A Comparison of Fresh Frozen vs. Formalin-Fixed, Paraffin-Embedded Specimens of Canine Mammary Tumors via Branched-DNA Assay

Ripoli, Florenza Lüder; Mohr, Annika; Hammer, Susanne Conradine; Willenbrock, Saskia; Hewicker‐Trautwein, M.; Hennecke, Silvia; Escobar, Hugo Murua; Nolte, Ingo

doi:10.3390/ijms17050724

Cited by 31 publications

(25 citation statements)

References 34 publications

(47 reference statements)

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“…This wide variability could be explained by heterogeneity in study design, sampling, analysis methodology, population, geographic location, or diet; these variations are summarized in Table 1 [ 38 , 46 - 48 , 52 , 63 , 64 ].For instance, higher F. nucleatum detection is seen when using CRC tissue samples and whole-genome shotgun metagenomics sequencing methods, as compared with fecal samples or bacterial 16s sequencing[ 10 , 26 , 50 ]. Furthermore, caution should be taken when interpreting studies of FFPE samples, because FFPE samples provide a less accurate assessment of the microbiome when compared with fresh-frozen samples[ 65 ]. Finally, patients typically undergo bowel preparation when tissue samples are collected, which may affect Fusobacterium detection or abundance in tissue samples[ 66 ].…”

Section: Resultsmentioning

confidence: 99%

Fusobacterium’s link to colorectal neoplasia sequenced: A systematic review and future insights

Hussan¹,

Clinton²,

Roberts³

et al. 2017

WJG

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AIMTo critically evaluate previous scientific evidence on Fusobacterium’s role in colorectal neoplasia development.METHODSTwo independent investigators systematically reviewed all original scientific articles published between January, 2000, and July, 2017, using PubMed, EMBASE, and MEDLINE. A total of 355 articles were screened at the abstract level. Of these, only original scientific human, animal, and in vitro studies investigating Fusobacterium and its relationship with colorectal cancer (CRC) were included in the analysis. Abstracts, review articles, studies investigating other colonic diseases, and studies written in other languages than English were excluded from our analysis. Ninety articles were included after removing duplicates, resolving disagreements between the two reviewers, and applying the above criteria.RESULTSStudies have consistently identified positive associations between Fusobacterium, especially Fusobacterium nucleatum (F. nucleatum), and CRC. Stronger associations were seen in CRCs proximal to the splenic flexure and CpG island methylator phenotype (CIMP)-high CRCs. There was evidence of temporality and a biological gradient, with increased F. nucleatum DNA detection and quantity along the traditional adenoma-carcinoma sequence and in CIMP-high CRC precursors. Diet may have a differential impact on colonic F. nucleatum enrichment; evidence suggests that high fiber diet may reduce the risk of a subset of CRCs that are F. nucleatum DNA-positive. Data also suggest shorter CRC and disease-specific survival with increased amount of F. nucleatum DNA in CRC tissue. The pathophysiology of enrichment of F. nucleatum and other Fusobacterium species in colonic tissue is unclear; however, the virulence factors and changes to the local colonic environment with disruption of the protective mucus layer may contribute. The presence of a host lectin (Gal-GalNAc) in the colonic epithelium may also mediate F. nucleatum attachment to CRC and precursors through interaction with an F. nucleatum protein, fibroblast activation protein 2 (FAP2). The clinical significance of detection or enrichment of Fusobacterium in colorectal neoplasia is ambiguous, but data suggest a procarcinogenic effect of F. nucleatum, likely due to activation of oncogenic and inflammatory pathways and modulation of the tumor immune environment. This is hypothesized to be mediated by certain F. nucleatum strains carrying invasive properties and virulence factors such as FadA and FAP.CONCLUSIONEvidence suggests a potential active role of Fusobacterium, specifically F. nucleatum, in CRC. Future prospective and experimental human studies would fill an important gap in this literature.

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Section: Resultsmentioning

confidence: 99%

Fusobacterium’s link to colorectal neoplasia sequenced: A systematic review and future insights

Hussan¹,

Clinton²,

Roberts³

et al. 2017

WJG

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“…In agreement with the human data, 50 out of the 76 common overrepresented pathways were also found overrepresented in the xenograft diabetic tumor compared to nondiabetic tumor, being mainly distributed in the same categories (Table S3). Using a more specific and focused annotation based on curated pathways involved in inflammation (Loza et al, 2007), the two types of human diabetic samples (TD and ND) were found enriched in genes participating significantly in 4 processes (Apoptosis, Glucocorticoid/PPAR, MAPK, and PI3K/AKT Signaling) when compared to respective nondiabetic samples (T and N; Table S4). Here, the overlap between both comparisons was even larger, TD having only one other term enriched (Adhesion-Extravasation-Migration).…”

Section: Tumor and Normal Colonic Mucosa Show A Common Signal In Respmentioning

confidence: 99%

Molecular evidence of field cancerization initiated by diabetes in colon cancer patients

et al. 2019

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The potential involvement of type 2 diabetes mellitus (T2 DM ) as a risk factor for colon cancer ( CC ) has been previously reported. While several clinical studies show a higher incidence of CC and a lower survival rate in diabetics, others report no association. Our own experience indicates that diabetes does not seem to worsen the prognosis once the tumor is present. Despite this controversy, there are no wide‐spectrum molecular studies that delve into the impact of T2 DM ‐related mechanisms in colon carcinogenesis. Here, we present a transcriptomic and proteomic profiling of paired tumor and normal colon mucosa samples in a cohort of 42 CC patients, 23 of which have T2 DM . We used gene set enrichment and network approaches to extract relevant pathways in diabetics, referenced them to current knowledge, and tested them using in vitro techniques. Through our transcriptomics approach, we identified an unexpected overlap of pathways overrepresented in diabetics compared to nondiabetics, in both tumor and normal mucosa, including diabetes‐related metabolic and signaling processes. Proteomic approaches highlighted several cancer‐related signaling routes in diabetics found only in normal mucosa, not in tumors. An integration of the transcriptome and proteome analyses suggested the deregulation of key pathways related to colon carcinogenesis which converged on tumor initiation axis TEAD / YAP ‐ TAZ as a potential initiator of the process. In vitro studies confirmed upregulation of this pathway in nontumor colon cells under high‐glucose conditions. In conclusion, T2 DM associates with deregulation of cancer‐related processes in normal colon mucosa adjacent to tissue which has undergone a malignant transformation. These data support that in diabetic patients, the local microenvironment in normal colon mucosa may be a factor driving field cancerization promoting carcinogenesis. Our results set a new framework to study links between diabetes and colon cancer, including a new role of the TEAD / YAP ‐ TAZ complex as a potential driver.

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“…Due to the lack of such studies on BC samples, we decided to perform a pilot research on those 28 BC confirmed patients who had all of our inclusion criteria (between December 2013 and April 2014). Moreover, most studies measuring miR expression level have used formalin-fixed paraffin-embedded (FFPE)-paired normal and tumor tissue samples; whereas our study was performed on fresh frozen tumor samples ( 23 - 27 ), that their RNA yield was expected to be higher ( 28 ). Clearly, obtaining and preparing fresh frozen samples are much more difficult and time- consuming.…”

Section: Methodsmentioning

confidence: 99%

MiR-328 May be Considered as an Oncogene in Human Invasive Breast Carcinoma

Saberi¹,

Danyaei²,

Neisi³

et al. 2016

Iran Red Crescent Med J

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BackgroundThe recent investigations have rendered microRNAs (miRs) as a novel biomarker in cancer research. In fact, alteration in miR expression may be associated with tumor suppression, tumorigenesis, metastasis, and poor prognosis in human breast cancer (BC).ObjectivesThe aim of this clinical experimental study was to measure the miR-328 expression level in breast cancer tissues, at first. Then, we tried to find out any possible correlation between miR-328 and prognostic and predictive biomarkers in BC. Both of these two objectives were investigated for the first time; and we did not find any similar survey measuring the expression level of miR-328 in both tumor and non-tumor breast tissues. This research was conducted in Iran (Ahvaz, Khuzestan), between December 2013 and April 2014. Furthermore, we did not find any previous document investigating the correlation between miR-328 expression level and prognostic factors in BC. Due to the lack of similar studies intending to measure the expression level of miR-328 in tumor and adjacent non-tumor tissues, we decided to carry out a pilot study.MethodsWe measured the expression level of miR-328 by Poly (A) real-time PCR based on SYBR Green-I in 28 fresh samples of BC tissues and 28 samples of normal adjacent tissues, including invasive ductal carcinoma (IDC), invasive lobular carcinoma (ILC), and ductal carcinoma in situ (DCIS). We tried to attribute the results to clinicopathologic features such as status of estrogen and progesterone receptors (ER/PR), HER2/neu (HER2), P53 and also Ki67 labeling (Ki67-LI).ResultsThe results showed that the miR-328 median level of expression was 0.88 (2-ΔΔCt) (25th-75th percentile, 0.07 - 2.34). It means that the expression level increased in tumor tissues compared to normal adjacent tissues (NATs). However, a statistically significant correlation between the miR-328 median expression level and prognostic factors, including pathologic diagnosis, age, and also the status of ER, PR, HER2, and Ki67-LI was not observed (P > 0.05).ConclusionsTherefore, it might be possible to consider miR-328 as an oncogene; but not necessarily an oncomiR, in human BC.

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A Comparison of Fresh Frozen vs. Formalin-Fixed, Paraffin-Embedded Specimens of Canine Mammary Tumors via Branched-DNA Assay

Cited by 31 publications

References 34 publications

Fusobacterium’s link to colorectal neoplasia sequenced: A systematic review and future insights

Fusobacterium’s link to colorectal neoplasia sequenced: A systematic review and future insights

Molecular evidence of field cancerization initiated by diabetes in colon cancer patients

MiR-328 May be Considered as an Oncogene in Human Invasive Breast Carcinoma

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