<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.oraloncology.com/?rss=yes"><title>Oral Oncology</title><description>Oral Oncology RSS feed: Current Issue.    
 Oral Oncology  is an international interdisciplinary journal which publishes high quality original research, clinical trials and 
review articles, editorials, and commentaries relating to the etiopathogenesis, epidemiology, prevention, clinical features, diagnosis, 
treatment and management of patients with neoplasms in the head and neck. 

 
 
 Oral Oncology  is of interest to head and neck 
surgeons, radiation and medical oncologists, maxillo-facial surgeons, oto-rhino-laryngologists, plastic surgeons, pathologists, scientists, 
oral medical specialists, special care dentists, dental care professionals, general dental practitioners, public health physicians, palliative 
care physicians, nurses, radiologists, radiographers, dieticians, occupational therapists, speech and language therapists, nutritionists, 
clinical and health psychologists and counselors, professionals in end of life care, as well as others interested in these fields. 


 
 Basic, translational, or clinical Research or Review papers of high quality and that make a contribution to new knowledge are invited 
on the following aspects of neoplasms arising in the head and neck (including lip, tongue, oral cavity, oropharynx, salivary glands, 
sinuses, nose, nasopharynx, larynx, skull base, thyroid, and craniofacial region, and the related hard and soft tissues and lymph nodes): 


 
 • Etiopathogenesis: natural history of cancer and pre-cancer; basic pathology, metastatic mechanisms; genetic changes; cellular 
and molecular changes; microorganisms; growth factors, adhesion and other molecules • Epidemiology; risk factors; biomarkers; 
protective factors; geographic factors; prevention; screening and intervention • Clinical features; orofacial effects of neoplasms 
at both local and distant sites; tumor staging and grading  • Diagnosis; detection of cancer and pre-cancer; cellular and molecular 
markers for diagnosis; advances in imaging and other functional diagnostic modalities for cancer and pre-cancer • Management 
and Prognosis; clinical, cellular and molecular markers for prognosis; treatment options including surgical, lasers, photodynamic therapy, 
cryosurgery, micro- vascular and other forms of surgery, medical, radiotherapy, chemotherapy, immunotherapy, biological and gene therapy 
advances; molecular targets and new therapeutics (new cytotonics and molecular-targeted therapies); multimodality treatment; advances 
in reconstruction and rehabilitation, including flaps and grafts, alloplasty, bone and connective tissue biology; multidisciplinary teamwork 
in cancer care and oral health care.  • Quality of life issues; issues of consent; psychosocial aspects; patient and health 
professional information; patient involvement; psychological interventions, improving outcomes; the prevention, diagnosis and management 
of complications, including, pain, hemorrhage, dysfunction, deformity, osteoradionecrosis, xerostomia, and others; rehabilitation; palliative 
and end of life care; and support teamwork.   </description><link>http://www.oraloncology.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Elsevier Ltd. All rights reserved. </dc:rights><prism:publicationName>Oral Oncology</prism:publicationName><prism:issn>1368-8375</prism:issn><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2011 Elsevier Ltd. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511009341/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511007998/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008232/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008220/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008396/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS136883751100813X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008141/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008128/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008177/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008190/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008815/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008062/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008086/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008074/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008219/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008207/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS136883751100827X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511007433/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511007718/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008025/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008244/abstract?rss=yes"/><rdf:li rdf:resource="http://www.oraloncology.com/article/PIIS1368837511008268/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511009341/abstract?rss=yes"><title>Editorial Board/Aims &amp; Scope</title><link>http://www.oraloncology.com/article/PIIS1368837511009341/abstract?rss=yes</link><description></description><dc:title>Editorial Board/Aims &amp; Scope</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1368-8375(11)00934-1</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511007998/abstract?rss=yes"><title>Is neck dissection needed in squamous-cell carcinoma of the maxillary gingiva, alveolus, and hard palate? A multicentre Italian study of 65 cases and literature review</title><link>http://www.oraloncology.com/article/PIIS1368837511007998/abstract?rss=yes</link><description>Summary: The occurrence of occult cervical metastases due to squamous-cell carcinoma of the hard palate and maxillary alveolar ridge has not been studied systematically. We have observed that many patients return with a delayed cervical metastasis following resection of a primary cancer at these sites. Some of these patients have died as a result of a regional or distant metastasis, despite control of the primary cancer. The literature contains few recommendations to guide the treatment of maxillary squamous-cell carcinoma; prospective studies are difficult due to the rarity of such tumours. The aim of this study is to define the incidence of cervical metastasis and to investigate whether elective neck dissection is justified.We present a retrospective multicentre study of 65 patients with squamous-cell carcinomas of the maxillary alveolar ridge and hard palate and review of the existing literature.The overall incidence of cervical metastases was 21%. We evaluated the significance of primary-site tumours as indicator of regional disease.The maxillary squamous-cell carcinoma cases in our multicentre study and in the literature review exhibited aggressive regional metastatic behaviour, comparable with that of carcinomas of the tongue, mouth floor, and mandibular gingiva. Based on our findings, we recommend selective neck dissection in clinically negative necks as a primary management strategy for patients with maxillary squamous-cell carcinomas involving the palate, maxillary gingiva, or maxillary alveolus.</description><dc:title>Is neck dissection needed in squamous-cell carcinoma of the maxillary gingiva, alveolus, and hard palate? A multicentre Italian study of 65 cases and literature review</dc:title><dc:creator>Giada A. Beltramini, Olindo Massarelli, Marco Demarchi, Chiara Copelli, Andrea Cassoni, Valentino Valentini, Antonio Tullio, Aldo B Giannì, Enrico Sesenna, Alessandro Baj</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.012</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-12</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-12</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>97</prism:startingPage><prism:endingPage>101</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008232/abstract?rss=yes"><title>In vitro influence of the extracellular matrix in myoepithelial cells stimulated by malignant conditioned medium</title><link>http://www.oraloncology.com/article/PIIS1368837511008232/abstract?rss=yes</link><description>Summary: In order to investigate the role of myoepithelial cell and tumor microenvironment in salivary gland neoplasma, we have performed a study towards the effect of different extracellular matrix proteins (basement membrane matrix, type I collagen and fibronectin) on morphology and differentiation of benign myoepithelial cells from pleomorphic adenoma cultured with malignant cell culture medium from squamous cell carcinoma. We have also analyzed the expression of α-smooth muscle actin (α-SMA) and FGF-2 by immunofluorescence and qPCR. Our immunofluorescence results, supported by qPCR analysis, demonstrated that α-SMA and FGF-2 were upregulated in the benign myoepithelial cells from pleomorphic adenoma in all studied conditions on fibronectin substratum. However, the myoepithelial cells on fibronectin substratum did not alter their morphology under malignant conditioned medium stimulation and exhibited a stellate morphology and, occasionally focal adhesions with the substratum. In summary, our data demonstrated that the extracellular matrix exerts an important role in the morphology of the benign myoepithelial cells by the presence of focal adhesions and also inducing increase FGF-2 and α-SMA expression by these cells, especially in the fibronectin substratum.</description><dc:title>In vitro influence of the extracellular matrix in myoepithelial cells stimulated by malignant conditioned medium</dc:title><dc:creator>Elizabeth F. Martinez, Ana Paula Dias Demasi, Marcelo Henrique Napimoga, Victor Elias Arana-Chavez, Albina Altemani, Ney Soares de Araújo, Vera Cavalcanti de Araújo</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.008</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-13</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-13</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>102</prism:startingPage><prism:endingPage>109</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008220/abstract?rss=yes"><title>Vesicular stomatitis virus matrix protein (VSVMP) inhibits the cell growth and tumor angiogenesis in oral squamous cell carcinoma</title><link>http://www.oraloncology.com/article/PIIS1368837511008220/abstract?rss=yes</link><description>Summary: The purpose of this study was to investigate the anticancer property of vesicular stomatitis virus matrix protein (VSVMP) in oral squamous cell carcinoma (OSCC) via in vitro and in vivo approaches. In this study, we found that OSCC cells treated with VSVMP showed retarded cell growth in vitro. The percentage of apoptotic cells in VSVMP group was much higher than that of the control groups. Moreover, our in vivo experiments showed that the growth of tumor xenografts was significantly suppressed by VSVMP treatment without any obvious side effects. Further studies revealed that the suppression of tumor growth may be caused by the synergistic effect of VSVMP related cell apoptosis enhancing and tumor angiogenesis suppression, and the latter is most likely correlated with the suppression of VEGF pathway. This study indicated that VSVMP treatment can effectively inhibited the cell growth and tumor angiogenesis in OSCC without obvious adverse effects. Therefore, VSVMP might be a potential and efficient strategy for OSCC treatment.</description><dc:title>Vesicular stomatitis virus matrix protein (VSVMP) inhibits the cell growth and tumor angiogenesis in oral squamous cell carcinoma</dc:title><dc:creator>Yu Zhou, Xiaohan Zhu, Rui Lu, Hongxia Dan, Fang Wang, Jing Wang, Jing Li, Xiaodong Feng, Hui Wang, Ning Ji, Min Zhou, Xin Zeng, Lu Jiang, Qianming Chen</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.007</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-28</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-28</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>110</prism:startingPage><prism:endingPage>116</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008396/abstract?rss=yes"><title>HNOCDB: A comprehensive database of genes and miRNAs relevant to head and neck and oral cancer</title><link>http://www.oraloncology.com/article/PIIS1368837511008396/abstract?rss=yes</link><description>Summary: In spite of the wide prevalence of head, neck and oral cancer, HNOC, there is no integrated database on genes and miRNAs associated with all the carcinoma subtypes of HNOC. The objective is to compile a multilayered and comprehensive database of HNOC as a user-friendly resource for researchers devising novel therapeutic strategies. We present HNOCDB, the head, neck and oral cancer database, with the following key features: (i) it tabulates all the different categories of HNOC separately under appropriate subtype-names, and then puts them together in a table headlined All; (ii) the oncogenes/oncomiRs that cause HNOC are listed; their mutations, methylations and polymorphisms loci are marked, and the variations in their expression profiles relative to the normal are recorded; (iii) HNOCDB contains a chromosomal map of HNOC genes and miRNA; (iv) contains references that experimentally validate the reason for the inclusion of the genes and the miRNAs in HNOCDB. HNOCDB is freely accessible for academic and non-profit users via http://gyanxet.com/hno.html.</description><dc:title>HNOCDB: A comprehensive database of genes and miRNAs relevant to head and neck and oral cancer</dc:title><dc:creator>Sanga Mitra, Smarajit Das, Shaoli Das, Suman Ghosal, Jayprokas Chakrabarti</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.014</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>117</prism:startingPage><prism:endingPage>119</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS136883751100813X/abstract?rss=yes"><title>Immunoexpression of p53 and hMSH2 in oral squamous cell carcinoma and oral dysplastic lesions in Yemen: Relationship to oral risk habits and prognostic factors</title><link>http://www.oraloncology.com/article/PIIS136883751100813X/abstract?rss=yes</link><description>Summary: Although several studies analyzed p53 and mismatch repair (MMR) gene expression separately in oral squamous cell carcinoma (SCC), no reports of combined assessment of both proteins in this cancer. The aim of this study was to investigate the roles of p53 and hMSH2 proteins in oral SCC as well as in oral dysplastic lesions (DL) in Yemen.Immunohistochemistry was used to examine the pattern of expression of p53 and hmsh2 proteins in 70 oral SCC and 21 oral DL obtained from Yemeni patients.p53 Immunoexpression was detected in 24 of the 70 oral SCC (34.3%) and 3 of 21 DL (14.3%) with no significant difference between the two groups. On the other hand, reduced expression of hMSH2 was detected in 26 of the 70 oral SCC (37.1%) and 2 of 21 oral DL (9.5%) with a statistically significant difference (P=0.03). Both proteins were significantly related to the grade of tumor differentiation (P=0.007 and 0.02, respectively). There was an inverse correlation between the levels of p53 and hMSH2 immunoexpression in the oral SCC (r=0.42, P=0.01).This study suggested that p53 may play a role in the early stages of oral carcinogenesis, while hMSH2 may be altered in the late stages. More importantly, the roles of p53 and hMSH2 in oral carcinogenesis seem to be interrelated in the pathogenetic pathway of oral SCC. Such a relationship has not been published previously in this type of cancer and needs to be clarified in future studies.</description><dc:title>Immunoexpression of p53 and hMSH2 in oral squamous cell carcinoma and oral dysplastic lesions in Yemen: Relationship to oral risk habits and prognostic factors</dc:title><dc:creator>Thanaa El. A. Helal, Mona T. Fadel, Abdalla K. El-Thobbani, Amira M. El-Sarhi</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.024</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-21</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-21</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>120</prism:startingPage><prism:endingPage>124</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008141/abstract?rss=yes"><title>Common genetic mutations in the start codon of the SDH subunit D gene among Chinese families with familial head and neck paragangliomas</title><link>http://www.oraloncology.com/article/PIIS1368837511008141/abstract?rss=yes</link><description>Summary: Head and neck paragangliomas (HNPGLs) are rare, and frequently associated with germline mutations of the succinate dehydrogenase (SDH) genes, especially for familial cases. The purpose of the study is to explore SDH mutations in Chinese families with familial HNPGLs in Taiwan.Four unrelated families with familial HNPGLs were screened for germline mutations in the SDHB, SDHC and SDHD genes by direct sequencing. One hundred healthy subjects without a diagnosis or family history of HNPGLs were screened as normal controls. Immunohistochemistry with SDHB antibody was performed for a carotid body tumor.Two allele variants were identified, including p.Met1Val (c.1A&gt;G) in the SDHD gene in one family and p.Met1Ile (c.3G&gt;C) in the SDHD gene in the other three families. Both variants are considered pathogenic because of the absence of these variants in 100 normal controls, 100% evolutionary conservation of the p.Met1 residue, co-segregation of the variants with the phenotype of HNPGL in pedigrees, and predicted abolishment of the translation start site. The tumor cells obtained from one proband harboring c.3G&gt;C mis-sense mutation were weak diffuse staining in the cytoplasm of tumors cells.This study demonstrates that two mis-sense mutations at the start codon of the SDHD gene, including p.Met1Val (c.1A&gt;G) and p.Met1Ile (c.3G&gt;C), might be mutation hotspots in Chinese patients with familial HNPGLs.</description><dc:title>Common genetic mutations in the start codon of the SDH subunit D gene among Chinese families with familial head and neck paragangliomas</dc:title><dc:creator>Cheng-Ping Wang, Tseng-Cheng Chen, Yih-Leong Chang, Jenq-Yuh Ko, Tsung-Lin Yang, Fei-Yun Lo, Ya-Ling Hu, Pei-Lung Chen, Chen-Chi Wu, Pei-Jen Lou</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.025</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-26</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-26</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>125</prism:startingPage><prism:endingPage>129</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008128/abstract?rss=yes"><title>A high HIF-1α expression genotype is associated with poor prognosis of upper aerodigestive tract carcinoma patients</title><link>http://www.oraloncology.com/article/PIIS1368837511008128/abstract?rss=yes</link><description>Summary: The aim of the present study was to evaluate the role of HIF-1α genetic polymorphisms and protein expression in the development of metastasis in upper aerodigestive tract cancer (UADTC) patients. The expression of pro-angiogenic markers was also evaluated. Protein expression was analysed using immunohistochemistry, and RFLP analysis was used to investigate HIF-1α C1779T and G1790A polymorphisms in 52 patients with UADTC. Primary lesions were divided into 2 groups according to the absence or presence of metastasis. Lymph node samples were divided into 3 groups: metastatic lymph nodes, non-metastatic lymph nodes (both derived from patients with metastatic disease), and control lymph nodes, which were obtained from patients without any metastasis. The allele T was more frequently found in patients with metastatic disease. HIF-1α protein expression in the lymph nodes was increased in the presence of the T allele. Metastatic lymph nodes showed lower levels of HIF-1α, VEGFR1, and MMP-9 proteins compared to lymph nodes without metastasis, while VEGFR2 protein levels were increased. In agreement, HIF-1α expression was correlated with MMP-9. Cox regression analysis demonstrated that higher HIF-1α and MMP-9 protein expression levels and GA and GG genotypes were associated with poor survival. Our findings show that the C1772T and G1790A polymorphisms of the HIF-1α gene are associated with increased expression of the HIF-1α protein in UADTC. The present data indicate that non-metastatic tissues express higher levels of HIF-1α, VEGFR1, and MMP-9, while in metastatic lymph nodes, VEGFR2 protein expression is elevated. The present study also shows that the HIF-1α G1790A polymorphism and its protein expression have an impact on the prognosis of UADTC patients.</description><dc:title>A high HIF-1α expression genotype is associated with poor prognosis of upper aerodigestive tract carcinoma patients</dc:title><dc:creator>Carlos Alberto de Carvalho Fraga, Marcos Vinícius Macedo de Oliveira, Érica Silva de Oliveira, Lucas Oliveira Barros, Francis Balduino Guimarães Santos, Ricardo Santiago Gomez, Alfredo Maurício Batista De-Paula, André Luiz Sena Guimarães</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.023</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-26</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-26</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>130</prism:startingPage><prism:endingPage>135</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008177/abstract?rss=yes"><title>Type I and III collagen degradation products in serum predict patient survival in head and neck squamous cell carcinoma</title><link>http://www.oraloncology.com/article/PIIS1368837511008177/abstract?rss=yes</link><description>Summary: Cancer invasion induces extracellular matrix remodeling and collagen degradation. The aim of this study was to assess whether serum levels of type I and III collagen degradation products were associated with patient survival in head and neck squamous cell carcinoma (HNSCC). A novel enzyme immunoassay was developed for measuring type III collagen N-terminal telopeptide (IIINTP) in human serum samples. In addition, type I collagen C-terminal telopeptide (ICTP), matrix metalloprotease-8 (MMP-8) and tissue inhibitor of metalloproteases-1 (TIMP-1) were assessed in 205 blood samples from HNSCC patients. High levels of serum ICTP and IIINTP and plasma TIMP-1 were associated with poor survival. The concentration of ICTP was associated with levels of IIINTP and TIMP-1. The plasma concentration of MMP-8 was associated with tumor stage, but not with survival or levels of ICTP, IIINTP or TIMP-1 suggesting that other collagenases/proteases are responsible for the cleavage of type I and type III collagens. The rate of type I and type III collagen degradation is associated with patient survival and can be used as a prognostic marker in HNSCC.</description><dc:title>Type I and III collagen degradation products in serum predict patient survival in head and neck squamous cell carcinoma</dc:title><dc:creator>Sini Nurmenniemi, Marja-Kaisa Koivula, Pia Nyberg, Taina Tervahartiala, Timo Sorsa, Petri S. Mattila, Tuula Salo, Juha Risteli</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.002</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-26</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-26</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>136</prism:startingPage><prism:endingPage>140</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008190/abstract?rss=yes"><title>Head and neck inflammatory myofibroblastic tumor (IMT): Evaluation of clinicopathologic and prognostic features</title><link>http://www.oraloncology.com/article/PIIS1368837511008190/abstract?rss=yes</link><description>Summary: Owing to rarity and awareness deficiency towards inflammatory myofibroblastic tumor (IMT), we sought to review on its clinicopathological features; arising awareness to achieve early diagnosis; exploring prognostic factors and then establishing a treatment protocol. Retrospective study was performed on patients with histological proven IMT between January 2003 and December 2010. Their demographic data, clinical and histological presentations were recorded. Overall survival (OS) and progression-free-survival (PFS) were estimated via Kaplan–Meier method. Cox regression model was applied to determine the significant of prognostic factors. Logistic regression model was established to predict the probability of relapse. A total of 28 patients. Five-year PFS was 65%. Surgical margins primarily and independently determined the survival, followed by size, pseudocapsule of the lesion, intra-lesional necrosis and lastly Ki-67 and ALK overexpression. Logistic model in prediction of relapse was established, with the formula as probability of relapse=1/(1+e−z) where e=exponential function, z=constant value (3.9)+B*margin+B*size+B*immunohistochemical expression+B*pseudocapsule+B*intra-lesional necrosis. Immunohistochemical overexpression was significant if Ki-67 was strongly expressed with a conditioned ALK overexpression simultaneously. Staining intensity must be at least moderate for those ALK nuclear staining was less than 25%. Weak ALK staining intensity is only significant if nuclear staining was more than 25%. Diagnosis of IMT is achieved via exclusion. Radical resection and obtaining negative margins remains the mainstay of treatment. Both high and moderate-risk groups required post-operative radiotherapy. In low-risk group, post-operative radiotherapy was recommended if the lesion is larger than 5cm in diameter with a conditioned ALK &amp; Ki-67 overexpression.</description><dc:title>Head and neck inflammatory myofibroblastic tumor (IMT): Evaluation of clinicopathologic and prognostic features</dc:title><dc:creator>Hui Shan Ong, Tong Ji, Chen Ping Zhang, Jiang Li, Li Zhen Wang, Rong Rong Li, Jian Sun, Chun Yue Ma</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.004</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-19</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-19</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>141</prism:startingPage><prism:endingPage>148</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008815/abstract?rss=yes"><title>Accuracy of MRI in prediction of tumour thickness and nodal stage in oral squamous cell carcinoma</title><link>http://www.oraloncology.com/article/PIIS1368837511008815/abstract?rss=yes</link><description>Summary: We aim to compare radiological with histological tumour thickness (RTT with HTT) for oral squamous cell carcinoma (OSCC), and the ability of both to predict cervical metastasis. The MRI images and histopathology reports of 102 consecutive OSCC cases were compared and therelationship between RTT and HTT, calculated as a “shrinkage factor” by the gradient of the best fitting regression line. Most (69%) tumours appeared thicker on MRI than was revealed by histopathology. Shrinkage factor was 0.70 (interquartile range 0.63–0.77, correlation co-efficient 0.63) for all cases, 0.87 (IQR 0.80–0.95, CC 0.88) for tongue and 0.65 (IQR 0.49–0.82, CC 0.45) for floor of mouth sub-sites. RTT did not correlate well with the presence of nodal metastases in any sub-site, i.e. there was no clinically applicable cut-off value of RTT to determine the prescription of elective neck dissection. Although RTT has some predictable relationship with HTT, this varies between sub-sites with tongue the most accurately predicted shrinkage using axial MRI. It is not possible from either the MRI staging of neck or tumour thickness to safely determine the need for neck dissection in OSCC. It is necessary to re-evaluate the benefit of MRI as a staging investigation (particularly for early stage OSCC) and further explore the contribution of molecular biomarkers and ultrasound.</description><dc:title>Accuracy of MRI in prediction of tumour thickness and nodal stage in oral squamous cell carcinoma</dc:title><dc:creator>Christine T Lwin, Rebecca Hanlon, Derek Lowe, James S. Brown, Julia A. Woolgar, Asterios Triantafyllou, Simon N. Rogers, Fazilet Bekiroglu, Huw Lewis-Jones, Hulya Wieshmann, Richard J. Shaw</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.11.002</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-12-09</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-12-09</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>149</prism:startingPage><prism:endingPage>154</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008062/abstract?rss=yes"><title>Radiation-associated head and neck sarcomas: Spectrum of imaging findings</title><link>http://www.oraloncology.com/article/PIIS1368837511008062/abstract?rss=yes</link><description>Summary: Sarcomas developing after radiation treatment for primary malignancies of the head and neck are often detected clinically when they are very aggressive. We reviewed the patient demographics and imaging findings in 21 patients with radiation-associated sarcomas (RAS) of the head and neck treated at our institution.Twenty-one RAS of the head and neck were retrospectively reviewed. The lesions were assessed for presence of a soft tissue mass, enhancement pattern, bone destruction, characteristics of tumor matrix, and FDG avidity.The RAS developed 4.5–25years (mean 12.7years) after irradiation. On both CT and MRI, all 21 lesions presented with a soft tissue mass. A variable imaging appearance was noted on CT, MR, and PET/CT, most, but not all, demonstrated aggressive features. At a median follow-up time of 19.1months, 11 of the 21 patients had died from the sarcoma.RAS have variable imaging appearances. While most demonstrate aggressive features, some appear benign, which can lead to misdiagnosis. Head and neck radiologists, surgeons and oncologists who manage patients after radiation treatment should be aware of the wide range of clinical presentations and imaging features of RAS, because failure to diagnose can delay appropriate treatment.</description><dc:title>Radiation-associated head and neck sarcomas: Spectrum of imaging findings</dc:title><dc:creator>J. Matthew Debnam, Nandita Guha-Thakurta, Yasser M.M. Mahfouz, Adam S. Garden, Robert S. Benjamin, Erich M. Sturgis, Lawrence E. Ginsberg</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.017</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-21</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-21</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>155</prism:startingPage><prism:endingPage>161</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008086/abstract?rss=yes"><title>Radical radiotherapy for nasopharyngeal carcinoma in elderly patients: The importance of co-morbidity assessment</title><link>http://www.oraloncology.com/article/PIIS1368837511008086/abstract?rss=yes</link><description>Summary: Elderly patients represent a unique challenge for radical treatment in nasopharyngeal carcinoma (NPC) because of age and co-morbid conditions. We sought to evaluate the outcome of this particular group of patients and to identify key factors affecting treatment outcome. From 1998 to 2008, 990 consecutive NPC patients without distant metastasis were treated with radical radiotherapy with planned total dose &gt;66Gy. Among them, 103 (10.4%) patients were elderly aged &gt;70 (group A). Their clinical characteristics and outcome were compared with those aged &lt;70 (group B). Mortality at 90days was used as a proxy of early deaths related to treatment. Co-morbidities were measured by the Adult Co-morbidity Evaluation 27 (ACE-27). Group A presented more commonly with poorer performance status. They showed higher rates of acute reaction, radiotherapy incompletion and mortality at 90days (7.8% vs. 1.2%, p&lt;0.001). The 5-year overall survival rates were 43.9% and 78.1% for groups A and B, respectively (p&lt;0.001). No difference in failure free survival rates was noted. For group A, ACE-27 was the only predicting factor for mortality at 90days [ACE-27 2–3 vs. 0–1: HR 15.86 (2.68–93.95), p=0.002], and the most important prognostic factors for overall survival included age, presenting stage and ACE-27 (p&lt;0.05). Elderly NPC patients had poorer tolerance to radiotherapy. Early deaths related to treatment were not uncommon. A reasonable disease control can still be attained after radical radiotherapy for those who were able to survive through the peri-radiotherapy period. Patient selection and treatment approach with reference to ACE-27 should be considered.</description><dc:title>Radical radiotherapy for nasopharyngeal carcinoma in elderly patients: The importance of co-morbidity assessment</dc:title><dc:creator>Henry C.K. Sze, W.T. Ng, Oscar S.H. Chan, Tracy C.Y. Shum, Lucy L.K. Chan, Anne W.M. Lee</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.019</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-19</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-19</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>162</prism:startingPage><prism:endingPage>167</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008074/abstract?rss=yes"><title>Role of larynx-preserving partial hypopharyngectomy with and without postoperative radiotherapy for squamous cell carcinoma of the hypopharynx</title><link>http://www.oraloncology.com/article/PIIS1368837511008074/abstract?rss=yes</link><description>Abstract: The purpose of this study was to examine the treatment outcomes of larynx-preserving partial hypopharyngectomies for hypopharyngeal carcinoma. Forty-three patients underwent partial hypopharyngectomy and reconstruction using faciocutaneous free flaps with and without postoperative radiotherapy between 1998 and 2009. Primary tumor sites were pyriform sinus in 35 and posterior pharyngeal wall in 8 patients. Thirty patients received postoperative radiotherapy. The 5-year overall and disease-specific survival rates were 63% and 67%, respectively. A significant positive correlation was found between pathologic N stage and primary site and disease-specific survival rates (N0/N1 stage; 93% vs. N2/N3 stage; 43%, p&lt;0.001 and pyriform sinus; 80% vs. posterior pharyngeal wall; 29%, p=0.012, respectively). Recurrences occurred in 15 (35%) patients. Among them, two patients were successfully rescued. Primary partial hypopharyngectomy with laryngeal preservation can be achieved with favorable oncologic outcomes. Factors that affected prognosis were advanced stage neck disease and posterior pharyngeal wall carcinoma.</description><dc:title>Role of larynx-preserving partial hypopharyngectomy with and without postoperative radiotherapy for squamous cell carcinoma of the hypopharynx</dc:title><dc:creator>Young-Hoon Joo, Kwang-Jae Cho, Jun-Ook Park, In-Chul Nam, Min-Sik Kim</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.018</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-19</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-19</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>168</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008219/abstract?rss=yes"><title>Impact of elective neck dissection on regional recurrence and survival in cN0 staged oral maxillary squamous cell carcinoma</title><link>http://www.oraloncology.com/article/PIIS1368837511008219/abstract?rss=yes</link><description>Summary: To evaluate the impact of elective neck dissection (END) on regional recurrence and survival in cN0 staged patients with maxillary squamous cell carcinoma (SCC).Eighty-six patients with maxillary SCC and clinically staged N0 cervical lymph-nodes were evaluated in this single center retrospective study.Seventy-four of 86 patients were included in this analysis, of which 36 patients were treated with END, 38 without END. Following END, pathohistologically verified regional lymph-nodes in the initially cN0 neck were found in three (8%) patients. In both the +END and non-END group regional recurrences occurred exclusively in patients with T4 primaries. The overall regional recurrence rate was 17% in the +END and 18% in the non-END group, respectively. The 5-year overall survival rate for all tumor stages combined (T1–T4) was 86% in the +END group and 82% in the −END group. Within the patients groups with T4 tumors, 5-year overall survival was 81% for the +END group and 56% for the −END group.Over all tumor stages combined (T1–T4), END did not significantly improve overall survival rates and did not prevent the rate of regional recurrence in cN0 staged patients with maxillary alveolar, gingival and palatal SCC. However, in the subgroup of patients with locally advanced T4 tumors, their seemed to be a clear tendency towards improvement of overall survival in the END group. END can therefore be recommended for these patients.</description><dc:title>Impact of elective neck dissection on regional recurrence and survival in cN0 staged oral maxillary squamous cell carcinoma</dc:title><dc:creator>Paul W. Poeschl, Rudolf Seemann, Cornelia Czembirek, Guenter Russmueller, Irene Sulzbacher, Edgar Selzer, Dzana Nuhic, Rolf Ewers</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.006</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>178</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008207/abstract?rss=yes"><title>Salivary gland carcinoma in Denmark 1990–2005: Outcome and prognostic factors: Results of the Danish Head and Neck Cancer Group (DAHANCA)</title><link>http://www.oraloncology.com/article/PIIS1368837511008207/abstract?rss=yes</link><description>Summary: To describe outcome and prognostic factors in a national Danish series of patients treated for salivary gland carcinoma. From three Danish nation-wide registries and supplementary patient records, 871 patients diagnosed with primary major or minor salivary gland carcinoma in the period from 1990 to 2005 were identified. A total of 796 (91%) histological specimens were revised according to the WHO 2005 classification. The median follow-up time was 78months. Three hundred and thirty-four patients (38%) experienced recurrence. Crude survival, disease-specific survival and recurrence-free survival after 5 and 10years were 66%, 76%, 64% and 51%, 69%, 58%, respectively. In multivariate analysis age, latency, stage, microscopic margins, vascular invasion and histological grade were all independent prognostic factors with regards to crude and disease-specific survival. Stage, microscopic margins, vascular invasion and histological grade were independent prognostic factors for recurrence-free survival. Age over 61years, latency under 8months, stage 3+4 disease, involved or close microscopic margins, vascular invasion and high histological grade are all independent prognostic factors with a negative impact on survival in salivary gland carcinoma patients. This knowledge can be helpful in guiding clinicians in daily work and choice of treatment across the large variety of salivary gland carcinoma subtypes.</description><dc:title>Salivary gland carcinoma in Denmark 1990–2005: Outcome and prognostic factors: Results of the Danish Head and Neck Cancer Group (DAHANCA)</dc:title><dc:creator>Kristine Bjørndal, Annelise Krogdahl, Marianne Hamilton Therkildsen, Jens Overgaard, Jørgen Johansen, Claus A. Kristensen, Preben Homøe, Christian Hjort Sørensen, Elo Andersen, Troels Bundgaard, Hanne Primdahl, Karin Lambertsen, Lisbeth Juhler Andersen, Christian Godballe</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.005</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-04</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-04</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>179</prism:startingPage><prism:endingPage>185</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS136883751100827X/abstract?rss=yes"><title>Impact of smoking status on clinical outcome in oral cavity cancer patients</title><link>http://www.oraloncology.com/article/PIIS136883751100827X/abstract?rss=yes</link><description>Summary: The association between smoking status and survival in oral cavity squamous cell carcinoma (OSCC) patients remains unclear. Therefore, we evaluated the association between smoking status before treatment and clinical outcome in OSCC patients. We conducted a retrospective cohort study of 222 OSCC patients who were treated at Aichi Cancer Center in Japan. Of these, 82 patients (36.9%) were non-smokers, 65 (29.3%) were light smokers (pack-years smoking (PY) &lt;30), 54 (24.3%) were moderate smokers (30⩽PY&lt;60), and 21 (9.5%) were heavy smokers (60⩽PY). The survival impact of pre-treatment smoking status was evaluated using multivariate proportional hazard models. Five-year overall survival for non-, light, moderate, and heavy smokers was 72.9% (95% confidence interval CI): (61.4–81.5), 85.5% (74.0–92.2), 59.9% (44.3–72.4) and 69.0% (42.8–85.0). Adjusted hazard ratios (HRs) for moderate and heavy smokers in comparison with light smokers were 2.44 (1.07–5.57, P=0.034) and 2.66 (0.97–7.33, P=0.058) and the dose–response relationship among smokers was statistically significance (Ptrend=0.024). In addition, adjusted HR for non-smokers relative to light smokers was 2.27 (0.84–6.15, P=0.108). We observed a suggestive heterogeneity in the impact of smoking status by treatment method (P for heterogeneity=0.069). Effect of smoking was evident only among the chemoradiotherapy or radiotherapy group. In this study, we found the significant positive dose–response relationship among smokers on clinical outcome in OSCC patients and that non-smokers were worse prognosis than light smokers. In addition, this effect might differ by treatment method.</description><dc:title>Impact of smoking status on clinical outcome in oral cavity cancer patients</dc:title><dc:creator>Daisuke Kawakita, Satoyo Hosono, Hidemi Ito, Isao Oze, Miki Watanabe, Nobuhiro Hanai, Yasuhisa Hasegawa, Kazuo Tajima, Shingo Murakami, Hideo Tanaka, Keitaro Matsuo</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.012</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-13</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-13</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>186</prism:startingPage><prism:endingPage>191</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511007433/abstract?rss=yes"><title>Ameloblastomas have already been treated successfully with intralesional chemotherapy in dogs, why not in humans?</title><link>http://www.oraloncology.com/article/PIIS1368837511007433/abstract?rss=yes</link><description>In 2010, Kelly et al. reported treating six dogs with acanthomatous ameloblastoma using weekly or bimonthly intralesional or perilesional injections of bleomycin; all exhibited complete remission within 4months of the commencement of treatment. A seventh dog, with a non-resectable tumor, received palliative treatment with bleomycin. The dogs exhibited no apparent systemic toxicity to the drug; local side effects included exposure of bone, swelling and infection, all of which were readily managed. Kelly et al. based their investigation on that of Yoshida et al. who, in 1998, reported treating four dogs successfully with intralesional bleomycin. While, as yet, only 11 dogs have been reported as having been treated in this manner, the results are impressive. Would this therapy work in humans?</description><dc:title>Ameloblastomas have already been treated successfully with intralesional chemotherapy in dogs, why not in humans?</dc:title><dc:creator>David G. Gardner, Emeritus</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.07.007</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-08-08</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-08-08</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Letters to the Editor - E-only</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e1</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511007718/abstract?rss=yes"><title>A case report of bevacizumab-related osteonecrosis of the jaw: Old problem, new culprit</title><link>http://www.oraloncology.com/article/PIIS1368837511007718/abstract?rss=yes</link><description>Osteonecrosis of the jaw (ONJ) is well-characterized syndrome predominantly reported in advanced stage cancer patients who had used long term bisphosphonates to treat bone metastases. Rarely, ONJ has been reported in patients who have not used bisphosphonates. Here we present an extremely rare occurrence of ONJ that occurred in a patient who received bevacizumab containing chemotherapy without bisphosphonate therapy.</description><dc:title>A case report of bevacizumab-related osteonecrosis of the jaw: Old problem, new culprit</dc:title><dc:creator>Umut Dişel, Ali Ayberk Beşen, Özgür Özyılkan, Efsun Er, Tuba Canpolat</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.07.030</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-08-24</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-08-24</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Letters to the Editor - E-only</prism:section><prism:startingPage>e2</prism:startingPage><prism:endingPage>e3</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008025/abstract?rss=yes"><title>Complex cannibalism: An unusual finding in oral squamous cell carcinoma</title><link>http://www.oraloncology.com/article/PIIS1368837511008025/abstract?rss=yes</link><description>Cellular cannibalism, defined as a large cell enclosing a slightly smaller one within its cytoplasm is a characteristic morphologic feature exclusively seen in aggressive malignancies. It was first described by Leyden in 1904 and he called them ‘‘bird-eye cells’’. They were also called as ‘‘signet-ring cells”, owing to their appearance. This phenomenon of “tumor cell within a tumor cell” is frequently seen in vivo in different types of cancers; it has, for instance, been referred to as “cellular phagocytosis”, “cell phagocytosis”, “cell in cell appearance”, “cell in cell pattern”, “one cell delicately wrapped around the next”, “phagocytosis of tumor cell by tumor cell”, and “tumor cell embraced by another tumor cell”. The fact, although often ignored, that “cannibalism” is commonly observed in vivo suggests that this phenomenon may represent a general growth behavior of tumor cells.</description><dc:title>Complex cannibalism: An unusual finding in oral squamous cell carcinoma</dc:title><dc:creator>Gargi S. Sarode, Sachin C. Sarode, Swarada Karmarkar</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.08.013</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-09-22</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-09-22</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Letters to the Editor - E-only</prism:section><prism:startingPage>e4</prism:startingPage><prism:endingPage>e6</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008244/abstract?rss=yes"><title>Oncocytic mucoepidermoid carcinoma with prominent tumour-associated lymphoid proliferation of the submandibular gland</title><link>http://www.oraloncology.com/article/PIIS1368837511008244/abstract?rss=yes</link><description>We report a peculiar oncocytic mucoepidermoid carcinoma (OMEC) with the unusually prominent lymphoplasmacytic component occurring in the submandibular gland.   A 70-year-old male patient presented with a painless mass in the right submandibular region. Magnetic resonance imaging revealed a well-defined and heterogeneously enhancing mass that measured approximately 2.0cm in diameter in the right submandibular gland. A core-cut biopsy was performed, which allowed for a diagnosis of OMEC. The patient underwent total excision of the right submandibular gland. He recovered fully and was free of disease at the 19-month follow-up.</description><dc:title>Oncocytic mucoepidermoid carcinoma with prominent tumour-associated lymphoid proliferation of the submandibular gland</dc:title><dc:creator>Hongbiao Jing, Qingda Meng, Yanhong Tai</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.009</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Letters to the Editor - E-only</prism:section><prism:startingPage>e7</prism:startingPage><prism:endingPage>e8</prism:endingPage></item><item rdf:about="http://www.oraloncology.com/article/PIIS1368837511008268/abstract?rss=yes"><title>Tumor induced osteomalacia: A forgotten paraneoplastic syndrome?</title><link>http://www.oraloncology.com/article/PIIS1368837511008268/abstract?rss=yes</link><description>Paraneoplastic syndromes are disorders that accompany benign or malignant tumors but are not directly related either to mass effect or to invasiveness of the tumor (primary or metastatic), nor are they associated with side-effects of anti-cancer treatment. They instead represent either the endocrinologic, hematologic, dermatologic and neurologic manifestations of ectopic hormone production by a tumor, or the immunological responses to the tumor. Recently, Toro et al. Chapireau et al. and Feller et al. separately reviewed the paraneoplastic syndromes related to oral neoplasms including, among others, hypercalcaemia, hypercalcaemia–leukocytosis syndrome, syndrome of inappropriate antidiuretic hormone production, ectopic production of beta-human chorionic gonadotrophin, Bazex syndrome, Sweet syndrome, and pemphigus. Those comprehensive studies did not review osteomalacia induced by oral tumors. The purpose of this communication is to present a concise review of the literature regarding this entity to enhance the awareness of oral practitioners.</description><dc:title>Tumor induced osteomalacia: A forgotten paraneoplastic syndrome?</dc:title><dc:creator>Yehuda Zadik, Dorrit W. Nitzan</dc:creator><dc:identifier>10.1016/j.oraloncology.2011.09.011</dc:identifier><dc:source>Oral Oncology 48, 2 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Oral Oncology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>48</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1368-8375(11)X0015-5</prism:issueIdentifier><prism:section>Letters to the Editor - E-only</prism:section><prism:startingPage>e9</prism:startingPage><prism:endingPage>e10</prism:endingPage></item></rdf:RDF>
