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Background And Aims: Oncogenic KRAS mutations are present in approximately 90% of pancreatic ductal adenocarcinoma (PDAC). However, Kras mutation alone is insufficient to transform precancerous cells into metastatic PDAC. This study investigates how KRAS-mutated epithelial cells acquire the capacity to escape senescence or even immune clearance, thereby progressing to advanced PDAC.

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Objective: We attempted to evaluate the immediate high-grade squamous intraepithelial lesion-cervical intraepithelial neoplasia grade 2/3 or worse (HSIL-CIN2+/3+, hereafter referred to as CIN2+/3+) risk of specific human papillomavirus (HPV) genotype and form the precise risk-based triage strategy for atypical squamous cells of undetermined significance (ASC-US) women.

Methods: The clinical data of ASC-US women who underwent HPV genotyping testing and colposcopy were retrospectively reviewed. The distribution and CIN2+/3+ risks of specific HPV genotype were assessed by three approaches.

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The ovarian oncobiome is subject to increasing scientific focus, but a potential link between bacterial dysbiosis and ovarian carcinogenesis remains controversial. Our primary aim was to characterize the bacterial microbiota in epithelial ovarian cancer samples. Secondarily, we aimed to compare results from the bacterial microbiota in formalin-fixed, paraffin-embedded ovarian tissue samples from 194 patients with epithelial ovarian cancer, fallopian tube tissue samples from 16 patients with serous tubal intraepithelial carcinomas and in benign fallopian tube tissue samples from 25 patients.

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Importance: As US health care systems shift to human papillomavirus (HPV)-based cervical cancer screening, more patients are receiving positive high-risk non-16/18 genotype HPV results and negative for intraepithelial lesion or malignancy (NILM) cytological findings. Risk-based management guidelines recommend 2 consecutive negative annual results to return to routine screening.

Objective: To quantify patterns of surveillance testing and associated outcomes for patients after an HPV-positive results and NILM cytologic findings.

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Cancers with activating mutations of KRAS show a high prevalence but remain intractable, requiring innovative strategies to overcome the poor targetability of KRAS. Here, we report that KRAS expression is post-translationally up-regulated through deubiquitination when the scaffolding function of NDRG3 (N-Myc downstream-regulated gene 3) promotes specific interaction between KRAS and a deubiquitinating enzyme, USP9X. In KRAS-mutant cancer cells KRAS protein expression, downstream signaling, and cell growth are highly dependent on NDRG3.

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