Shipping to United States We Offer Worldwide Shipping
Login Wishlist

Apigenin 7-diglucuronide

$1,520

  • Brand : BIOFRON

  • Catalogue Number : BN-O1866

  • Specification : 98%(HPLC)

  • CAS number : 74696-01-8

  • Formula : C27H26O17

  • Molecular Weight : 622.5

  • Volume : 20mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BN-O1866

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

622.5

Appearance

Botanical Source

Structure Type

Category

SMILES

Synonyms

IUPAC Name

Applications

Density

Solubility

Flash Point

Boiling Point

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:74696-01-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

28242577

Abstract

Keratinocyte carcinoma (KC), which includes basal-cell carcinoma (BCC) and squamous-cell cancer (SCC), has been associated with an increased risk of second primary cancers (SPCs), although the reason for this increase is unknown. We assessed the effects of smoking, alcohol, and obesity prior to the diagnosis of KC on the development of SPCs, as these are well-established risk factors for multiple cancers and may also contribute to the increased risk of SPCs among those with KC. A total of 15,628 women with self-reported KC were identified in the Nurses’ Health Study. Incident SPCs were assessed throughout the follow-up until June 2012. Cox proportional hazards models were used to calculate the hazard ratios (HRs) of SPC associated with pre-diagnostic smoking, alcohol and body mass index (BMI). We also compared these risk estimates to those for first cancers in all cohort participants. During 193,695 person-years of follow-up, we recorded 2839 SPC cases. Compared with never smokers, current smokers had a significantly elevated risk for SPC overall and specifically for lung, colorectal, and bladder cancers. We also found a positive association between higher BMI and risk for SPC overall as well as for endometrial and bladder SPCs. Women with KC who consumed alcohol ≥30 g/day had a marginally higher risk of SPC compared to non-drinkers. The associations between incident SPC risk among KC cases and smoking, alcohol, and obesity appeared similar to the associations between these risk factors and the incident first primary cancers in the whole cohort. Only in the heavy smoking (≥25 cigarettes/day) category was the HR for SPC after KC (2.34; 95% CI 1.98-2.76) slightly higher than that for the first cancer in the overall cohort (HR 1.86; 95% CI 1.75-1.98, Pheterogeneity = 0.01). In conclusion, pre-diagnostic smoking, alcohol and obesity prior to KC diagnosis were associated with risk of SPCs.

KEYWORDS

Smoking, Alcohol, Body mass index, Second primary cancer, Keratinocyte carcinoma

Title

Risk of second primary cancer associated with pre-diagnostic smoking, alcohol, and obesity in women with keratinocyte carcinoma

Author

Sang Min Park,a,b Tricia Li,c Shaowei Wu,c,d Wen-Qing Li,c,e Abrar A. Qureshi,a,c,e Meir Stampfer,a and Eunyoung Choa,c,e,*

Publish date

2018 May 7.

PMID

30646906

Abstract

Background
It has been found that chronic rhinosinusitis (CRS) increases the risk of developing nasopharyngeal carcinoma (NPC). CRS can be caused by gastro-oesophageal reflux (GOR) that may reach nasopharynx. The major component of refluxate, bile acid (BA) has been found to be carcinogenic and genotoxic. BA-induced apoptosis has been associated with various cancers. We have previously demonstrated that BA induced apoptosis and gene cleavages in nasopharyngeal epithelial cells. Chromosomal cleavage occurs at the early stage of both apoptosis and chromosome rearrangement. It was suggested that chromosome breaks tend to cluster in the region containing matrix association region/scaffold attachment region (MAR/SAR). This study hypothesised that BA may cause chromosome breaks at MAR/SAR leading to chromosome aberrations in NPC. This study targeted the AF9 gene located at 9p22 because 9p22 is a deletion hotspot in NPC.

Methods
Potential MAR/SAR sites were predicted in the AF9 gene by using MAR/SAR prediction tools. Normal nasopharyngeal epithelial cells (NP69) and NPC cells (TWO4) were treated with BA at neutral and acidic pH. Inverse-PCR (IPCR) was used to identify chromosome breaks in SAR region (contains MAR/SAR) and non-SAR region (does not contain MAR/SAR). To map the chromosomal breakpoints within the AF9 SAR and non-SAR regions, DNA sequencing was performed.

Results
In the AF9 SAR region, the gene cleavage frequencies of BA-treated NP69 and TWO4 cells were significantly higher than those of untreated control. As for the AF9 non-SAR region, no significant difference in cleavage frequency was detected between untreated and BA-treated cells. A few breakpoints detected in the SAR region were mapped within the AF9 region that was previously reported to translocate with the mixed lineage leukaemia (MLL) gene in an acute lymphoblastic leukaemia (ALL) patient.

Conclusions
Our findings suggest that MAR/SAR may be involved in defining the positions of chromosomal breakages induced by BA. Our report here, for the first time, unravelled the relation of these BA-induced chromosomal breakages to the AF9 chromatin structure.

Electronic supplementary material
The online version of this article (10.1186/s12920-018-0465-4) contains supplementary material, which is available to authorized users.

KEYWORDS

Chronic rhinosinusitis, Nasopharyngeal carcinoma, Gastro-oesophageal reflux, Bile acid, Apoptosis, AF9, Matrix association region/scaffold attachment region

Title

Matrix association region/scaffold attachment region: the crucial player in defining the positions of chromosome breaks mediated by bile acid-induced apoptosis in nasopharyngeal epithelial cells

Author

Sang-Nee Tan and Sai-Peng Simcorresponding author

Publish date

2019;

PMID

29850039

Abstract

The asymmetric unit of the title compound, [Fe(C8H11N2)(C17H14PS)], contains two independent mol­ecules (A and B) with very similar conformations. Each mol­ecule is built up from a ferrocene unit substituted in the 1 and 1′ positions by a protected sulfur di­phenyl­phosphine and by a di­methyl­hydrazine, -C(H)=N—N(CH3)2, fragment. The two independent mol­ecules are linked by a C—H⋯N hydrogen bond. In the crystal, the A-B dimer is linked by a pair of C—H⋯S hydrogen bonds, forming a centrosymmetric four-mol­ecule arrangement. These units are linked by C—H⋯π inter­actions, forming a supra­molecular three-dimensional structure.

KEYWORDS

crystal structure, ferrocenyl P,N ligands, thio­phosphine, hydrazine, catalysis, hydrogen bonding, C—H⋯π inter­actions

Title

The crystal structure of a new ferrocenyl P,N ligand: 1-[(2,2-di­methyl­hydrazin-1-yl­idene)meth­yl]-1′-(di­phenyl­phospho­rothio­yl)ferrocene

Author

Toma Nardjes Mouas,a,b,c Jean-Claude Daran,a,* Hocine Merazig,b and Eric Manourya

Publish date

2018 Feb 1