High-density bin-based genetic map reveals a 530-kb chromosome segment derived from wild peanut contributing to late leaf spot resistance.

KEY MESSAGE: Twenty-eight QTLs for LLS disease resistance were identified using an amphidiploid constructed mapping population, a favorable 530-kb chromosome segment derived from wild species contributes to the LLS resistance. Late leaf spot (LLS) is one of the major foliar diseases of peanut, causing serious yield loss and affecting the quality of kernel and forage. Some wild Arachis species possess higher resistance to LLS as compared with cultivated peanut; however, ploidy level differences restrict utilization of wild species. In this study, a synthetic amphidiploid (Ipadur) of wild peanuts with high LLS resistance was used to cross with Tifrunner to construct TI population. In total, 200 recombinant inbred lines were collected for whole-genome resequencing. A high-density bin-based genetic linkage map was constructed, which includes 4,809 bin markers with an average inter-bin distance of 0.43 cM. The recombination across cultivated and wild species was unevenly distributed, providing a novel recombination landscape for cultivated-wild Arachis species. Using phenotyping data collected across three environments, 28 QTLs for LLS disease resistance were identified, explaining 4.35-20.42% of phenotypic variation. The major QTL located on chromosome 14, qLLS14.1, could be consistently detected in 2021 Jiyang and 2022 Henan with 20.42% and 12.12% PVE, respectively. A favorable 530-kb chromosome segment derived from Ipadur was identified in the region of qLLS14.1, in which 23 disease resistance proteins were located and six of them showed significant sequence variations between Tifrunner and Ipadur. Allelic variation analysis indicating the 530-kb segment of wild species might contribute to the disease resistance of LLS. These associate genomic regions and candidate resistance genes are of great significance for peanut breeding programs for bringing durable resistance through pyramiding such multiple LLS resistance loci into peanut cultivars.

CD44+ fibroblasts increases breast cancer cell survival and drug resistance via IGF2BP3-CD44-IGF2 signalling.

CD44, a cell adhesion protein, involves in various process in cancer such as cell survival and metastasis. Most researches on CD44 in cancer focus on cancer cells. Recently, it is found that CD44 expression is high in fibroblasts of tumour microenvironment. However, its role in communication between fibroblasts and breast cancer cells is seldom known. In this study, CD44-positive (CD44+ Fbs) and CD44-negative carcinoma-associated fibroblasts (CD44- Fbs) were isolated and cocultured with breast cancer cells for analysis of cell survival and drug resistance. We found that CD44+ Fbs promoted breast cancer cell survival and paclitaxel resistance and inhibited paclitaxel-induced apoptosis. Our further research for the molecular mechanism showed that IGF2BP3 bound to CD44 mRNA and enhanced CD44 expression, which increased IGF2 levels of fibroblasts and then stimulated breast cancer cell proliferation and drug resistance. IGF2 was found to activate Hedgehog signal pathway in breast cancer cells. In conclusion, the results illustrated that in CD44+ Fbs, binding of IGF2BP3 and CD44 promotes IGF2 expression and then accelerates breast cancer cell proliferation, survival and induced chemotherapy resistance likely by activating Hedgehog signal pathways.

A presenting with obstructive jaundice in pulmonary adenocarcinoma: a case report.

INTRODUCTION: Obstructive jaundice caused by metastases to the distal common bile duct or the ampulla of Vater is often observed in patients with various advanced cancers; however, metastasis of lung cancer to the ampulla of Vater with subsequent development of jaundice is rare. CASE PRESENTATION: The patient was a 41-year-old Chinese female who presented with apparent jaundice and itching. An enlarged right supraclavicular lymph node was found during physical examination. Laboratory tests revealed significantly elevated bilirubin and aminotransferase. Imaging examinations, including ultrasonography, computed tomography (CT), and magnetic resonance cholangiopancreatography (MRCP) revealed a 3.1×2.5×2 cm mass in the distal common bile duct and the ampulla of Vater. The routine chest x-ray film revealed a 4-cm nodule in the upper lobe of the left lung and further CT scan confirmed the diagnosis of left lung cancer. A biopsy of supraclavicular lymph node was performed and the histopathology showed poorly differentiated adenocarcinoma with cytokeratin-7 (CK-7) and thyroid transcription factor-1 (TTF-1) being positive immunohistochemically. The patient underwent a pylorus preserving pancreaticoduodenectomy and the histology of the resected specimen revealed characteristic of pulmonary adenocarcinoma. Thus, the final diagnosis was periampullary metastasis from pulmonary adenocarcinoma. The patient's postoperative recovery was uneventful and the jaundice was disappeared one month later. A pulmonary lobectomy was followed by chemotherapy with combination of vinorelbine and cisplatin for six cycles. CONCLUSION: Similar situations are bound to occur again in the future and we believe that this report could demonstrate that there is a case for aggressive surgical management in patients with periampullary metastasis from pulmonary adenocarcinoma.

Recombinant adenovirus with human indoleamine-2,3-dioxygenase and hepatitis B virus preS was constructed and expressed in HepG2 cells.

BACKGROUND: Indoleamine-2,3-dioxygenase (IDO) is proven to suppress hepatitis B virus (HBV) specific immune response and depletion of IDO may be a useful approach for HBV therapy. To test this concept, we constructed recombinant adenovirus with human IDO and HBV preS, which would form the basis for future in vivo experiments. METHODS: The fragment of human IDO and HBV preS cDNA were subcloned into multiple cloning sites in an adenoviral vector system containing two cytomegalovirus (CMV) promoters. Recombination was conducted in the Escherichia coli BJ5183. The recombinant adenovirus containing hIDO gene and HBVpreS gene was packaged and amplified in 293 cells. Integration was confirmed by polymerase chain reaction as well as the quantification of viral titers. HepG2 cells were infected with the recombinant adenovirus and mRNA and protein specific for hIDO and HBVpreS was detected by RT-PCR and Western blotting respectively. RESULTS: The recombinant adenovirus was produced successfully. Its titer was 2.5 × 10(9) efu/ml. IDO and HBVpreS mRNA as well as the encoded proteins could be found in transfected HepG2 cells, but not in control HepG2 cells. CONCLUSION: The transfer of hIDO-HBVpreS with double-promoter adenoviral vector was efficient. The recombinant adenovirus with hIDO and HBV preS would provide the experimental basis for future studies.