Malignantly transformed cells must alter their metabolic status to stay viable in a harsh microenvironment and maintain their ability to invade and spread. Anoikis, a specific detachment‐related form of apoptotic cell death, is a potential barrier to cancer cell metastasis. Several molecular/pathway alterations have been implicated in preventing anoikis in metastatic cancers. Specific alterations in the lipid metabolism machinery (such as an increase in fatty acid uptake and synthesis) and modifications in the carbohydrate and amino acid metabolism are partially identified mechanisms associated with the anoikis resistance in various types of cancers, among other survival benefits. Following a summary of the molecular basis of the anoikis pathway, its resistance mechanisms, and the fundamentals of lipid metabolism in cancer, this article aims to elucidate the impact of lipid metabolism deviations recruited by cancer cells to escape anoikis.

Purpose Esophageal cancer is the second most common cancer among men and women. There is a need to systematically assess the current evidence to map out the contribution of genetic factors in the development of esophageal squamous cell carcinoma (ESCC). Methods A literature search was carried out on published and unpublished studies up to August 2021 in Medline (PubMed), Embase (Ovid), Scopus, Proquest, Web of Science, and Google scholar. Studies that have reported the frequency of genetic mutations in ESCC were included in this study. Results A total of 1238 titles were retrieved through searches, and finally, 56 articles, including 8114 samples, met our predefined inclusion criteria. Of the included studies, 31 were conducted in China, 12 in Japan, and the remaining were conducted in various nations, including Brazil, Korea, and Iran. Most of our included studies evaluated the TP53 (n = 37 studies) and PIK3CA (n = 30 studies) gene mutations.

Background: Papillary thyroid carcinoma (PTC) is the most prevalent endocrine malignancy. Despite nearly three-fold increase in incidence over three decades, the mortality rate remains unchanged. Biomarkers related to early diagnosis and prognosis of PTC are poorly investigated. Autophagy pathways and related miRNAs is considered to play an important role in PTC pathophysiology.Methods and Results: Tissue samples from patients with PTC undergoing thyroidectomy were collected. Total RNA content of tumor and margin samples were purified and converted to cDNA. Gene expression levels of mRNA (FOXO1) and miRNAs (miR-30d-5p, miR- 182-5p and miR-183-5p) were evaluated using qPCR method in PTC and adjacent normal tissue. A 6.51-fold decrease in miR-30d-5p level was detected in tumor samples compared to adjacent tissues. Moreover, miR-182-5p and miR-183-5p (FOXO1 as the main target) showed 1.73- and 4.31-fold increases in their levels, respectively. We also observed a 2.66-fold decrease in FOXO1 mRNA level in relation to these miRNA fold changes indicating a possible correlation between autophagy-linked molecular events and PTC.Conclusions: Significant increase in miR-183-5p and miR-182-5p expression, as well as a decrease in FOXO1 and miR-30d-5p expression, suggest that PTC has active autophagy machinery. This can possibly be used as a novel diagnostic or prognostic biomarker.

BackgroundHPV infection can cause cancer, and standard treatments often result in recurrence. The extent to which liquid biopsy using HPV circulating tumor DNA (HPV ctDNA) can be used as a promising marker for predicting recurrence in HPV‐related cancers remains to be validated. Here we conducted a systematic review and meta‐analysis to assess its effectiveness in predicting treatment response.MethodsWe conducted a systematic literature search of online databases, including PubMed, Embase, Scopus, and the Cochrane Library, up to December 2022. The goal was to identify survival studies that evaluated the potential of plasma HPV ctDNA at baseline and end‐of‐treatment (EoT) in predicting recurrence of related cancers. Hazard ratios were estimated directly from models or extracted from Kaplan–Meier plots.ResultsThe pooled effect of HPV ctDNA presence on disease recurrence was estimated to be HR = 7.97 (95% CI: [3.74, 17.01]). Subgroup analysis showed that the risk of recurrence was HR = 2.17 (95% CI: [1.07, 4.41]) for baseline‐positive cases and HR = 13.21 (95% CI: [6.62, 26.36]) for EoT‐positive cases. Significant associations were also observed between recurrence of oropharyngeal squamous cell carcinoma (HR = 12.25 (95% CI: [2.62, 57.36])) and cervical cancer (HR = 4.60 (95% CI: [2.08, 10.17])) in plasma HPV ctDNA‐positive patients.ConclusionsThe study found that HPV ctDNA detection can predict the rate of relapse or recurrence after treatment, with post‐treatment measurement being more effective than baseline assessment. HPV ctDNA could be used as a surrogate or incorporated with other methods for detecting residual disease.