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Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer deaths worldwide. Recent studies have shown that cancer stem cells (CSCs) are an important cause of tumor recurrence and metastasis. We hypothesized that CSCs marker CD166-positive CRC and colorectal adenoma (CAD) cells consist of more hotspot mutations than CD166-negative CRC and colorectal adenoma cells. To verify this, formalin fixed paraffin embedded tissue specimens from 42 patients each with CRC and CAD were recruited and CD166 immunohistochemical (IHC) staining followed by macrodissection was performed. DNA extracted was used for quantitative polymerase chain reaction detection on a somatic mutation array. Results showed that the immunoreactivity of CD166 protein had significant difference among CRC, CAD, and normal colorectal epithelial tissues (NCET) (P < 0.0001, Kruskal-Wallis test). Moreover, nucleotide changes were found in APC, KRAS, P53, PIK3CA, FBXW7 and SRC genes. Among those genes, KRAS exon 2 mutations were validated in another cohort of 70 CRC and 72 CAD specimens. Results showed that the difference in percentage of KRAS exon 2 mutations between CD166 positive and CD166 negative CRC specimens was significant (P < 0.05, chi-square test). Long term follow-up of the CRC patients showed that CD166-positive KRAS exon 2 mutations was useful in discriminating CRC patients with worse outcome. This study has provided evidence that KRAS exon 2 mutations are concentrated in CD166-positive cancer cells, with prognostic significance in CRC, and those mutations are also detected in CAD.

Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer deaths worldwide. Recent studies have shown that cancer stem cells (CSCs) are an important cause of tumor recurrence and metastasis. We hypothesized that CSCs marker CD166-positive CRC and colorectal adenoma (CAD) cells consist of more hotspot mutations than CD166-negative CRC and colorectal adenoma cells. To verify this, formalin fixed paraffin embedded tissue specimens from 42 patients each with CRC and CAD were recruited and CD166 immunohistochemical (IHC) staining followed by macrodissection was performed. DNA extracted was used for quantitative polymerase chain reaction detection on a somatic mutation array. Results showed that the immunoreactivity of CD166 protein had significant difference among CRC, CAD, and normal colorectal epithelial tissues (NCET) (P < 0.0001, Kruskal-Wallis test). Moreover, nucleotide changes were found in APC, KRAS, P53, PIK3CA, FBXW7 and SRC genes. Among those genes, KRAS exon 2 mutations were validated in another cohort of 70 CRC and 72 CAD specimens. Results showed that the difference in percentage of KRAS exon 2 mutations between CD166 positive and CD166 negative CRC specimens was significant (P < 0.05, chi-square test). Long term follow-up of the CRC patients showed that CD166-positive KRAS exon 2 mutations was useful in discriminating CRC patients with worse outcome. This study has provided evidence that KRAS exon 2 mutations are concentrated in CD166-positive cancer cells, with prognostic significance in CRC, and those mutations are also detected in CAD.

Treatment of LnCl3(THF)x with one equivalent of Na2[nido-7,8-C2B9H11] in THF gave the half-sandwich lanthanacarborane chloride compound (η5-C2B9H11)Ln(THF)2(μ-Cl)2Na(THF)2 (Ln=Y (1), Er (2), Yb (3), Lu (4)). Recrystallization of 1 or 3 from a wet THF–toluene solution afforded the ionic compound [LnCl2(THF)5][nido-C2B9H12] (Ln=Y (5), Yb (6)). Reaction of 1 or 3 with Na2[nido-7,8-C2B9H11] in a molar ratio of 1:1 in THF generated the full-sandwich lanthanacarborane {(η5-C2B9H11)2Ln(THF)2}{Na(THF)2} (Ln=Y (7), Yb (8)). All of these new compounds were characterized by 1H-, 13C-, and 11B-NMR spectra and elemental analyses. The solid-state structures of 5 and 6 were further confirmed by single-crystal X-ray analyses.

Treatment of anhydrous LaCl3 with 1 equiv of Na2[7,8-R2-nido-7,8-R2C2B9H9] in THF afforded sandwich complexes closo-{(THF)2Na}{(R2C2B9H9)2La(THF)2} (R = H (1), R = C6H5CH2 (2)) in good yield. React...

The rapid emergence of molecular diagnostic platforms has revolutionized the diagnostic approaches in hematology laboratory. Fluorescence in-situ hybridization, polymerase chain reaction and DNA sequencing are common techniques used in routine clinical laboratories for the diagnosis of hematological diseases. Different molecular techniques are indicated in different situations. This paper describes the utility of common molecular techniques. Fluorescence in-situ hybridization is specific for detection of chromosomal abnormalities using fluorescent labeled targeting probe. Polymerase chain reaction amplifies target DNA and reverse transcription polymerase chain reaction amplifies target RNA for the analysis of gene and its expression level. Real-time polymerase chain reaction is highly sensitive for detection of minimal residual disease in hemic malignancies. Gap-polymerase chain reaction is often employed for diagnosis of large deletions such as in alpha thalassemia. Allele-specific polymerase chain reaction is commonly used for single nucleotide polymorphism detection which is common in beta thalassemia, myeloproliferative neoplasm and acute leukemia. Inverse shifting-polymerase chain reaction can be employed for the detection of large genetic rearrangements such as those seen in hemophilia A. For genetically complex diseases such as hemophilia A, which involves a great variety of mutations in large genes, high resolution melting analysis can be used to scan for point mutations. Any suspected mutations are confirmed using post-PCR technologies, such as DNA sequencing. Although conventional diagnostic methods are able to provide a basic analysis in most cases, molecular technologies generate valuable genetic information that can refine diagnosis, better predict prognosis and facilitate disease monitoring.

SmI3 can be prepared by the reaction of SmI2 with O2 in dry condition. It crystallizes as an ionic complex, [SmI2(THF)5][SmI4(THF)2], from THF, rather than the simple coordination compound SmI3(THF)3.