Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MALT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Molecular analysis of mucosa-associated lymphoid tissue (MALT) lymphoma of ocular adnexa.

Lymphomas of mucosa-associated lymphoid tissue (MALT) are a distinct subgroup of extranodal B-cell non-Hodgkin's lymphomas. Most studies have failed to demonstrate the clonal rearrangement of BCL-1, BCL-2 or c-MYC genes for MALT lymphomas. Further, alteration of the p53 gene is rarely demonstrated in low-grade MALT lymphomas, but can be detected in high-grade disease. Lymphomas of the ocular adnexa represent approximately eight percent of all extranodal lymphomas, most of which are MALT lymphomas, but few studies had explored the alterations of BCL-1, BCL-2, c-MYC and p53 genes specifically for ocular MALT lymphomas. We investigated the changes to BCL-1, BCL-2, c-MYC and p53 genes in these lymphomas for Taiwanese patients. Clonal rearrangement for immunoglobulin heavy-chain (IgH), BCL-1, BCL-2, c-MYC and p53 genes was examined for 16 cases of ocular MALT lymphoma. Restriction-length polymorphism and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) of the DNA, corresponding to exons 5 through 9, followed by DNA sequencing, were utilized to analyze the possible mutations of the p53 gene for these tumors. Thirteen of the cases revealed rearranged IgH genes using Southern blotting or PCR. No rearrangement of BCL-1, BCL-2, c-MYC or p53 genes was discovered, with point mutation of the p53 gene in one case. As for other types of MALT lymphomas, BCL-1, BCL-2 and c-MYC genes are not implicated in the pathogenesis of the ocular sub-group. Although alteration of the p53 gene is rare for low-grade ocular MALT lymphoma, its role in disease progression merits further research.

Adolescent↗

CD5 expression in a lymphoma of the mucosa-associated lymphoid tissue (MALT)-type as a marker for early dissemination and aggressive clinical behaviour.

Mucosa associated lymphoid tissue (MALT) developing in response to chronic infection or autoimmune stimuli has been recognized as a possible site of origin for a distinct type of B-cell lymphoma. While preferentially occurring in the stomach, MALT-type lymphomas can be found in virtually all organs. MALT-type lymphomas normally follow an indolent course, with a tendency to remain localized at their site of origin for a prolonged period of time. Histologically, MALT-type lymphomas are heterogeneous covering a cytological spectrum ranging from centrocyte-like cells to smaller lymphoid cells or monocytoid B-cells. Usually a small number of transformed blasts are also present. Immunohistochemically, the malignant cells express markers of B-cell lineage, but are distinct from follicular lymphomas (which express CD10), mantle cell lymphomas (expressing cyclin D1 and CD5) and small lymphocytic lymphoma, which express CD5 and CD23. In contrast to the usual phenotype CD20+CD10-CD5-Cyclin D1-, scattered reports in the literature have documented expression of CD5 in marginal zone B-cell lymphomas of MALT-type. However, these cases are rare, and aberrant CD5-expression has been thought to be a marker for early dissemination and aggressive behavior in some patients, while other reports have also found CD5 expression in localized indolent MALT-type lymphomas. We report a patient with a CD5+ MALT-type lymphoma following an aggressive clinical course without histological progression who relapsed only 18 months after local radiotherapy at the initial localizations (conjunctiva of the right upper eye lid and hypopharynx), and showed a rapid generalization to the contralateral conjunctiva, mediastinal lymph nodes and the esophagogastric junction. Our case lends further support to the notion that CD5+ MALT-lymphomas arising in the head-and-neck area and/or the ocular adnexa might be characterised by an aggressive clinical course.

Aged↗

Expression of CD86 and increased infiltration of NK cells are associated with Helicobacter pylori-dependent state of early stage high-grade gastric MALT lymphoma.

AIM: A high percentage of early-stage high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori (H pylori)-dependent. However, unlike their low-grade counterparts, high-grade gastric MALT lymphomas may progress rapidly if unresponsive to H pylori eradication. It is mandatory to identify markers that may predict the H pylori-dependent status of these tumors. Proliferation of MALT lymphoma cells depends on cognate help and cell-to-cell contact of H pylori-specific intratumoral T-cells. To examine whether the expression of co-stimulatory marker CD86 (B7.2) and the infiltration of CD56 (+) natural killer (NK) cells can be useful markers to predict H pylori-dependent status of high-grade gastric MALT lymphoma. METHODS: Lymphoma biopsies from 26 patients who had participated in a prospective study of H pylori-eradication for stage I(E) high-grade gastric MALT lymphomas were evaluated. Tumors that resolved to Wotherspoon grade II or less after H pylori eradication were classified as H pylori-dependent; others were classified as H pylori-independent. The infiltration of NK cells and the expression of CD86 in pre-treatment paraffin-embedded lymphoma tissues were determined by immunohistochemistry. RESULTS: There were 16 H pylori-dependent and 10 H pylori-independent cases. CD86 expression was detected in 11 (68.8%) of 16 H pylori-dependent cases but in none of 10 H pylori-independent cases (P = 0.001). H pylori-dependent high-grade gastric MALT lymphomas contained significantly higher numbers of CD56 (+) NK cells than H pylori-independent cases (2.8+/-1.4% vs 1.1+/-0.8%; P = 0.003). CD86 positive MALT lymphomas also showed significantly increased infiltration of CD56 (+) NK cells compared to CD86-negative cases (2.9+/-1.1% vs 1.4+/-1.3%; P = 0.005). CONCLUSION: These results suggest that the expression of co-stimulatory marker CD86 and the increased infiltration of NK cells are associated with H pylori-dependent state of early-stage high-grade gastric MALT lymphomas.

Adult↗

Gastric MALT-lymphoma, gastrin and cyclooxygenases.

Malt-lymphoma, gastrin and COX-2 interaction. Low grade, mucosal associated lymphoid tissue (MALT)-lymphoma is an unique among gastric malignancies where causal involvement of Helicobacter pylori (H. pylori) infection has been proposed based on complete regression of the tumor following the eradication therapy. In this report ten primary, low-grade MALT-lymphomas have been examined before and 6 months after one week of successful eradication therapy (clarithromycin + amoxicillin + omeprazole). Gastric biopsy samples from tumor and intact antrum and corpus mucosa were obtained during endoscopy before and after eradication for assessment of expression of gastrin and gastrin receptor (CCKB-R) as well as cyclooxygenase (COX)-1 and COX-2 using RT-PCR. The gastric lumen and serum gastrin and mucosal and tumor tissue PGE2 biosynthesis were determined by RIA before and after H. pylori eradication. Eradication of H. pylori resulted in complete endoscopic and histological remission of MALT-lymphoma in 9 out of 10 patients as assessed 6 months after this eradication. Before eradication, the mRNA expression for gastrin and CCKB-R as well as mRNA expression for COX-1 and COX-2 were observed in tumor tissue and infected mucosa, while corpus mucosa expressed only CCKB-R and antrum mucosa only gastrin. Six months upon the eradication when MALT-lymphoma completely regressed both endoscopically and histologically in 9 of 10 tested subjects, the expression of gastrin and COX-2 disappeared from the former area of MALT-lymphoma tumor. Gastrin mRNA remained detectable only in antrum mucosa, CCKB-R mRNA in corpus mucosa and COX-1 mRNA both in antrum and corpus mucosa. Gastric luminal and serum gastrin levels and gastric mucosa and tumor PGE2, which were greatly elevated before eradication, became normalized after this procedure. This study demonstrates that low-grade MALT-lymphoma is linked to H. pylori infection which may promote the expression and excessive release of gastrin and COX-2 expression that could be involved in the pathogenesis of MALT-lymphoma.

Amoxicillin↗

Purification and properties of the MalT protein, the transcription activator of the Escherichia coli maltose regulon.

Expression of the Escherichia coli maltose regulon is controlled by MalT, a transcriptional activator (Mr = 102,288) encoded by the malT gene. Activation of transcription depends on the presence of the inducer, maltotriose. Using an in vitro transcription/translation assay to monitor the protein, we have purified MalT in native form from MalT-overproducing bacteria. The purified protein is able to promote transcription from different MalT-controlled promoters in well-defined in vitro systems. Maltotriose and the MalT protein suffice to stimulate initiation of transcription at malPp by the E. coli RNA polymerase holoenzyme. In contrast, both MalT protein and cAMP receptor protein are required with their respective effectors, maltotriose and cyclic AMP, for activation of malEp. These data are in agreement with in vivo observations. In addition, we present evidence that MalT is an ATP-binding protein, a result suggesting that ATP may play a role in transcription initiation.

Adenosine Triphosphate↗

Helicobacter pylori, gastric MALT and B-cell clonality.

MALT, or mucosa associated lymphoid tissue, is normally not present in gastric tissue. Its presence is often associated with persistent antigenic stimulation. MALT is a precursor of gastric MALT lymphoma, a low-grade lymphoma whose incidence recently appears to have increased. Although much epidemiologic and clinical evidence has linked both MALT and MALT lymphoma to Helicobacter pylori infection, it is not known whether other agents and or mechanisms may also play a role and whether there is a clearly defined pre-neoplastic lesion. In particular, the clinical significance of B-cell clonality remains unknown. In a recent study we attempted to define the role of H. pylori and MALT in the genesis of B-cell clonality in a northern Italian patient population referred to us for simple dyspepsia. The results show that B-cell clonality is unexpectedly frequent in these patients regardless of the presence of H. pylori infection. These observations raise the possibility that agents and mechanisms other than H. pylori may be involved in the genesis of MALT lymphoma. Indeed, other studies conducted by our group in patients with Sjögren's syndrome indicate that genetic/immunologic factors and possibly viruses may play a role. The high prevalence of B-cell clonality in an otherwise healthy population suggests either that most of these patients are at risk of developing MALT lymphoma (in which case this condition at the moment may be greatly underdiagnosed) or that B-cell clonality is a very early step in the development of neoplasia, which requires several other factors and which will occur only in a restricted fraction of these patients. Careful follow-up studies will provide an answer to this question.

Autoimmunity↗

Gastric MALT lymphoma and Helicobacter pylori.

Primary gastric low-grade B-cell lymphomas are neoplastic mimics of mucosa associated lymphoid tissue (MALT) as exemplified by Peyer's patches in the terminal ileum. Architectural and immunophenotypic properties of the neoplastic cells suggest that they originate from MALT-derived marginal zone B-cells. Paradoxically, the normal human stomach is devoid of organized MALT within which a lymphoma can develop. Lymphoid tissue is acquired in the stomach in response to antigenic stimulation, predominantly associated with Helicobacter pylori infection. Studies of patients with low-grade MALT lymphoma have confirmed a high incidence of H. pylori infection and suggest that the infection predates neoplastic transformation. Certain morphological features of MALT lymphomas suggest that the tumor cells remain responsive to antigen drive. Given the close association between gastric MALT lymphoma and H. pylori, it is possible that this organism provides such a drive. In vitro studies have shown that the tumor cells proliferate in a T-cell-dependent way to the presence of H. pylori. Several studies have now demonstrated that eradication of the organism in patients with low-grade gastric MALT lymphoma can result in regression of the tumor. In cases with a high-grade component, the associated low-grade part may regress, but most high-grade gastric MALT lymphomas are unresponsive to this conservative therapy.

Helicobacter Infections↗

Detection of BCL-6 rearrangements and p53 mutations in Malt-lymphomas.

Twenty-seven lymphomas of mucosa-associated lymphoid tissue (MALT) derived from distinct anatomical sites were tested for the presence of genetic lesions commonly involved in B-cell lymphomagenesis, including activation of proto-oncogenes (BCL-1, BCL-2, BCL-6, and c-MYC), disruption of tumor suppressor loci (p53, 6q), and infection by viruses [Epstein-Barr virus (EBV), and Kaposi's sarcoma-herpesvirus/human herpesvirus-8 (KSHV/HHV-8)]. Sixteen low-grade and 11 high-grade MALT-lymphomas were included in the study. The presence of genetic lesions was tested by a combination of molecular approaches, including Southern blot hybridization, polymerase chain reaction (PCR), and PCR-single strand conformation polymorphism followed by DNA direct sequencing. Alterations of BCL-1, BCL-2, or c-MYC, as well as infection by KSHV/HHV-8, scored negative in all MALT-lymphomas analysed. Conversely, rearrangements of BCL-6 and mutations of p53 clustered with a fraction of high-grade MALT-lymphomas. Deletions of 6q occurred in selected cases of both low- and high-grade MALT-lymphomas, whereas a monoclonal infection by EBV was restricted to one single patient. These data corroborate the notion that the molecular pathogenesis of MALT-lymphomas differs substantially from that of nodal B-cell lymphomas. Occasionally, however, a proportion of high-grade MALT-lymphomas may harbor selected genetic lesions among the ones commonly involved in nodal B-cell lymphomagenesis.

Blotting, Southern↗

Splenic marginal zone expansion in B-cell lymphomas of gastrointestinal mucosa-associated lymphoid tissue (MALT) is reactive and does not represent homing of neoplastic lymphocytes.

It has been suggested that lymphocytes of mucosa-associated lymphoid tissue (MALT) arise from marginal zone cells and that MALT-derived lymphomas may spread to other extra-nodal sites by homing to marginal zones in different tissues. Marginal zone expansion has been observed in spleens removed during surgery for gastrointestinal MALT lymphoma, which was sufficiently extreme in some cases to suggest neoplastic involvement. To investigate this phenomenon, polymerase chain reaction (PCR) amplification of immunoglobulin heavy chain gene fragments was performed to demonstrate B-cell clonality in gastrointestinal MALT lymphomas and spleens from 11 patients. Monoclonal PCR products were obtained from 9 of the 11 gastrointestinal tumours but from none of the accompanying spleens. One additional spleen, for which the accompanying gastric lymphoma tissue was unavailable for review, yielded a monoclonal product. However, obvious lymphoma deposits were present in this specimen, in addition to marginal zone enlargement. It is concluded that splenic marginal zone expansion accompanying gastrointestinal MALT lymphoma is correctly interpreted as being reactive. Splenic involvement by MALT lymphoma is uncommon and does not show preferential colonization of the marginal zone to suggest homing of MALT-derived cells to this site.

B-Lymphocytes↗

MALT lymphoma with t(14;18)(q32;q21)/IGH-MALT1 is characterized by strong cytoplasmic MALT1 and BCL10 expression.

Mucosa-associated lymphoid tissue (MALT) lymphoma is specifically associated with t(11;18)(q21;q21), t(1;14)(p22;q32) and t(14;18)(q32;q21). t(11;18)(q21;q21) fuses the N-terminus of the API2 gene to the C-terminus of the MALT1 gene and generates a functional API2-MALT1 product. t(1;14)(p22;q32) and t(14;18)(q32;q21) bring the BCL10 and MALT1 genes respectively to the IGH locus and deregulate their expression. The oncogenic activity of the three chromosomal translocations is linked by the physiological role of BCL10 and MALT1 in antigen receptor-mediated NFkappaB activation. In this study, MALT1 and BCL10 expression was examined in normal lymphoid tissues and 423 cases of MALT lymphoma from eight sites, and their expression was correlated with the above translocations, which were detected by molecular and molecular cytogenetic methods. In normal B-cell follicles, both MALT1 and BCL10 were expressed predominantly in the cytoplasm, high in centroblasts, moderate in centrocytes and weak/negative in mantle zone B-cells. In MALT lymphoma, MALT1 and BCL10 expression varied among cases with different chromosomal translocations. In 9/9 MALT lymphomas with t(14;18)(q32;q21), tumour cells showed strong homogeneous cytoplasmic expression of both MALT1 and BCL10. In 12/12 cases with evidence of t(1;14)(p22;q32) or variants, tumour cells expressed MALT1 weakly in the cytoplasm but BCL10 strongly in the nuclei. In all 67 MALT lymphomas with t(11;18)(q21;q21), tumour cells expressed weak cytoplasmic MALT1 and moderate nuclear BCL10. In MALT lymphomas without the above translocations, both MALT1 and BCL10, in general, were expressed weakly in the cytoplasm. Real-time quantitative RT-PCR showed a good correlation between MALT1 and BCL10 mRNA expression and underlining genetic changes, with t(14;18)(q32;q21)- and t(1;14)(p22;q32)-positive cases displaying the highest MALT1 and BCL10 mRNA expression respectively. These results show that MALT1 expression pattern is identical to that of BCL10 in normal lymphoid tissues but varies in MALT lymphomas, with high cytoplasmic expression of both MALT1 and BCL10 characterizing those with t(14;18)(q32;q21).

Adaptor Proteins, Signal Transducing↗

Gastric low-grade B-cell MALT lymphoma: treatment, response, and genetic alteration.

Approximately 10% of gastric low-grade B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) type are unresponsive to Helicobacter pylori ( H. pylori) eradication treatment, and many of them contain an API2-MALT1 chimeric transcript mediated by t(11;18)(q21;q21) translocation. We here review the current status on the interrelationship among clinical features, H. pylori infection status, responsiveness to antibacterial treatment, and API2-MALT1 chimeric transcript of gastric MALT lymphoma in a unicenter study experience and discuss the clinicopathologic significance of API2-MALT1 chimeric transcript in gastric MALT lymphoma. We enrolled 59 patients with gastric MALT lymphoma in a unicenter study. H. pylori infection status and clinical stages were investigated. Antibacterial treatment and subsequent follow-up endoscopy were performed for the assessment of responsiveness of MALT lymphoma in every patient. All cases were examined for API2-MALT1 chimeric transcript by means of RT-PCR and sequencing analyses using RNA extracted from tissues. H. pylori infection status was assessed as positive in 50 patients and negative in 9. Antibacterial treatment achieved complete or partial remission in 41 patients and no change in 12. API2-MALT1 chimeric transcript was detected in 9 patients, all of whom showed no change in response to treatment. Notably, responsiveness to H. pylori eradication treatment most clearly delineated the enrolled cases into two groups, indicating that six factors ( H. pylori infection, API2-MALT1 chimeric transcript, cobblestone mucosa and submucosal tumor in gross appearance, nodal involvement, and clinical stage) were statistically significant. On the other hand, comparison of two groups from the standpoint of H. pylori or API2-MALT1 chimeric transcript status revealed a lesser number of the statistically significant factors (two and three, respectively). Gastric MALT lymphoma characterized by unresponsiveness to antibacterial treatment contains all API2-MALT1 chimeric transcript-positive cases and may constitute a distinct group often seen with nodal involvement and an advanced clinical stage. This group is thought to be unrelated to H. pylori infection in its pathogenesis, and might share a unifying feature of genetic alteration such as involving the MALT1 locus on chromosome 18. Investigation in the future will clarify this issue and establish the clinical implication of such genetic alteration as the predictive factor for gastric MALT lymphoma.

Chromosome Aberrations↗

Immunological and molecular analysis of B lymphocytes in low-grade MALT lymphoma of the stomach. Are there any useful markers for predicting outcome after Helicobacter pylori eradication?

BACKGROUND: Although Helicobacter pylori eradication is effective in treating low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, the condition in some patients deteriorates even after the eradication. Therefore, it is important to predict the disease outcome before starting H. pylori eradication. We investigated the usefulness of flow cytometry, quantifying CD19- and CD20-positive B lymphocytes in MALT lymphoma tissue, for predicting the disease outcome after H. pylori eradication. METHODS: Tissue specimens from 14 patients with H. pylori-positive low-grade gastric MALT lymphoma were examined by histology, Southern blotting, and flow cytometry before therapy. Serum levels of soluble interleukin (IL)-2 receptor were also measured. The relationship between the data and the prognosis after H. pylori eradication was analyzed. RESULTS: Remission occurred in 10 of the 14 patients. The condition in the 4 remaining patients deteriorated even after H. pylori eradication. The percentages of CD19- and CD20-positive cells in MALT lymphoma tissue from the patients in remission were both significantly lower than those in the tissue from patients not in remission. Indeed, 4 of the 5 patients in whom both CD19- and CD20-positive cells accounted for more than 50% of the total number of lymphocytes had gastrectomy, whereas all patients in whom both CD19- and CD20-positive cells accounted for less than 50% of the total number of lymphocytes achieved remission. Although immunoglobulin gene rearrangement was present in all patients operated on, there were also 6 patients whose MALT lymphoma was ameliorated in spite of the presence of gene rearrangement. The serum level of soluble IL-2 receptor was in the normal range in all patients tested. CONCLUSIONS: Analysis of mature B-cell markers in MALT lymphoma tissue is more useful than the examination of immunoglobulin gene rearrangement or serum levels of soluble IL-2 receptor in predicting the outcome of low-grade gastric MALT lymphoma after H. pylori eradication.

Antigens, CD19↗

MALT Lymphoma in Children: Case Report and Review of the Literature.

Mucosa-associated lymphoid tissue (MALT) lymphoma predominantly occurs in adults, and is rare in children. We report a case of MALT lymphoma involving minor salivary gland of the lip in an otherwise healthy 12-year-old boy. This is the second case report of MALT lymphoma of minor salivary gland in an immunocompetent child. Of 24 cases of MALT lymphomas in children reported in the English literature, parotid MALT lymphomas in human immunodeficiency virus (HIV) patients and H. pylori infection-associated gastric MALT lymphomas are the most common. As in adult cases, most MALT lymphomas in the pediatric age group are localized and follow an indolent clinical course, respond well to therapy, and have an excellent outcome.

Antigens, CD↗

The nucleotide sequence of the malT gene encoding the positive regulator of the Escherichia coli maltose regulon.

The molecular organization of the malT region of the Escherichia coli K-12 chromosome has been elucidated by nucleotide sequence studies. A single open reading frame of 901 codons comprises the malT gene which is separated by a repetitive extragenic palindromic unit from an unidentified gene, orfX, divergently oriented with respect to malT. The predicted Mr of the MalT protein is 102988, making it the largest transcriptional regulatory protein yet described in E. coli. By deleting in vitro the 3'-end of the gene or constructing malT-lacZ gene fusions, it was found that the integrity of the C-terminus of MalT is indispensable for the activity of the protein. Furthermore, it was found that truncated MalT proteins lacking up to 300 amino acids at the C-terminus blocked the activity of the wild type protein. No sequence homology can be found either with the other activators known in E. coli or with the other proteins of the maltose regulon.

Amino Acid Sequence↗

Immunisation against Helicobacter felis infection protects against the development of gastric MALT Lymphoma.

UNLABELLED: The formation of mucosa-associated lymphoid tissue (MALT) in response to Helicobacter pylori infection is closely associated with the development of primary gastric MALT lymphoma. AIM: To examine whether immunisation against Helicobacter felis can protect against development of MALT lymphoma. RESULTS: The majority of control infected mice demonstrated MALT formation (13/15) and five developed lymphoma. Fifteen immunised mice were protected against bacterial challenge, of which only five had evidence of MALT formation and none developed lymphoma. Interestingly, of the four mice in which immunisation failed, all developed MALT and two of these had lymphoma. CONCLUSION: Effective immunisation against Helicobacter infection can protect against gastric MALT lymphoma. To our knowledge this is the first demonstration of vaccination protecting against a bacteria-induced malignancy.

Animals↗

Effect of kilning on the antioxidant and pro-oxidant activities of pale malts.

Pale malts were prepared using standard and rapid kilning regimes that differed in the temperature and moisture profiles in the kiln. Samples were taken over the last 9 h of kilning, that is, at 18, 20, 22, 25, and 27 h. Antioxidant activity, assessed by redox potential, scavenging of the 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) radical cation (ABTS*+), and ferric reducing/antioxidant power (FRAP), increased at moisture levels below 6.7% for both regimes. The 27 h malt exposed to the rapid regime (moisture content of 4.8%) had a higher activity than the 27 h standard regime sample (moisture content of 4.8%). None of the malts scavenged oxygen. Pro-oxidant activity profiles were different for the malts obtained using each regime and, at 27 h, the rapid procedure gave malt with higher activity. Levels of (+)-catechin and ferulic acid (the most abundant phenolic compounds identified) generally increased as the moisture content of malt fell below 6.7%. Differences in antioxidant and pro-oxidant activities of the 27 h malts are partly attributed to the Maillard reaction, as evidenced by lower L* and higher b* values and higher levels of Maillard-derived flavor compounds, in the sample obtained by the rapid procedure. Levels of lipid-derived flavor compounds were significantly higher after 27 h of kilning using the rapid procedure.

Antioxidants↗

The product of the t(11;18), an API2-MLT fusion, is an almost exclusive finding in marginal zone cell lymphoma of extranodal MALT-type.

BACKGROUND: Extranodal marginal zone cell lymphoma (MZCL) of MALT-type share similar features with nodal and splenic MZCL regarding morphology and immunophenotype. At the genetic level, recent cytogenetic studies have shown that t(11;18) is a recurring abnormality in extranodal MALT-type MZCL but has hitherto never been reported in nodal or splenic MZCL. The aim of the present study was to determine the prevalence of t(11;18) in a large series of nodal, splenic and extranodal MALT-type MZCL, using a sensitive real-time RT-PCR method. MATERIALS AND METHODS: Ninety-three MZCL cases were divided on clinical grounds into 61 extranodal MALT-type, 19 splenic and 12 nodal MZCL. One case that presented with a massive splenomegaly but for which also gastro-intestinal localisations were found, was left unclassified. A real-time RT-PCR method for the detection of the API2-MLT fusion resulting from t(11;18) was performed on RNA extracted from frozen tissue sections. RESULTS: The API2-MLT fusion was detected in 12 cases, which were all extranodal MALT-type lymphomas of the stomach, except for one case. The remaining positive case was the unclassified case, for which the translocation was detected in the spleen and in hilar lymph node tissue. CONCLUSIONS: While similarities between MZCL from different anatomic sites have lend us to propose that all MZCL have a common normal counterpart, the almost exclusive detection of t(11;18) in gastric MALT-type lymphoma favours its recognition as a separate lymphoma entity. The absence of the translocation in nodal and splenic MZCL challenges the idea of these lymphomas being secondary to MALT-type lymphomas of the gut. The unclassified case illustrates the inadequate approaches available at present to identify and define the various MZCL.

Apoptosis↗

Gastric MALT lymphoma: from concept to cure.

Gastric MALT lymphomas are clinically and histologically quite distinct from comparable low-grade B-cell lymphomas of lymph nodes. Their histology suggests that immunological mechanisms might be operative in their growth. Given that there is normally no lymphoid tissue in gastric mucosa and that Helicobacter pylori (H. pylori), the only common bacterial antigen in the stomach, results in the accumulation of gastric MALT, the possibility that this organism is implicated in the pathogenesis of gastric lymphoma has been extensively investigated. It appears that most, but not necessarily all, gastric MALT lymphomas arise in MALT acquired in response to H. pylori infection and develop by stepwise accumulation of genetic abnormalities. Early molecular events in the evolution of gastric MALT lymphoma from 'acquired' MALT include trisomy 3, t(11;18)(q21;q21), genetic damage leading to genetic instability, as indicated by the so-called replication error repair (RER) phenotype, and both p53 and c-myc mutations. At this stage in their development, the growth of the lymphomas is driven by contact between the neoplastic B cells and H. pylori specific intra-tumoral T cells. Eradication of H. pylori causes the tumour to enter a latent phase resulting in clinical regression. Later events, such as t(1;14)(p22;q32), appear to be linked to a capacity for autonomous growth, loss of sensitivity to H. pylori and dissemination of the lymphoma beyond the stomach and gastric lymph nodes. Cloning of the breakpoint in t(1;14) has allowed the identification of a new tumour suppresser gene, bc110. High grade transformation of MALT lymphoma has been associated with p53 inactivation, deletions of p16 and t(8;14).

Chromosome Aberrations↗