Heterotopic hip ossification resection: monocentric experiences of associated factors, outcomes, and complications.

PURPOSE: The exponential increase in total hip arthroplasty (THA) has led to acute and chronic surgery-related complications. Common chronic and local complications are represented by hip ossification (HO). The aim of our study was to assess the clinical and radiological correlates of patients undergoing surgical removal of heterotopic ossifications after THA and the possible association between HO and prosthetic joint infection. METHODS: Data of 26 patients who underwent surgical removal of periprosthetic calcifications after THA from 2000 to 2022 were analyzed and compared with characteristics of 156 subjects without HO. RESULTS: The preoperative radiographs of patients showed a high-grade Brooker, 3 or 4, later reduced to 1 or 2 in the postoperative radiographs. Ten (38.5%) patients underwent radiotherapy prophylaxis, administered as a single dose 24 h before surgery. In 19 (73%) patients, pharmacological prophylaxis with indomethacin was added in the 30 postoperative days. Only one patient who underwent radiotherapy had a recurrence, while new ossifications were found in three patients without prophylaxis (11.5%). Intraoperative cultures were performed for suspected periprosthetic infection in 8 study group patients. In logistic regression, the presence of HO was significantly and inversely associated with the ASA score (OR = 0.27, 95% CI = 0.09-0.82; P = 0.021) after adjusting. CONCLUSION: Surgical HO removal in symptomatic patients with high-grade disease produces good clinical and radiographic results. Radiotherapy was a good perioperative and preventive strategy for recurrence, also associated with NSAIDs and COX-2 inhibitors.

Data of postoperative complications related to fibrinogen-to-albumin ratio in pancreatic resections.

Pancreatic surgery is one of the surgeries burdened with the highest mortality and morbidity rate. This is due both to the aggressive biological nature of the pathology affecting the organ and to the technical difficulties associated with surgery. A further aspect on which research is focusing is represented by inflammation related to oncological pathology. Inflammation plays an important role in tumor progression, and growing evidence has confirmed that the fibrinogen-to-albumin ratio (FAR) is an important prognostic factor for overall survival (OS) in malignant tumors. Inflammatory markers had demonstrated also a role in the prediction of postoperative complication after pancreatic surgery. We speculate that FAR, as an easily available, cost-effective, and non-invasive prognostic indicator for pancreatic cancer patients, could help to identify patients at increased risk of postoperative pancreatic fistula (POPF). We therefore retrospectively analyzed the data relating to 117 pancreatic resections relating direct and indirect markers of inflammation with the incidence of post-operative complications.

Topographic lymph node staging system shows prognostic superiority compared to the 8th edition of AJCC TNM in gastric cancer. A western monocentric experience.

INTRODUCTION: The current Tumor Node Metastasis staging system (TNM) for gastric cancer classifies the extent of lymph node metastasis based upon the number of lymph nodes involved. Choi et al. have recently proposed a new anatomical classification based upon the regionality of the involved nodes. This new classification seems to have a better predictive prognostic value than the traditional one. We investigated the prognostic role of the new anatomical based classification, reviewing our institutional gastric cancer database. METHODS: We performed a retrospective chart review of 329 patients who underwent gastrectomy at our Institution from 2003 to 2017. We excluded from data analysis any patient with distant metastases at the time of first diagnosis and or surgery, pathology other than adenocarcinoma, lymphadenectomy less than D2, impossibility to identify location of lymph nodes (LNs) on pathological report and neoadjuvant chemotherapy. The extent of D2 lymphadenectomy was defined according to Japanese Gastric Cancer Association criteria. LN metastasis were reclassified into three topographic groups (lesser, greater curvature, and extraperigastric nodes) and staged according to Choi. The new N stage was combined with the current pT according to the 8th edition of TNM and a new hybrid TNM stage was established. All patients were followed up until June 2019. The prognostic performance of the new stage and of the current anatomical numeric based system (TNM) was analyzed and assessed by the C-index, AIC and likelihood ratio χ2 value. RESULTS: In predicting both Overall Survival (OS) and Disease free Survival (DFS) the new N stage and the new TNM staging system had the highest C-index and likelihood ratio χ2 value and the lowest Akaike Information Criterion (AIC), showing a better accuracy and displaying a better prognostic performance. CONCLUSIONS: Our study is the first from the Western world to compare the new hybrid classification, based on the anatomical location of metastatic nodes, to the 8th of American Joint Committee on Cancer (AJCC) TNM staging system. Our findings on a small, monocentric sample suggest that hybrid topographic lymph node staging system is more accurate than TNM.

The Von Willebrand Factor Antigen Plasma Concentration: a Monitoring Marker in the Treatment of Aortic and Mitral Valve Diseases.

Von Willebrand disease is a commonly inherited bleeding disorder caused by defects of von Willebrand factor (vWF). In the most common valve diseases, aortic valve stenosis (AVS) and mitral valve regurgitation (MVR), a bleeding tendency has been described in a number of patients. This has been associated to a high turbulence of blood flow through the compromised valve, promoting degradation of vWF with loss of high-molecular-weight multimers of vWF (HMWM), leading to an acquired von Willebrand syndrome (AvWS). We analysed three groups of patients, one affected by AVS, treated with transcatheter aortic valve implantation (TAVI), the second group of patients affected by MVR, treated with Mitraclip® mitral valve repair. The third group was represented by patients also affected by AVS, but not eligible for TAVI and treated with standard surgery. A fourth group of patients that underwent percutaneous coronary intervention (PCI) with stenting was used as a control. Our results demonstrated that the level of vWF measured as antigen concentration (vWF:Ag) increases in all cohorts of patients after treatment, while in control PCI patients, no modification of vWF:Ag has been registered. Western blot analysis showed only a quantitative loss of vWF in the pre-treatment time, but without significant HMWM modification. The monitoring of the vWF:Ag concentration, but not the quality of HMWM, can indicate the status of blood flow in the treated patients, thus introducing the possibility of using the vWF antigen detection in monitoring the status of replaced or repaired valves.

Effect of GLP-1 and GIP on C-peptide secretion after glucagon or mixed meal tests: Significance in assessing B-cell function in diabetes.

BACKGROUND: The aim of the study was to investigate the different B-cell responses after a glucagon stimulation test (GST) versus mixed meal tolerance test (MMTT). METHODS: We conducted GST and MMTT in 10 healthy people (aged 25-40 years) and measured C-peptide, gastric inhibitory peptide (GIP) and glucagon-like peptide-1 (GLP-1) at different time points after the administration of 1 mg i.v. glucagon for GST or a liquid mixed meal for MMTT. RESULTS: The GST stimulated C-peptide showed a mean increase of 147.1%, whereas the mean increase of MMTT stimulated C-peptide was 99.82% (Δincrease = 47.2%). Maximum C-peptide level reached with the MMTT was greater than that obtained with the GST (C-pept max MMTT = 2.35 nmol/L vs C-pep max GST = 1.9 nmol/L). A positive and linear correlation was found between the GST incremental area under the curve C-peptide and the MMTT incremental area under the curve C-peptide (r = 0.618, P = .05). After GST, there was no increment of GIP and glucagon like peptide-1 levels compared to baseline levels. A positive and linear correlation between GIP and C-peptide levels was observed only for the MMTT (r = 0.922, P = .008) indicating that in the GST, the C-peptide response is independent of the incretin axis response. CONCLUSIONS: Although the 2 stimulation tests may elicit a similar response in C-peptide secretion, B-cell response to MMTT depends on a functionally normal incretin axis. These results may have implications when investigating the B-cell response in people with diabetes and for studies in which stimulated C-peptide secretion is used as primary or secondary outcome for response to therapy.

Procalcitonin as diagnostic marker of infection in solid tumors patients with fever.

In oncologic patients fever is a non-specific clinical marker of different clinical settings. Procalcitonin (PCT) seems to be the most promising infection marker. We aimed to define the potential role of PCT as an earlier diagnostic marker in patients with fever and solid tumor. This retrospective study enrolled 431 patients. All of them performed hemoculture (HE) and basal PCT assessment (reference laboratory cut-off: ≤0.5 or >0.5 ng/dL) before starting antibiotic therapy. Gram positive (G+), negative (G-) or Fungi infection were detected. A statistically significant difference in PCT levels between patients with positive and negative HE was observed (P < 0.0001). Moreover comparing PCT values in patients with positive and negative HE, we obtain in the positive HE subpopulation an AUC of 0.7 and a cut-off of 1.52 ng/dL reached high sensitivity (61.6%) and specificity (70.1%). Using this last cut-off, instead of the normal reference value, we achieve a risk reduction to overestimate an infection status of 23.4%. We support the clinic usefulness of serum PCT dosage in febrile advanced solid tumor patients. A PCT cut-off of 1.52 ng/dL could be helpful in the management of the antibiotic therapy preventing delays of oncologic treatments.

Epigenetic modifications of Dexras 1 along the nNOS pathway in an animal model of multiple sclerosis.

The development of multiple sclerosis, a major neurodegenerative disease, is due to both genetic and environmental factors that might trigger aberrant epigenetic changes of the genome. In this study, we analysed global DNA methylation in the brain of mice upon induction of experimental autoimmune encephalomyelitis (EAE), and the effect of environmental enrichment (EE). We demonstrate that global DNA methylation decreased in the striatum, but not in the cortex, of EAE mice compared to healthy controls, in particular in neuronal nitric oxide synthase (nNOS)-positive interneurons of this brain area. Also, in the striatum but again not in the cortex, decreased DNA methylation of the nNOS downstream effector, dexamethasone-induced Ras protein 1 (Dexras 1), was observed in EAE mice, and was paralleled by an increase in its mRNA. Interestingly, EE was able to revert EAE effects on mRNA expression and DNA methylation levels of Dexras 1 and reduced gene expression of nNOS and 5-lipoxygenase (Alox5). Conversely, interleukin-1ß (IL-1ß) gene expression was found up-regulated in EAE mice compared to controls and was not affected by EE. Taken together, these data demonstrate an unprecedented epigenetic modulation of nNOS-signaling in the pathogenesis of multiple sclerosis, and show that EE can specifically revert EAE effects on Dexras 1 along this pathway.

Activation of beta-catenin signalling increases StarD7 gene expression in JEG-3 cells.

StarD7 gene encodes a protein that belongs to the StAR-related lipid transfer proteins involved in intracellular transport and metabolism of lipids. It has been previously documented that StarD7 has a wide-spread mRNA expression in trophoblastic tissues and several tumour cell lines with highest levels in both choriocarcinoma JEG-3 and JAR cells, hepatocellular carcinoma HepG2, and colorectal adenocarcinoma HT-29 cells. To understand the molecular mechanisms that regulate the expression of the human StarD7 gene, we have cloned and characterized the 5'-flanking region of the gene. Transient transfections of several 5'deleted StarD7-promoter-firefly luciferase constructs into JEG-3 cells indicated that the -312/+157 region contains the gene minimal promoter. In addition, sequence analysis of a 1.6kb gene fragment revealed the presence of a TATA-less promoter as well as multiple regulatory motifs, including one regulatory element corresponding to the T-cell factor 4 (TCF4) binding site. Inhibition of glycogen synthase kinase-3beta (GSK3beta), a component of Wnt/beta-catenin signalling, increased both StarD7 mRNA and protein expression as well as its promoter activity. Co-transfection experiments in JEG-3 cell line revealed that the StarD7 promoter is activated by TCF4 transcription factor and by its beta-catenin coactivator. Moreover, site-directed mutagenesis of the TCF4 site located -614/-608bp relative to the transcription start site markedly diminished StarD7 promoter activity. Chromatin immunoprecipitation analysis demonstrated that beta-catenin and TCF4 are bound in vivo to the StarD7 gene promoter in JEG-3 cells treated with lithium chloride. Collectively, these studies show that beta-catenin and TCF4 activate the human StarD7 gene interacting with its promoter region through Wnt/beta-catenin signalling.

Toll-like receptor 4 Asp299Gly and Thr399Ile polymorphisms in gastric cancer of intestinal and diffuse histotypes.

In the present study we investigated the potential role of Toll-like receptor 4 (TLR-4) Asp299Gly and Thr399Ile polymorphisms as risk factors in the development of gastric cancer. TLR-4 Asp299Gly and Thr399Ile polymorphisms were investigated in 171 Italian patients with sporadic gastric cancer and in 151 controls. Unconditional regression (odds ratio and 95% confidence intervals) were used to investigate the association of the studied polymorphisms with gastric cancer. TLR-4 Thr399Ile polymorphism is linked with an increased susceptibility to gastric cancer (P = 0.023 and hazard ratio = 3.62). No significant association for TLR-4 Asp299Gly polymorphism was found. In the subgroup of patients with intestinal-type gastric cancer, a significant risk of gastric cancer was associated with TLR-4 Thr399Ile genotype (P = 0.006). Our results demonstrated that TLR-4 Thr399Ile polymorphism is linked with an increased susceptibility to gastric cancer. An increased risk for intestinal gastric cancer in carriers of the TLR4 Thr399Ile allele was observed. Future epidemiological studies should consider the possible interactions between proinflammatory genotypes (such as TLR and interleukin-1R polymorphisms) and other risk factors for cancer such as dietary habits and/or exposure to environmental carcinogens.

Expression and localization of StarD7 in trophoblast cells.

The StAR-related lipid transfer (START) domain is defined as a motif of around 200 amino acids implicated in lipid/sterol binding. In a previous study, we identified the StarD7 transcript encoding one of the 15 family members with START domain present in the human genome. This transcript was found to be overexpressed in choriocarcinoma JEG-3 cells. In addition, we demonstrated that the recombinant StarD7 protein forms stable Gibbs and Langmuir monolayers at the air-buffer interface, showing marked surface activity and interaction with phospholipid monolayers, mainly with phosphatidylserine, cholesterol and phosphatidylglycerol. This study was undertaken to evaluate the expression and localization of StarD7 protein in trophoblastic samples. Here, we show for the first time the presence of StarD7 protein in human trophoblast cells. Western blot assays revealed a unique specific 34 kDa protein in JEG-3 cell line, choriocarcinoma tissue, complete hydatidiform mole, early and normal term placenta. Immunohistochemical data from early and normal term placentas and complete hydatidiform moles showed that this protein is abundant in the syncytiotrophoblasts, mainly at the apical side of the syncytium, with a weak and focal reaction in the cytotrophoblast cells. Furthermore, an increased StarD7 mRNA and protein expression, as well as a change in its sub-cellular localization was observed in in vitro differentiating cytotrophoblast isolated from normal term placenta. Taken together, these findings support and allow future studies to explore the possibility that StarD7 protein mediates transplacental lipid transport and/or is involved in syncytialization.

Rhabdomyolysis due to severe hypokaliemia in a Crohn's disease patient after budesonide treatment.

Patients with Crohn's disease may experience several non-digestive complications, including muscle disorders. Rabdomyolysis has rarely been reported in patients with inflammatory bowel disease, however a number of factors may cause muscular damage in this setting. We report the case of a young woman with Crohn's disease who developed a severe, symptomatic skeletal muscle damage associated with severe hypokaliemia. Reversal of the potassium levels to normal ranges led to clinical resolution. The possible causes that might have lead to hypokalemia development and subsequent rhabdomyolysis are discussed with special emphasis for the potential causative role of medical treatment, especially budesonide for which similar side effects have been previously reported. Physicians should be aware that hypokalemia is possible in the setting of Crohn's disease and muscle damage can present as a complication.

Cell cycle alterations and lung cancer.

It is now widely accepted that human carcinogenesis is a multi-step process and phenotypic changes during cancer progression reflect the sequential accumulation of genetic alterations in cells. The recent progress of scientific research has notably increased knowledge about biological events involved in lung cancer pathogenesis and progression, thanks to the use of molecular biology and immunohistochemistry techniques. Lots of the genetic alteration found in small cells lung cancer (SCLC) and in not small cells lung cancer (NSCLC) concern the expression of cell cycle genes, actually recognized as onco-suppressor genes and the lack of equilibrium between oncogenes and oncosuppressor genes. The present review of literature widely describes the cell cycle control, the lung cancer molecular pathogenesis, the catalog of known genetic alterations and the recent advances in global expression profiles in lung tumors, on the basis of the various hystological types too. Such data suggest the potential use of this knowledges in clinical practice both as prognostic factors and innovative therapeutic possibilities and they impose the necessity of new studies about cell cycle control and lung carcinogenesis.

Does an 'autoimmune' profile affect the clinical profile of chronic hepatitis C? An Italian multicentre survey.

Nonorgan-specific autoantibodies (NOSA) are common in patients with chronic hepatitis C virus infection. It is unclear whether serological markers of autoimmunity segregate in a cohort of cases with more severe liver damage. We assessed the relationship between NOSA and demographic, biochemical and histological features in 502 subjects with anti-HCV positive, HCV-RNA positive, HBsAg negative chronic hepatitis consecutively referred to four Italian liver units. Percutaneous liver biopsy was performed in all subjects. A single pathologist scored the biopsies using histology activity index classification. The overall prevalence of positivity for any NOSA was 36.9%. Antinuclear antibodies, anti-smooth muscle antibodies, and anti-liver/kidney microsomal antibodies were found in 15.7, 27.3 and 2.2% of cases. Multivariate analysis showed that gamma-globulin >2 g/dL was the only independent predictor of the likelihood of NOSA positivity (OR, 2.1; 95% CI, 1.3-3.4). No other clinical (age, gender, ALT, HCV genotype) or histological features (grading and staging score, bile ductular damage) were linked to NOSA. Antiviral therapy in 155 subjects with NOSA did not cause any adverse events related to autoimmunity during and after treatment. The presence of NOSA in patients with chronic HCV hepatitis is not related to specific demographic features and has no impact on the biochemical and histological profile of the liver disease at presentation and the response to antiviral treatment.

Utility of combined use of plasma levels of chromogranin A and pancreatic polypeptide in the diagnosis of gastrointestinal and pancreatic endocrine tumors.

BACKGROUND: Chromogranin A (CgA) is considered the most accurate marker in the diagnosis of gastro-entero-pancreatic (GEP) endocrine tumors. Pancreatic polypeptide (PP) has also been proposed to play this role, but then not used due to its low sensitivity. The aim of the present study was to determine whether the assessment of PP would improve the diagnostic reliability of CgA in patients with GEP tumors. PATIENTS AND METHODS: Both markers were assessed in 68 patients [28 functioning (F), 40 non functioning (NF)]. Twenty-seven patients disease-free (DF) after surgery, and 24 with non-endocrine tumors (non-ETs) were used as control groups. RESULTS: CgA sensitivity was: 96% in F, 75% in NF, 74% in pancreatic, and 91% in gastrointestinal (GI) tumors. Specificity was 89% vs DF, and 63% vs non-ETs. PP sensitivity was: 54% in F, 57% in NF, 63% in pancreatic, and 53% in GI tumors. Specificity was 81% vs DF, and 67% vs non-ETs. By combining the two markers a significant gain in sensitivity vs CgA alone was obtained: overall in GEP tumors (96% vs 84%, p = 0.04), in NF (95% vs 75%, p = 0.02), and in pancreatic (94% vs 74%, p = 0.04). More specifically, a 25% gain of sensitivity was obtained in the subgroup of NF pancreatic tumors (93% vs 68%, p = 0.04). CONCLUSION: The combined assessment of PP and CgA leads to a significant increase in sensitivity in the diagnosis of GEP tumors, particularly in pancreatic NF.

GTT1/StarD7, a novel phosphatidylcholine transfer protein-like highly expressed in gestational trophoblastic tumour: cloning and characterization.

We report the cDNA cloning and characterization of GTT1/StarD7, a novel gestational trophoblastic tumour gene, initially identified by its up-regulated expression in the choriocarcinoma JEG-3 cell line with respect to their nonmalignant counterpart, complete hydatidiform mole and normal trophoblastic tissue. Using the differential display fragment as a probe we screened placenta and HeLa cDNA libraries and isolated a clone carrying a 3315 bp insert (accession number AF270647). This cDNA encodes a protein of 295 amino acid residues with a molecular weight of approximately 34.7 kDa and a pI of 5.79. Computer-mediated homology search revealed that the deduced amino acid sequence had similarity to phosphatidylcholine transfer protein (PCTP) with a conserved StAR-related lipid transfer (START) domain extending between the amino acids 66 to 250. The GTT1 gene contains at least 9 exons spread nearly 30 kb on chromosome 2p12-2p11.2. Northern blot assays of total RNA derived from normal early placenta (NEP), complete hydatidiform mole (CHM) and JEG-3 cell line revealed a 3.5 kb mRNA expressed exclusively in the JEG-3 cell line. However, semiquantitative RT-PCR analysis performed with the same RNA samples demonstrated GTT1 expression throughout all of them with the highest level in JEG-3 cell line. Examination of GTT1 mRNA expression by semiquantitative RT-PCR assays in a series of tumour cell lines indicated wide-spread GTT1 expression with predominance in both choriocarcinoma JEG-3 and JAR cells, colorectal adenocarcinoma HT29 and hepatocellular carcinoma HepG2 cells. In conclusion, the highly GTT1 expression profile in JEG-3 and JAR cell lines and its lipid binding domain suggest that GTT1 may play an important role in the phospholipid-mediated signalling of trophoblastic tumour cellular events.

Bad to the bone: the effects of liver diseases on bone.

Metabolic bone disease (MBD) is a relevant complication of long-standing liver disease. It has been described in association with most types of chronic liver disease both cholestatic and non-cholestatic. It can significantly affect morbidity, and quality of life of these patients. Fractures are also associated with an excess mortality. Recently, the issue of MBD in liver disease has been considered to be such an hot topic to be the subject of 2 recent review/guideline articles produced by the British Society of Gastroenterology and the American Gastroenterological Association. Aim of this paper is to summarize some practical issues regarding this topic and to provide a rapid overview of the main pathophysiological and pharmacological aspects.

A third-line levofloxacin-based rescue therapy for Helicobacter pylori eradication.

BACKGROUND: Helicobacter pylori infection persists in a considerable proportion of patients after both first- and second-line current treatments. A standard therapy for re-treatment in such refractory patients is still lacking. This study aimed to evaluate the efficacy of a levofloxacin-amoxycillin combination in patients who previously failed two or more therapeutic attempts. PATIENTS AND METHODS: Consecutive patients with persistent Helicobacter pylori infection were enrolled. Bacterial infection was assessed by rapid urease test and histology on gastric biopsies at endoscopy. Patients were assigned to receive a 10-day triple therapy, comprising rabeprazole 20 mg b.d., levofloxacin 250 mg b.d., and amoxycillin 1 g b.d. Four to 6 weeks after therapy, Helicobacter pylori eradication was assessed by a further endoscopy or 13C urea breath test. RESULTS: Overall, 36 patients were enrolled, but two patients were lost to follow-up. Helicobacter pylori was successfully cured in 30 patients, giving an 83.3% (95% CI=71.2-95.5) and 88.2% (95% CI=77.4-99) eradication rate at intention-to-treat and per protocol analysis, respectively. Compliance was good in all but two patients, who discontinued the treatment at 8 and 6 days, respectively, on account of glossitis. No major side-effects were reported, whilst 7 (20.1%) patients complained of mild side-effects. CONCLUSIONS: This study demonstrates that a 10-day levofloxacin-amoxycillin triple therapy is a safe and successful third-line therapeutic approach for Helicobacter pylori eradication.

Staging of digestive endocrine tumours using helical computed tomography and somatostatin receptor scintigraphy.

BACKGROUND: In patients with digestive endocrine tumours, complete pre-operative staging is essential in planning proper management and evaluating treatment efficacy. To date, somatostatin receptor scintigraphy (SRS) is considered the 'gold standard' imaging procedure, and very few data are available concerning the use of helical computed tomography (hCT). This study aimed to determine the diagnostic accuracy and the ability to modify the surgical management of hCT, alone or combined with SRS. PATIENTS AND METHODS: Sixty patients were staged before surgery by hCT, SRS and tumour markers, and included in group 1 if suitable for radical surgery, otherwise in group 2. All patients underwent laparotomy followed by subsequent re-staging. RESULTS: SRS sensitivity was 77%, 48% and 67% for primary, lymph-node and liver lesions, respectively. hCT sensitivity was 94%, 69% and 94% for primary, lymph-node and liver lesions, respectively (P = 0.02 versus SRS, for liver lesions). During pre-operative evaluation, hCT correctly staged 92% and SRS 75% of patients (P = 0.02). hCT provided additional information in 17% of patients. CONCLUSIONS: Since hCT has been shown to be extremely accurate, providing essential information for the planning of surgical treatment compared with that of SRS, both techniques should be used in the pre-operative work-up of digestive endocrine tumours.

Identification of multiple differentially expressed messenger RNAs in normal and pathological trophoblast.

In an attempt to assess the molecular basis of phenotypic alterations present in the gestational trophoblastic diseases (GTDs) and to identify genes whose expression is specifically associated to these placental proliferative disorders we performed differential display techniques. Initially 19 candidate gene fragments were identified and differential expression was confirmed in eight of these fragments by Northern blot analysis. At the mRNA level ribosomal L26 (rL26), ribosomal L27 (rL27), a new Krüppel type zinc finger protein and TIS11d were preferentially expressed in normal early placenta (NEP) relative to complete hydatidiform mole (CHM), persistent gestational trophoblastic disease (PGTD) and choriocarcinoma JEG-3 cell line. In contrast, heterogeneous ribonucleoprotein A1 (hnRNPA1), the ferritin light chain mRNA, and the uncharacterized protein KIAA0992 were predominantly expressed in JEG-3 cell line. Finally, decorin, a prototype member of an expanding family of small leucine-rich proteoglycans, showed high expression in CHM. In addition we demonstrated by immunohistochemistry analysis that increased decorin mRNA in CHM reflected a genuine augmentation in average steady state mRNA levels within cells. Taken together, these findings provide several interesting candidates for regulation of tumorigenic expression as well as early placentation development, including those involved in protein synthesis (rL26 and rL27), metabolism (ferritin light chain), intercellular communication (decorin) and regulation of gene expression (Krüppel-like zinc finger, TIS11d and hnRNPA1). Information about such alterations in gene expression could be useful for elucidating the genetic events associated to gestational trophoblastic pathogenesis, developing new diagnostic markers, or determining novel therapeutic targets.