Table 2: Characteristics of studies included in investigating prevalence of myofibroblasts in oral cancer
| References |
Year of publication |
Journal of publication |
Details of the study | ||||
| Zidar et al17 | 2002 | Oncology | Sample - n1 = 42 (resected larynx) n2 = 40 (laryngeal biopsies of epithelial hyperplastic lesions and squamous carcinoma-myofibroblast found exclusively in squamous carcinoma) | ||||
| Barth et al18 | 2004 | Virchows Arch | Sample - n = 39 (OSCC and tumor-free oral mucosa) 31 carcinomas showed increased stromal a SMA positive myofibroblast | ||||
| Lewis et al19 | 2004 | Br J Cancer | Sample - n = 25 (15 OSCC and 10 fibro epithelial hyperplasia) Myofibroblasts differentiation is commonly seen in the stroma of OSCC (11), particularly at the invasive front of the tumor, no a SMA positive myofibroblast in the connective tissue of fibroepithelial hyperplasia | ||||
| Vered et al20 | 2005 | Oral Oncol | Sample - n = 53, high frequency of stromal myofibroblast in known aggressive odontogenic lesion, such as odontogenic keratocyst parakeratinized type and solid ameloblastoma implies that myofibroblast can contribute to the biological behavior of these odontogenic lesions | ||||
| Kellermann et al21 | 2007 | Histopathology | Sample - n = 117, myofibroblast in the stroma of the oral carcinoma are associated with poor prognosis | ||||
| Kellermann et al22 | 2008 | Oral Oncol | 60% of the OSCC contain myofibroblast in the stroma of the tumor During tumor invasion OSCC-derived TGF-p 1 promote fibroblast myofibroblast transdifferentiation and tumor cell proliferation can be induced by factors released from myofibroblast favoring tumor growth | ||||
| Verad et al23 | 2009 | Cancer Microenviron | Sample - n = 19 (pair matched-oral tongue SCC and metastatic tumor to regional lymph node), expression of cancer-associated fibroblast is common to both primary and metastatic SCC | ||||
| Franz et al24 | 2009 | Histochem Cell Biol | Sample - n = 152, Snail-positive cell in the stroma of OSCC invasive front without statistically significant correlation, histological grade, or nodal metastasis. | ||||
| Kawashiri et al25 | 2009 | Head Neck | Sample - n = 84, high level of stromal collagen fibers in invasive tumors, myofibroblast appearance increased with increasing tumor invasiveness with frequent lymph node metastasis | ||||
| Etemad-Moghadam et al26 | 2009 | J Oral Pathol Med | Sample - n = 70, presence of myofibroblast in the stroma of OSCC but not in dysplasia and normal mucosa | ||||
| Franz et al27 | 2010 | J Oral Pathol Med | Sample - n = 5, mediated by myofibroblast OSCC development is associated with a stromal upregulation of laminin isoform possibly contributing to a migration promoting microenvironment | ||||
| Seifi et al28 | 2010 | Asian Pac J Cancer Pre | v Sample - n = 54, increase in the number of myofibroblast and change in the distribution pattern occur during carcinogenesis signifying their role in tumor invasion characteristics | ||||
| Sobral et al29 | 2011 | Oral Oncol | Sample - n = 30, myofibroblast in the stroma of OSCC may influence proliferation and invasion | ||||
| Salgueiredo-Giudice et al30 | 2011 | Oral Surg Oral Med Oral Pathol Oral Radiol Endod | Sample - n = 3, demonstration of IHC profile of oral inflammatory myofibroblastic tumor along with morphological analysis reveals positive for calponin, vimentin, a-SMA, fibronectin | ||||
| Angadi et al13 | 2011 | J Oral Pathol Med | Sample - n = 85, statistically significant increase in the myofibroblast between early and advance stages was observed | ||||
| Sridhara et al31 | 2013 | J Oral Maxillofac Pathol | Sample - n = 10, a-SMA cases were more in the metastatic group than in the nonmetastatic tumor | ||||
| Lucio et al32 | 2013 | Braz J Otorhinolaryngol | Myofibroblasts are important components of the stroma for SCC | ||||
| Angadi et al33 | 2014 | Ada Odontol Scand | Sample - n = 65, (50-OSCC and histologically normal mucosa adjacent to OSCC, 15-control) significant co-relation was established for the presence of myofibroblast in the stroma of OSCC and HNMAOSCC. Myofibroblasts are early stromal change in the HNMAOSCC that highlights the possible role of myofibroblast as likely mediator for field cancerization | ||||
| Routray et al34 | 2014 | Oral Dis | Myofibroblast can arise locally from endothelial mesenchymal transformation at the invasive edge of the cancer leading to development of high-grade malignancies and poor prognosis | ||||
| Pinisetti et al35 | 2014 | J Oral Maxillofac Pathol | Myofibroblast in focal epithelial dysplasia and SCC revealed a higher number of myofibroblast in OSCC | ||||
| Rao et al36 | 2014 | J Clin Diagn Res | Sample n = 62 (41 - OSMF, 10 - OSMF with dysplasia and 11 - OSCC). Presence of myofibroblasts was significantly higher in OSCC | ||||
| Luksic et al49 | 2015 | Int J Oral Maxillofac Surg | Sample n = 152, myofibroblast proliferation was suggested to facilitate tumor invasion and distant metastasis | ||||
| Guan et al50 | 2015 | Histopathology | Immunohistochemically, significant difference was observed in a-SMA expression in between normal controls and adenoid cystic carcinoma. This study demonstrated presence of myofibroblasts in adenoid cystic carcinoma. | ||||
| Jensen et al51 | 2015 | J Oral Pathol Med | In this study, budding tumor cells had decreased expression of E-cadherin. Thus, it is suggested that budding tumor cells in OSCC is not dependent upon either myofibroblast or complete epithelial― mesenchymal transition. |
OSCC: Oral squamous cell carcinoma; HNMAOSCC: Histologically normal mucosa adjacent to oral squamous cell carcinoma; IHC: Immunohistochemistry; SMA: Smooth muscle actin; OSMF: Oral submucous fibrosis