45 - The Washington Post
The Food and Drug Administration expanded its approval of the HPV vaccine to include men and women between 27 and 45, an effort to protect more people from several types of cancer caused by the human papillomavirus. via Pocket
via-IFTTT  via-Pocket  health  hpv  medicine  news  vaccines  via-Diigo 
27 days ago by evansthompson
HPV Vaccine Expanded for People Ages 27 to 45 - The New York Times
older people will need three shots, spaced a few months apart

If a person has already been exposed to a particular strain of HPV, the vaccine will not work against that strain. For that reason, vaccination has been strongly recommended for young people before they become sexually active.

But even someone who has already been exposed to a few strains — but not to all nine in the vaccine — can still gain protection against the strains they have not encountered.
HPV  vaccine  health  breakthrough 
5 weeks ago by dandv
Australia to 'eliminate' cervical cancer by 2028 - CNN
Australia will be free of cervical cancer within 20 years, says a new study, thanks to national vaccination and screening programs.
5 weeks ago by dougleigh
Attenuated TRAF3 Fosters Activation of Alternative NF-κB and Reduced Expression of Antiviral Interferon, TP53, and RB to Promote HPV-Positive Head and Neck Cancers | Cancer Research
combine tnfa with cisplatin for chemotherapy ?

Human papilloma viruses (HPV) are linked to an epidemic increase in oropharyngeal head and neck squamous cell carcinomas (HNSCC), which display viral inactivation of tumor suppressors TP53 and RB1 and rapid regional spread. However, the role of genomic alterations in enabling the modulation of pathways that promote the aggressive phenotype of these cancers is unclear. Recently, a subset of HPV+ HNSCC has been shown to harbor novel genetic defects or decreased expression of TNF receptor–associated factor 3 (TRAF3). TRAF3 has been implicated as a negative regulator of alternative NF-κB pathway activation and activator of antiviral type I IFN response to other DNA viruses. How TRAF3 alterations affect pathogenesis of HPV+ HNSCC has not been extensively investigated. Here, we report that TRAF3-deficient HPV+ tumors and cell lines exhibit increased expression of alternative NF-κB pathway components and transcription factors NF-κB2/RELB. Overexpression of TRAF3 in HPV+ cell lines with decreased endogenous TRAF3 inhibited NF-κB2/RELB expression, nuclear localization, and NF-κB reporter activity, while increasing the expression of IFNA1 mRNA and protein and sensitizing cells to its growth inhibition. Overexpression of TRAF3 also enhanced TP53 and RB tumor suppressor proteins and decreased HPV E6 oncoprotein in HPV+ cells. Correspondingly, TRAF3 inhibited cell growth, colony formation, migration, and resistance to TNFα and cisplatin-induced cell death. Conversely, TRAF3 knockout enhanced colony formation and proliferation of an HPV+ HNSCC line expressing higher TRAF3 levels. Together, these findings support a functional role of TRAF3 as a tumor suppressor modulating established cancer hallmarks in HPV+ HNSCC.

Significance: These findings report the functional role of TRAF3 as a tumor suppressor that modulates the malignant phenotype of HPV+ head and neck cancers. Cancer Res; 78(16);
HPV  HNSCC  chemotherapy  nfkb 
10 weeks ago by Segalllab
The molecular landscape of head and neck cancer | Nature Reviews Cancer
good summary of hnscc development and molecular evaluations
HNSCC  tcga  HPV  p53  E6  E7 
10 weeks ago by Segalllab
Human papillomavirus type 16 E5-mediated upregulation of Met in human keratinocytes - ScienceDirect
E5 may stabilize EGFR leading to increase met transcription in foreskin keratinocytes. E5 expressing alone cells could not be made...

Human papillomaviruses (HPVs) cause benign lesions that can lead to malignancy. How cellular changes induced by viral oncogenes contribute to the progeny virion production is not always clear. Stromally-derived growth factors and their receptors are critical for development of malignancy, but their impact on the pre-malignant HPV life cycle is unknown. We show that HPV16 increases levels of Met, a growth factor receptor critical for tumor cell invasion, motility, and cancer metastasis. The viral oncogene E5 is primarily responsible for Met upregulation, with E6 playing a minor role. Met induction by E5 requires the epidermal growth factor receptor, which is also increased by E5 at the mRNA level. E5-induced Met contributes motility of HPV-containing cells. Finally, Met signaling is necessary for viral gene expression, particularly in the differentiation-dependent phase of the viral life cycle. These studies show a new role for E5 in epithelial-stromal interactions, with implications for cancer development.
HPV  E5  EGFR  cmet  keratinocytes 
august 2018 by Segalllab
HPV16 E6 and E7 upregulate the histone lysine demethylase KDM2B through the c-MYC/miR-146a-5p axys | Oncogene
E6 and E7 effects on miRNA in human foreskin keratinocytes. Intriguingly they did not list mir375 as affected?!? Need to check the data further...

"Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. In this study, we demonstrated that miR-146a-5p was down-regulated by E6 and, less efficiently, by E7 of high-risk HPV16 in keratinocytes and the presence of low levels of this miRNA in cervical carcinoma cell lines and in high-risk HPV-positive cervical specimens. Down-regulation of miR-146a-5p was mediated at least in part by the transcription repressor c-MYC, through binding sites in the miR-146a promoter. Overexpression of miR-146a-5p significantly inhibited proliferation and migration of keratinocytes and cervical cancer cells. The histone demethylase KDM2B was validated as a new direct target of miR-146a-5p and two putative binding sites for miR-146a-5p were identified in its 3′UTR sequence. Western blot analysis and immunohistochemistry showed that KDM2B was overexpressed in HPV16 E6/E7-positive keratinocytes, in cervical cancer cell lines, and in a subset of invasive cervical carcinomas and HPV-positive laryngeal squamous cell carcinomas. In these tumors, KDM2B overexpression was associated with c-MYC copy number gain. In vitro, silencing of KDM2B inhibited proliferation of cervical cancer cells. In conclusion, this study identified a novel player,
miRNA  keratinocytes  HPV  E6  E7 
july 2018 by Segalllab

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