HPV(52) Antigen ELISA Quantitation Kit (DEIASL120)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
Serum, plasma
Species Reactivity
Human
Intended Use
HPV(52) Antigen ELISA Quantitation Kit is designed for quantitatively detection of the contents of HPV-52 antigen in the samples.
Storage
1. All components remain stable under the condition of 2-8°C;
2. Avoid light. Valid for six months
Precision
CV% ≤15% (n=10)
Detection Range
7.5~480ng/ml
Sensitivity
Sensitivity: ≤7.5ng/ml
General Description
Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes. L1 is a major capsid protein of human papilloma virus. Infection with specific types of HPV has been associated with an increased risk of developing cervical neoplasia.

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References


High-risk human papilloma virus was not detected in a Norwegian cohort of oral squamous cell carcinoma of the mobile tongue

CLINICAL AND EXPERIMENTAL DENTAL RESEARCH

Authors: Soland, Tine M.; Bjerkli, Inger-Heidi; Georgsen, Jeanette B.; Schreurs, Olaf; Jebsen, Peter; Laurvik, Helene; Sapkota, Dipak

Objectives The presence of and the causative role of high-risk human papilloma virus (HPV) is a subject of controversy in oral squamous cell carcinoma (OSCC). The disagreement can be related to the misclassification of OSCC as oropharyngeal squamous cell carcinoma and/or lack of standard detection methods. This study aimed to examine the presence of transcriptionally active high-risk HPV in a homogenous Norwegian cohort of primary and second primary OSCC of the mobile tongue (oral tongue squamous cell carcinoma-OTSCC). Methods Tissue microarrays containing formalin-fixed and paraffin-embedded cores of 146 OTSCC from the anterior 2/3 of the tongue (n = 128 primary and n = 18 second primary) from a multicentric Norwegian cohort were examined for the presence of high-risk HPV by DNA- and RNA-in situ hybridization (ISH) assays and p16 immunohistochemistry. Results Transcriptionally active HPV (E6/E7 mRNA) was not identified in any of the OTSCC specimens. In parallel, no tumors were positive for HPV by DNA ISH. Although, 61 (42%) OTSCC demonstrated p16 positivity with varying staining intensity and subcellular localization, only two cases demonstrated strong and uniform p16-staining (both cytoplasmic and nuclear) in >70% of cancer cells. The absence of transcriptionally active high-risk HPV in this cohort of OTSCC indicates that high-risk HPV is an unlikely causative factor in the present material.

Association Between CD4 Count and Chemoradiation Therapy Outcomes Among Cervical Cancer Patients With HIV

JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES

Authors: Grover, Surbhi; Mehta, Priyanka; Wang, Qiao; Bhatia, Rohini; Bvochora-Nsingo, Memory; Davey, Sonya; Iyengar, Meera; Shah, Sidrah; Shin, Sanghyuk S.; Zetola, Nicola M.

Background: In Botswana, nearly two-thirds of cervical cancer patients are HIV-positive. This study examined the relationship between CD4 count and chemoradiation therapy outcomes among cervical cancer patients with HIV. Setting: A prospective cohort study of 231 HIV-positive women with locally invasive cervical cancer was conducted in Gaborone, Botswana from January 2015 to February 2018. Methods: Primary outcome was survival, defined as time from scheduled end of chemoradiation therapy to death or last contact with patient. Nadir CD4 count was defined as lowest CD4 available before cancer diagnosis. Delta CD4 count was defined as improvement from nadir CD4 to CD4 at cancer diagnosis. Hazard ratio (HR) analyses were adjusted for presenting variables (age, baseline hemoglobin, cancer stage, and performance status) and treatment variables (chemotherapy cycles and radiation dose). Results: Two hundred thirty-one patients were included in nadir CD4 analysis; 139 were included in delta CD4 analysis. Higher delta CD4 was significantly associated with reduced mortality after adjusting for presenting and treatment variables (CD4 100-249: HR 0.45, 95% CI: 0.21 to 0.95; CD4 >= 250: HR 0.45, 95% CI: 0.20 to 1.02). Higher nadir CD4 showed a trend toward reduced mortality after adjusting for presenting and treatment variables (HR 0.94, 95% CI: 0.84 to 1.06). Conclusions: Higher delta CD4 (greater improvement from nadir CD4 to CD4 at cervical cancer diagnosis) is significantly associated with lower mortality. Although not statistically significant, data suggest that higher nadir CD4 may reduce mortality. These results reinforce the importance of early HIV diagnosis and antiretroviral therapy initiation, as their effects influence cervical cancer outcomes years later.

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