Hwal Woong Kim

The Prevention of Vocal Fold Scarring Using Autologous Adipose Tissue-Derived Stromal Cells

Prevention and treatment of vocal fold scarring and atrophy remain challenging. The aim of this study was to treat injured vocal folds using autologous adipose tissue-derived stromal cells (ADSCs) and evaluate the ability to prevent vocal fold scarring and atrophy by ADSCs in a canine animal model. Ten adult dogs were used for this experiment. ADSCs from the adipose tissue from the inguinal area were isolated and cultured in all dogs. Immediately after being mixed with atelocollagen, the ADSCs (1–3 × 106) were injected into the right vocal fold of each animal, using a syringe with a 23-gauge needle. As a control, atelocollagen was injected into the left vocal fold of the same dog. The effects of the prevention of vocal fold scarring and atrophy were measured by morphological and histological assessment. At 8 weeks, there was a difference in granuloma and atrophic changes between the ADSC-injected and control sides in the majority of the dogs. This difference continued to be present at the 24 weeks’ follow-up. On histopathologic examination, a large number of cells labeled with a fluorochrome were observed in ADSC-injected vocal folds 8 weeks after the initial treatment. This study demonstrates the multipotential ability of ADSCs in the regeneration of injured vocal folds. Injecting ADSCs into a damaged vocal fold appears to be useful in preventing vocal fold scarring and atrophy 24 weeks after initial damage.

Gene expression in mixed type liposarcoma

Aims: Mixed type liposarcomas are rare. Here, we analysed the characteristics of an unusual case of mixed type liposarcoma, which consisted of a well‐differentiated liposarcoma (WDL) and a pleomorphic liposarcoma (PL), with a special emphasis on molecular alterations. Methods: Microscopic and immunohistochemical approaches were used to investigate this case of mixed type liposarcoma, and to identify molecular alterations in this tumour, gene expression was examined in PL, WDL, and normal adipose tissue (NA) samples using a 17 000 cDNA microarray. Results: The tumour mass, 9×5×5 cm, was located in the left upper arm of a 76‐year‐old man. Grossly, the proximal portion of the tumour was composed of a yellowish fatty lesion, whereas the distal portion of the tumour was whitish and necrotic in nature. Histologically, the tumour was composed of two distinct components. The proximal component of the tumour was a WDL and the distal component was a PL. Immunohistochemically, S100 protein immunoreactivity highlighted lipoblasts in both tumour portions. The Ki‐67 proliferation index was <1% in the WDL and 20% in the PL. MDM2 was positive in the WDL, but negative in the PL. p53 was negative in both areas. Numerous differentially expressed genes were found, which included genes coding for signal transduction, transcription, cell cycle, enzyme, structural protein, immune system and others. Conclusions: Our data demonstrate that multiple genes are differentially expressed in mixed type liposarcoma and suggest that these genes are associated with the differences in the morphological characteristics and pathogenesis of mixed type liposarcoma.

Clinicopathological significance of BGP expression in non-small-cell lung carcinoma: relationship with histological type, microvessel density and patients’ survival

Aims: Brain‐type glycogen phosphorylase (BGP) is the major isoform of glycogen phosphorylase found in fetal and neoplastic tissues, and is generally thought to induce glucose supply during an ischaemic period. This study was performed to investigate BGP expression in non‐small‐cell lung carcinoma (NSCLC). Methods: A total of 119 cases of NSCLC, including 63 squamous cell carcinomas (SqCCs) and 56 adenocarcinomas (ACs), were imunohistochemically evaluated for BGP expression, and its expression was correlated with clinicopathological parameters. Results: In total, 76.5% were positive, while non‐neoplastic bronchial epithelial cells were weakly positive and pneumocytes were negative. High BGP expression was noted in 78.6% of ACs and 36.5% of SqCCs (p = 0.001). Microvessel density was higher in the low BGP expression tumours (29.6 ± 16.9/mm2) than in the high expression tumours (22.8 ± 13.8/mm2) (p = 0.017). BGP expression did not correlate with patient age or tumour stage, but was more frequent in females than males. Kaplan–Meier analysis showed that high BGP expression was associated with poorer survival (p = 0.032). Conclusions: BGP is expressed in NSCLC, particularly AC, and is an independent poor prognostic factor.