Gastric cancer has high mortality and case fatality rate worldwide,especially in East Asia.Che-moresistance or chemotherapeutic resistance remains an important issue affecting the prognosis of gastric cancer patients.Mutations in the AT-rich interactive domain 1A(ARID1A)gene,an important member of the chromatin remodeling complex,are common in gastric cancer and are closely related to the clinical manifesta-tions of patients as well as the response to chemotherapy.Deletion or mutation of the ARID1A gene may lead to increased resistance of gastric cancer cells to platinum-based chemotherapeutic agents.In this paper,the bi-ological role of ARID1A gene,the alteration of DNA damage repair and metabolic remodeling in cisplatin re-sistance,and the possible mechanism of ARID1A gene involved in chemoresistance in gastric cancer are re-viewed.

Objective:To identify causative genes for autosomal recessive woolly hair (ARWH) in a family.Methods:Clinical data were collected from two patients and other family members in a Chinese pedigree of Han nationality with ARWH. Peripheral blood samples were obtained from the two patients, their unaffected parents and 100 unrelated healthy individuals, and DNA was extracted from the blood samples. A next-generation skin-targeted sequencing panel was used to detect gene mutations in the patients, and Sanger sequencing was performed to verify the sequencing results. The function of protein encoded by the mutant gene was predicted.Results:Two missense mutations c.530T>G (p.Leu177Arg) and c.736T>A (p.Cys246Ser) were both identified in the LIPH gene of the two patients, which were inherited from their father and mother respectively. Neither of the two mutations was identified in the 100 unrelated healthy controls. Interspecies sequence alignment showed that leucine at amino acid position 177 and cysteine at amino acid position 246 of the protein encoded by the LIPH gene were highly evolutionarily conserved. As SIFT and Polyphen-2 softwares showed, the mutations c.530T>G (p.Leu177Arg) and c.736T>A (p.Cys246Ser) were both predicted to be detrimental variations.Conclusion:Two missense mutations c.530T>G (p.Leu177Arg) and c.736T>A (p.Cys246Ser) in the LIPH gene may contribute to the clinical phenotype of the two patients with ARWH in this family.

Objective To evaluate the interference of ALP on cTnI assays. Methods One normal mixed plasma sample and 2 abnormal mixed plasma samples with different cTnI levels were prepared, and then divided them into 8 groups respectively. One group was randomly chosen as control while different amounts of ALP were added into the other seven groups. The concentrations of cTnI and ALP in each plasma portion were detected by ACCESS2 (Beckman-Coulter, Inc ) and AXSYM (Abbott Laboratories )separately. The results of the seven tested groups were then compared with those of the control, so as to evaluate whether ALP could interfere with the cTnI assay. Results When the chemiluminescent Access cTnI assay was carried out for detection of normal plasma, the concentration of ALP was up to 3 716 U/L and did not interfere with the test results of cTnI [(0. 04 ±0.01) μg/L] compared with those of the control portion [(0. 04 ± 0. 01 ) μg/L] (t = 0. 40, P ＞ 0. 05 ). Once the concentration of ALP went beyond 917 U/L, the AXSYM cTnI assay results [( 0.08 ± 0. 01 ) μg/L] were higher than those of the normal control ( t =-4. 89, P＜0. 01 ); When the concentration of ALP was up to 3 534 U/L, the test results of abnormal plasma cTnI detected by the Access assay [( 13.41 ±0. 17) μg/L] did not show significant differences from those of the control [(13.48±0.16) μg/L] (t=0. 52,P＞0.05).Conclusions High concentration ofALP did not interfere with the Access cTnI assay or lead to false positive results. However, the high level of ALP( ＞ 917 U/L) could interfere with the AXSYM cTnI assay and cause a false positive result.