Molar-Incisor Hypomineralisation: Severity, caries and hypersensitivity.

Objectives: To investigate distribution of affected teeth and severity of molar-incisor hypomineralisation (MIH) in 8-9-year-old children. A second aim was to study association between severity of MIH and hypersensitivity, caries, and affection of incisors and second primary molars (SPM).

Methods: A total of 3013 children in one age cohort participated in a cross-sectional study, of which 851 children were diagnosed with MIH.

Molar-incisor hypomineralisation in Norwegian children: Prevalence and associated factors.

This study investigated the prevalence and associations of molar-incisor hypomineralisation (MIH) in 8-9 year-old children in Oslo. A total of 3013 children in one age cohort participated in the study during their regular dental examination at the Public Dental Service. Hypomineralised enamel defects were recorded according to the European Academy of Paediatric Dentistry criteria for MIH.

Long-Term Effects of a Randomized Maternal Education Trial in Rural Uganda: Implications for Child Oral Health.

The aim was to examine oral health among 5-6-year-old children whose mothers participated in a 6 months' cluster-randomized education trial in rural Uganda starting when their children were 6-8 months old. The education focused on nutrition, oral hygiene, and child stimulation. In the current follow-up study, 357/511 (70%) children from the original trial were available for data collection (200 in the intervention and 157 in the control group).

p38 differentially regulates ERK, p21, and mitogenic signalling in two pancreatic carcinoma cell lines.

Whereas the p38 MAP kinase has largely been associated with anti-proliferative functions, several observations have indicated that it may also have positive effects on proliferation. In hepatocytes, we have found that p38 has opposing effects on DNA synthesis when activated by EGF and HGF. Here we have studied the function of p38 in EGF- and HGF-induced DNA synthesis in the two pancreatic carcinoma cell lines AsPC-1 and Panc-1.

Molar incisor malformation in six cases: description and diagnostic protocol.

Objective: The term molar-incisor malformation (MIM) has recently been presented in the scientific literature, where it is described as a condition with localized impaired root development. Here we present 6 recently discovered cases referred to our departments.

Study Design: The patients were enrolled in the study after referral and were examined clinically and radiologically.

HGF-induced DNA synthesis in hepatocytes is suppressed by p38.

Previous studies in rat hepatocytes have shown that the MEK/ERK, PI3K/Akt and p38 pathways are all involved in the activation of DNA synthesis by EGF and that sustained activation of MEK/ERK is required. Here, we show that although HGF stimulated DNA synthesis and activated signaling in the same manner as EGF, the contribution of the signaling pathways to the induction of DNA synthesis differed. While HGF-induced DNA synthesis was dependent on MEK/ERK, with no significant contribution from PI3K/Akt, p38 suppressed HGF-induced DNA synthesis.

The TGFβ-SMAD3 pathway inhibits IL-1α induced interactions between human pancreatic stellate cells and pancreatic carcinoma cells and restricts cancer cell migration.

Background: The most abundant cells in the extensive desmoplastic stroma of pancreatic adenocarcinomas are the pancreatic stellate cells, which interact with the carcinoma cells and strongly influence the progression of the cancer. Tumor stroma interactions induced by IL-1α/IL-1R1 signaling have been shown to be involved in pancreatic cancer cell migration. TGFβ and its receptors are overexpressed in pancreatic adenocarcinomas.

PI3K is required for both basal and LPA-induced DNA synthesis in oral carcinoma cells.

Background: The glycerophospholipid lysophosphatidic acid (LPA), which is present in most tissues and in high concentrations in saliva, may exert profound effects on oral cancer cells. We have investigated mitogenic signalling induced by LPA in the two oral carcinoma cell lines, D2 and E10, focusing on the role of EGFR transactivation and downstream pathways.

Methods: Two oral squamous carcinoma cell lines, D2 and E10, were analysed for effects of LPA on signalling pathways and induction of DNA synthesis.

Lysophosphatidic acid induces both EGFR-dependent and EGFR-independent effects on DNA synthesis and migration in pancreatic and colorectal carcinoma cells.

Lysophosphatidic acid (LPA) is a small glycerophospholipid ubiquitously present in tissues and plasma. It acts through receptors belonging to the G-protein-coupled receptor (GPCR) family, is involved in several biological processes, and is strongly implicated in different cancers. In this paper, we have investigated the effects of LPA on DNA synthesis and migration in a panel of pancreatic and colon cancer cells, with particular focus on the involvement of the epidermal growth factor (EGF) receptor (EGFR) in LPA-induced signaling.

Gab1 amplifies signaling in response to low-intensity stimulation by HGF.

The receptor tyrosine kinases EGFR and Met induce phosphorylation of the docking protein Gab1, and there is evidence that Gab1 may have a role in the signaling from these receptors. Studying hepatocytes, we previously found that although Gab1 mechanistically interacted in different ways with EGFR and Met, it was involved in mitogenic signaling induced by both EGF and HGF. It has been reported that in EGFR, Gab1 is required particularly at a low dose of EGF.

Role of LPAR3, PKC and EGFR in LPA-induced cell migration in oral squamous carcinoma cells.

Background: Oral squamous cell carcinoma is an aggressive neoplasm with serious morbidity and mortality, which typically spreads through local invasive growth. Lysophosphatidic acid (LPA) is involved in a number of biological processes, and may have a role in cancer cell migration and invasiveness. LPA is present in most tissues and can activate cells through six different LPA receptors (LPAR1-6).

Prognostic molecular markers in cancer - quo vadis?

Despite the tremendous number of studies of prognostic molecular markers in cancer, only a few such markers have entered clinical practise. The lack of clinical prognostic markers clearly reflects limitations in or an inappropriate approach to prognostic studies. This situation should be of great concern for the research community, clinicians and patients.

Migration induced by epidermal and hepatocyte growth factors in oral squamous carcinoma cells in vitro: role of MEK/ERK, p38 and PI-3 kinase/Akt.

Background: Cell migration is a necessary part of malignant invasiveness. Oral squamous cell carcinomas (OSCC) have a great tendency for local invasive growth. We have investigated signalling pathways involved in cell migration induced by epidermal growth factor (EGF) and hepatocyte growth factor (HGF) in OSCC cells and examined the effects of various experimental and clinically approved anti-tumour signal inhibitors on the migratory activity.

Nuclear and cytoplasmic expression of Met in oral squamous cell carcinoma and in an organotypic oral cancer model.

Met, the hepatocyte growth factor receptor, is important in transducing signals for tumour growth and metastasis. The aim of this study was to examine the pattern of Met expression and its value as a prognostic factor in oral squamous cell carcinomas (OSCCs). The material consisted of 53 OSCCs and five healthy controls from normal oral mucosa supplied with cell lines, 10 organotypic models supplied with oral cancer cells, and three organotypic models supplied with normal keratinocytes.

Induction of invasion in an organotypic oral cancer model by CoCl2, a hypoxia mimetic.

Invasion is a hallmark of malignancy. The aim of this study was to develop an in vitro model that can be used for experimental studies of cancer cell invasion. The organotypic oral cancer model was constructed by growing oral squamous cell carcinoma (OSCC) cells on a collagen matrix in which normal human fibroblasts were incorporated.