The stability of the inserted genes in the viral expression vector varied depending on the sequence introduced and the position of insertion. Infectious cDNA to Clover yellow vein virus (pClYVV) was modified to insert a foreign gene at two independent sites: one, along with a polylinker, between the NIb and CP genes (pClYVV/CP/ W) and the other between P1 and HC-Pro (pClYVV-Pst/ CP). The green fluorescent protein (GFP) gene was inserted into either pClYVV/CP/W or pClYVV-Pst/CP. GFP gene was stably maintained and expressed in both vectors following serial passages in plants. Progeny viruses from both constructs accumulated in similar amounts and at rates of 70%-80% of that of the wild-type virus. On the other hand, progeny viruses carrying the human interferon-α (hIFN) gene cloned in pClYVV-Pst/CP were genetically unstable owing to frequent deletions of the cloned gene during passage through plants. In contrast, the hIFN sequence cloned in pClYVV/CP/W was stably maintained in viruses after several passages in broad bean plants, and the progeny virus accumulated at the rate of about 50%-100% of that of the wild-type virus. The nucleotide sequence analyses indicated that the genetic instability of the inserted sequence results from homologous recombination of viral vector and inserted DNA sequences; it is not due to the inserted sequence alone.

Background Cystic angiomatosis is a rare benign disease manifesting as multiple lytic and sclerotic bone lesions, described as the proliferation of vascular and lymphatic channels lined by a single layer of endothelial cells. However, the potential pathogenetic mechanism of the disease still remains unknown. Here, we reported a case of cystic angiomatosis with multifocal bone lesion evaluated by whole exome sequencing. Case description In this presentation, we reported a case of an 11-year-old boy with pain in his chest. Computed tomography (CT) revealed the multiple lytic of the bone in the ribs, clavicle, vertebra thoracalis, skull, mandibula, shoulder blade, etc. The blood test showed ALP to be 393U/L and VEGF to be 287.26 pg/ml. The patient was performed with an open biopsy in the ribs and was diagnosed with cystic angiomatosis. Besides, the whole exome sequencing reported the single-nucleotide substitutions in the coding region of BRIP1, CHEK2, GRM4, and MUC16. Then, the upregulated genes involved CASC15, CENPF, ABCA13, ALK, BLM, and FGFR3. Conclusions In this article, we report a rare case of cystic angiomatosis in a child with abnormal VEGF and ALP reported by peripheral blood examination. The whole exome sequencing could provide the reference for the potential molecular mechanism in the diagnosis and treatment of cystic angiomatosis.

Background: Cystic angiomatosis is a rare disease characterized by the proliferation of vascular and lymphatic channels lined by a single layer of endothelial cells. Here, we reported a child of cystic angiomatosis with multifocal lesion in bone, who was diagnosed by biopsy surgery and evaluated by whole exome sequencing. Case Description: In this case presentation, we report a case of 11-year-old boy who had the pain in chest. Computed tomography revealed the multiple lytic of bone in ribs, clavicle, vertebra thoracalis, skull, mandibula, shoulder blade and so on. Blood test showed that ALP was 393U/L with the normal of 20–110 U/L and VEGF was 287.26 pg/ml with the normal of 0-142 pg/ml. The patient was performed by the biopsy surgery in ribs and diagnosed of cystic angiomatosis by pathological examination. The whole exome sequencing showed the single nucleotide substitutions in the coding region including BRIP1, CHEK2, GRM4, and MUC16. Besides, the up-regulated genes were involved of CASC15, CENPF, ABCA13, ALK, BLM, FGFR3.Conclusions: In this article, we report a rare case of cystic angiomatosis in a child with multiple lesions of bone and abnormal VEGF and ALP in peripheral blood examination. Then, the whole exome sequencing could be performed in order to explore the potential molecular mechanism in the development of cystic angiomatosis.

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