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Albert Roessner

Publications and source records attributed to Albert Roessner.

At least 73 records · Page 4Linked to original sources
PubMed2003

Skull base and nonskull base chordomas: clinicopathologic and immunohistochemical study with special reference to nuclear pleomorphism and proliferative ability.

BACKGROUND: To the authors' knowledge, little is known regarding the relation between the proliferative ability and clinicopathologic parameters in skull base chordomas (SBCs) and nonskull base chordomas (NSBCs). METHODS: The authors investigated 122 conventional chordomas for their clinicopathologic parameters, proliferative ability (MIB-1 labeling index [LI]) and clinical outcome. RESULTS: Primary NSBCs were found to affect more elderly patients and demonstrated a higher MIB-1 LI compared with primary SBCs. Mitosis was more commonly noted in recurrent NSBCs compared with primary NSBCs. Apoptosis was more frequent in elderly patients than in younger patients with regard to both SBCs and NSBCs. Apoptosis also was found to be correlated with necrosis in SBCs, suggesting a common factor for the two different types of cell death. Mucoid matrix was reported to be more abundant in NSBCs than in SBCs, and appeared to occur more often in elder NSBC patients compared with younger NSBC patients. This indicates that it is produced in the later stages of tumorigenesis. In SBCs, several clinicopathologic parameters were found to be correlated with MIB-1 LI. Among them, increased age, recurrence, and nuclear pleomorphism were the only independent factors found to indicate a higher MIB-1 LI. No such parameters were found in NSBCs. However, in these lesions, prognosis was significantly poorer in those cases with nuclear pleomorphism compared with those without. CONCLUSIONS: The results of the current study suggest that nuclear pleomorphism is a prognostic indicator in NSBCs. The proliferative ability of SBCs appears to be closely associated with patient age, clinical status (recurrence), and nuclear pleomorphism.

Adolescent↗
PubMed2003

p16INK4A alterations are accompanied by aberrant protein immunostaining in endometrial carcinomas.

PURPOSE: To date, the significance of p16INK4A tumor suppressor gene inactivation in sporadic endometrial cancer (EC) has only rarely been described. In this study, we examined the alteration type and frequency of gene alterations [point mutations, aberrant promoter methylation and loss of heterozygosity (LOH)] in 50 sporadic ECs, and correlated the genetic findings with the immunohistochemical expression of the p16INK4A protein and the classical clinicopathological features. METHODS: Gene mutations were detected by PCR-SSCP-sequencing analysis, promoter hypermethylation by methylation-specific PCR (MSP), and LOH by PCR of the STS-marker c5.1. RESULTS: In total, p16INK4A alterations were found in 14 of 50 (28%) sporadic ECs. In six (12%) cases, two alterations occurred simultaneously. Partial p16INK4A deletions were found in four of 50 (8%) samples. There was one missense mutation (codon 70; CCC-->GCC) and one frameshift mutation (1-bp deletion in exon 2). Only 2 of 47 (4.2%) tumors exhibited aberrant promoter methylation. An allelic loss was detected in 12 of 50 (24%) carcinomas with a higher incidence in advanced endometrial carcinomas than in early-stage uterine tumors. p16INK4A alterations were generally accompanied by gene silencing, confirmed by aberrant protein immunostaining ( r=-0.442; P=0.001). There was a significant difference in the frequency of p16INK4A alterations between early (stage I; 18%) and advanced (stages II-IV; 58%) ECs ( P=0.022). One case showed complete protein loss, but absence of genetic alterations. CONCLUSIONS: Our data indicate that p16INK4A inactivation plays a role in the tumorigenesis of the subset of sporadic ECs, particularly in cases exhibiting an aggressive clinical behavior. We demonstrate that p16INK4A methylation can act efficiently and similarly to other genetic alterations as one of the two necessary hits according to the Knudson two-hit hypothesis of tumor suppressor gene inactivation.

Adult↗
PubMed2003

Telomerase activity in juxtacortical and conventional high-grade osteosarcomas: correlation with grade, proliferative activity and clinical response to chemotherapy.

Seven samples from seven patients with juxtacortical osteosarcomas, and 27 samples from 19 patients with conventional high-grade osteosarcomas were investigated for a possible correlation between telomerase activity and clinicopathological features such as age, sex, and response to chemotherapy. Of seven juxtacortical osteosarcomas, telomerase activity was weakly positive in three parosteal osteosarcomas, and highly positive in one parosteal osteosarcoma. In contrast, of 27 conventional high-grade osteosarcomas, telomerase activity was weakly positive in eight tumors and highly positive in three. Of all samples, 44.1% of the osteosarcomas showed telomerase activity (57.1% of juxtacortical and 40.7% of conventional osteosarcomas). The majority of poor responders to chemotherapy showed no telomerase activity (nine of 11), whereas five of seven good responders showed strong or weak telomerase activity. There was a significant correlation between telomerase activity and the response to chemotherapy (P<0.05). Telomerase activity was not correlated with MIB-1 proliferation index, age at the time of surgery, or sex. These findings suggest that telomerase activation occurs early in the oncogenesis of osteoblastic tumors without having an effect on the progression of these tumors. In malignant osteoblastic tumors, the biological significance of telomerase activation is different from that described for most epithelial cancers.

Adolescent↗
PubMed2003

High prognostic value of p16INK4 alterations in gastrointestinal stromal tumors.

PURPOSE: Gastrointestinal stromal tumors (GISTs) represent a distinctive (but histologically heterogeneous) group of neoplasms, the malignant potential of which is often uncertain. To determine the prognostic relevance of p16INK4 alterations in GISTs, we investigated a larger group of GISTs and correlated the genetic findings with clinicopathological factors and patient survival. MATERIAL AND METHODS: We evaluated the methylation status of the promotor by methylation-specific polymerase chain reaction (PCR), the presence of mutations by PCR-SSCP-sequencing, the loss of heterozygosity at the p16INK4 locus (using the c5.1 marker), and the immunohistochemical expression of p16INK4 protein in 43 GISTs in 39 patients. RESULTS: p16INK4 alterations were found in 25 of 43 GISTs (58.1%), with benign, borderline, or malignant GISTs showing no differences in the type and frequency of alteration. p16INK4 alterations were correlated with a loss of p16INK4 protein expression (P <.01). Patients who had tumors with p16INK4 alterations had a poorer prognosis than patients with tumors without such alterations (P =.02). There was a high predictive value for p16INK4 alterations only in the group of benign and borderline GISTs (P <.01) with regard to clinical outcome. Univariate Cox's proportional hazard regression analysis revealed a strong correlation between p16INK4 alterations, tumor size, mitotic index, and overall survival (P <.02), whereas multivariate Cox's analysis confirmed only p16INK4 alterations as an independent prognostic factor. CONCLUSION: We believe that the evaluation of p16INK4 alteration status is a helpful prognosticator, particularly in the benign and borderline groups of GISTs.

Adult↗
PubMed2003

Feasibility of histological grading and staging of chronic viral hepatitis using specimens obtained by thin-needle biopsy.

We performed a retrospective study to investigate the feasibility of grading and staging of chronic viral hepatitis on specimens obtained by means of thin-needle biopsy (TNB; 20G) using the modified Ishak-system (J Hepatol 1995; 22:696-699). Specimens obtained using large-needle biopsy (LNB; 17G) served as a control. A total of 100 biopsy specimens from 88 patients were included in the study. Of the patients, 30 suffered from chronic hepatitis B, 54 from chronic hepatitis C, and 4 from both; 59 specimens were obtained by TNB and 41 by LNB. All four categories of the Ishak-system, i.e., interface hepatitis, confluent necrosis, lobular inflammation and portal inflammation, could be applied to TNB specimens and provided similar total scores to those observed in LNB specimens. Specimens obtained by TNB facilitated the diagnosis of liver cirrhosis. However, they bore the risk of underestimating the presence of cirrhosis in favor of advanced bridging fibrosis, whereas no differences were found in the overall recognition of liver fibrosis. Intra- and interobserver variabilities were not affected by the needle size. For the interobserver agreement, the kappa values for the category of inflammation ranged from 0.003 to 0.419 (TNB) and 0.096 to 0.470 (LNB) and for staging we noted kappa values of 0.351 (TNB) and 0.456 (LNB). Reproducibility increased when a tolerance of +/-1 was accepted for grading (total score) and staging; in this case, observer variability was less than 20%. This study showed that grading and staging of chronic viral hepatitis is feasible in TNB specimens and that intra- and interobserver variability poses a greater problem than needle size.

Adult↗
PubMed2003

Elevated telomerase activity, c-MYC-, and hTERT mRNA expression: association with tumour progression in malignant lipomatous tumours.

The role of telomerase activity in tumour progression of liposarcomas is not well understood. Therefore, we investigated 72 liposarcomas of different histological subtypes for an association between telomeric lengths and telomerase activity, and assessed the association between the catalytic subunit human telomerase reverse transcriptase (hTERT) and its activator c-MYC. Telomeric repeat fragment lengths were determined using radioactive DNA-fingerprint analysis with the telomere-specific probe (TTAGGG)(3), whereas telomerase activity was ascertained using the non-radioactive TRAP-assay. To evaluate the expression of hTERT and c-MYC, we applied real-time RT-PCR using a LightCycler. Eight tumours were investigated by microdissection. The MIB1-proliferation index and hTERT and c-MYC protein expression were determined immunohistochemically. Genetic alterations showed a high degree of tumour specificity. Highly malignant myxoid/round cell liposarcomas showed the longest telomeres, the strongest telomerase activity, and the highest hTERT and c-MYC expression levels compared with the pure myxoid variants (p < 0.001), which are of low malignancy. Pleomorphic liposarcoma was characterized by zero or low hTERT and c-MYC expression and telomerase activity, but long telomeres, underlining their different pathogenetic pathway. Elevated gene expression was accompanied by protein immunopositivity. MIB1-proliferation index did not correlate with other molecular markers. We conclude that hTERT and c-MYC expression are associated with telomerase activity in liposarcomas. Elevated hTERT and c-MYC expression as well as high telomerase activity play a role in the tumour progression of this sarcoma type. Nevertheless, each histological subtype of liposarcomas is defined by a specific molecular pattern. Telomerase activation is the most common pathway in liposarcomas maintaining telomeric length.

Biomarkers, Tumor↗
PubMed2003

KIT 1530ins6 mutation defines a subset of predominantly malignant gastrointestinal stromal tumors of intestinal origin.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. GISTs express KIT and show gain-of-function KIT mutations. Most of these mutations affect the KIT juxtamembrane domain, but other KIT domains are mutated at a lower frequency. In this study, frequency of GCC TAT insertion mutation (1530ins6) in KIT exon 9 (extracellular domain) and its possible clinicopathologic significance was investigated. Screening of 520 GISTs identified 26 cases with 1530ins6 KIT mutation and confirmed the previously reported low frequency of this type of KIT mutation among GISTs of different locations. Of the 26 tumors with 1530ins6 KIT mutation studied, 21 originated from the small intestine, 1 from the colon, and 3 from the rectum. In 1 case, primary small intestinal versus colonic localization could not be clearly established because of intra-abdominal dissemination. No distinctive morphological features were identified for the cohort of tumors defined by 1530ins6 KIT mutations. Most of the tumors showed predominant spindle cell morphology, and a few cases had epithelioid or pleomorphic histological features. Following previously published criteria based on tumor size and mitotic rate, 22 of 26 (85%) tumors were classified as malignant or potentially malignant, and 4 (15%) were classified as probably benign. A malignant clinical course was documented in 18 of 19 tumors from the malignant category. The survival times of 11 patients who died of disseminated GISTs ranged from 1 month to 105 months (median survival time, 26 months). In contrast, 2 of 4 GISTs assigned as probably benign tumors with follow-up information had long disease-free survival. GISTs carrying 1530ins6 occur exclusively in the intestinal location, and a great majority of these tumors follow a malignant course.

Adult↗
PubMed2003

Inhibitory effect of antisense aminopeptidase N (APN/CD13) cDNA transfection on the invasive potential of osteosarcoma cells.

Aminopeptidase N (APN/CD13), a Zn2+-dependent ectopeptidase, is localized on the cell surface and functions as a transmembrane protein. Increased expression and activity of APN have been postulated to correlate with the aggressive behavior of several tumor types. In this study, the osteosarcoma cell line MNNG/HOS was stably transfected with an expression vector capable of expressing the antisense transcript of APN. Four stably transfected clones, the control clones and parental cells were characterized. Stable integration of the antisense vector was confirmed by PCR analysis of genomic DNA. Competitive RT-PCR revealed that mRNA expression of antisense-transfectants was decreased to approximately 37% of the control cell line. The activity assay showed that the enzymatic activity of APN was inhibited to approximately 51% of the control cell line. Antisense-transfection had no influence on the cellular proliferation measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, on the motility in Transwell chambers, and on the adhesive potential to collagen I. However, an in vitro invasion assay revealed a significant decrease in the number of cells that migrated through a reconstituted membrane (51% of the control cell line). The adhesive potential to Matrigel was also affected (73% of the control cell line). Furthermore, under in vivo conditions, a reduced potency to metastasize to the lung was shown in an experimental metastasis assay in nude mice. These findings demonstrate that APN plays an active role in the cellular attachment and proteolytic degradation of the extracellular matrix in the metastatic process of osteosarcomas.

Animals↗
PubMed2003

Hypermethylation of the CDKN2/p16INK4A promotor in thyroid carcinogenesis.

Functional inactivation of the p16INK4A gene has been reported to be involved in the development of a variety of human malignancies. In thyroid carcinomas, mutations of the p16INK4A gene or homozygous deletions of the gene locus 9p21 are rare. This study investigated whether p16INK4A promotor methylation is an alternative mechanism for p16INK4A gene inactivation during thyroid carcinogenesis. A methylation-specific polymerase chain reaction protocol was applied. A total of 77 thyroid tumor specimens, including 18 follicular adenomas, 18 follicular carcinomas, 16 papillary carcinomas, 12 poorly differentiated carcinomas, and 13 undifferentiated carcinomas were analyzed longitudinally. In addition, 15 tumor-free thyroid tissues were investigated. The p16INK4A promotor status was compared with p16INK4A protein expression and patient-specific data. p16INK4A promotor hypermethylation was detected in 13% of non-tumorous tissue; in 33% of follicular adenomas; in 44% of papillary carcinomas; in 50% of follicular carcinomas; in 75% of poorly differentiated carcinomas; and in 85% of undifferentiated carcinomas. With the exception of two cases, the p16INK4A protein was lost as a result of promotor hypermethylation. Comparing the methylation status with tumor stage, no correlation was found. However, lymph node and distant metastasis status showed a statistically significant prevalence for the p16INK4A promotor methylation (p = 0.035). There was no association between p16INK4A promotor methylation and age and sex. These results suggest that hypermethylation of the p16INK4A promotor region is a frequent and an early event during thyroid carcinogenesis and is associated with tumor progression and dedifferentiation.

Adult↗
PubMed2003

Intermuscular chondrolipoma of the thigh: the diagnostic way of a rare entity.

Cartilaginous metaplasia in lipomas (chondrolipoma) is rare and mainly encountered in large-sized, long-standing lipomas. Chondrolipomas can be found at almost any site of the body, particularly in the connecting tissue of the skeletal system, breast, pharynx, and nasopharynx. We report on an intermuscular tumor of the thigh in a patient who suffered from lipomatosis in his past medical history. We describe how the diagnosis of chondrolipoma was reached and discuss the differential diagnoses.

Adult↗
PubMed2003

Function of HSP90 and p23 in the telomerase complex of thyroid tumors.

Recently, studies on endocrine tumors revealed a potential role of telomerase in the dedifferentiation and/or malignant transition of these tumors. Telomerase is a ribonucleoprotein complex that includes the telomerase RNA component (hTR), the telomerase-associated protein (TP1), and the telomerase catalytic subunit (hTERT). Previously, the chaperones p23 and HSP90 have been described as additional telomerase regulators. To test whether the interactions of these genes are reflected in the dedifferentiation of thyroid tumors, we determined their mRNA and/or protein expression in 30 normal (tumor-free) thyroid tissues (NT), 35 follicular adenomas (FAD), 42 papillary carcinomas (PTC), 38 follicular carcinomas (FTC), 25 poorly differentiated carcinomas (PDTC), and 34 undifferentiated carcinomas (UTC). We then compared the results with telomerase activity. RT-PCR analysis revealed that TP1 was ubiquitously expressed. hTR was found in 50-94% of malignant tumors, in contrast to 7% of NT and 26% of FAD. hTERT was clearly associated with aggressive biological behavior. Ninety-two to 100% of the malignant tumors were positive for hTERT protein, whereas NT and FAD were negative in 100% and 94%, respectively. HSP90 mRNA and protein showed a close relationship to hTERT. p23 protein was negative in NT and positive in 3% of FAD, 39% of FTC, 40% of PTC, 44% of PDTC and 47% of UTC. High telomerase activity was measurable in hTERT and HSP90-positive tissues only. Our data show that the common expression of hTERT and HSP90 regulates telomerase activity in thyroid carcinomas. Chaperone p23 is involved in the telomeric complex to a lesser extent, but its expression is stronger in carcinomas than in non-malignant thyroid tissues. The expression profile of telomerase components represents an additional prognostic marker that may identify more aggressive thyroid tumors.

Adenoma↗
PubMed2003

Gastrointestinal stromal tumors with internal tandem duplications in 3' end of KIT juxtamembrane domain occur predominantly in stomach and generally seem to have a favorable course.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. GISTs express KIT and have KIT mutations. Majority of these mutations cluster in the 5' end of the KIT juxtamembrane domain. Little is known about the clinicopathological profile of GIST carrying internal tandem duplications in the 3' end of KIT juxtamembrane domain (ITDs in the 3' KIT-JM). In this study, 500 immunohistochemically KIT-positive GISTs were screened for this type of mutation, and 18 cases were identified (3.6%). The majority of the ITDs consisted of 1 to 18 codon duplications, with Tyr(578), Asp(579), and Leu(576) being the most commonly duplicated codons. There were 14 gastric (78%), 2 small intestinal (11%), and 2 anal (11%) primary tumors diagnosed in 12 females and 6 males with median age of 71 years. The frequency of IDTs in gastric GISTs was 6.5% and was only 0.5% in intestinal GISTs. There was a strong female predominance (79%) among the patients with gastric tumors. Histologically, 16 GISTs were spindle cell, and 2 had epithelioid morphology. The sizes of primary tumors varied from 1 to >20 cm. Based on the combination of tumor size and mitotic activity, six tumors were classified as benign or probably benign, eight as having uncertain malignant potential, and only four as malignant. Follow-up data available in 17 patients confirmed the malignant course of disease in 3 cases. Only one of the tumors classified as potentially malignant metastasized, although the follow-up was limited in some cases. In summary, the great majority of GISTs with ITDs in the 3' KIT-JM were mitotically inactive tumors occurring predominantly in the stomach and that seemed to have a favorable course. This suggests that presence of these IDTs may define a clinicopathologically favorable subset of GISTs. The consequence of these mutations to KIT signaling should be investigated.

Aged↗
PubMed2003

Expression profile of the telomeric complex discriminates between benign and malignant pheochromocytoma.

Telomerase, a ribonucleoprotein complex that includes the telomerase RNA component, the telomerase-associated protein (TP1), the telomerase catalytic subunit (hTERT), and the heat shock protein 90 (HSP90), is closely related to the malignant potential of human tumors. In pheochromocytomas (PC) it is very difficult to predict malignant potential by conventional histology or immunohistochemical and molecular markers. To test whether the expression of telomerase subunits is reflected in the malignant transition of PCs, we determined their mRNA and/or protein expression in 28 benign and nine malignant PCs and compared the results with telomerase activity. RT-PCR analysis revealed that TP1 was ubiquitously expressed. The telomerase RNA component was found in all malignant (100%) and in 13 of 28 (46%) benign PCs. In contrast, hTERT was clearly associated with aggressive biological behavior. All of the malignant (100%), but only two of 28 benign (7%) PCs expressed hTERT. HSP90 was increased in malignant PCs, but was also expressed at a lower level in benign tumors. High telomerase activity was measurable in hTERT-positive tissues only. Our data indicate that hTERT, HSP90, and telomerase activity are up-regulated in malignant cells of the adrenal medulla. The common expression of hTERT and telomerase activity thus represents an additional prognostic marker that may identify more aggressive tumors.

Adrenal Gland Neoplasms↗
PubMed2003

Detection of hepatitis C virus RNA in formalin-fixed, paraffin-embedded thin-needle liver biopsy specimens.

We examined the feasibility of detecting hepatitis C virus (HCV) RNA in formalin-fixed, paraffin-embedded (FFPE) specimens obtained by thin-needle biopsy (TNB). Specimens obtained by large-needle biopsy (LNB) and unfixed frozen tissue served as controls. A total of 23 biopsy specimens, 13 obtained by TNB and 10 by LNB, from 20 patients with chronic hepatitis C were included in the study. HCV RNA was detected by nested reverse transcription-polymerase chain reaction (RT-PCR). HCV RNA was found in FFPE archival specimens obtained by TNB (11 [85%]) or LNB (7 [70%]). The sensitivity was similar in unfixed tissue in which HCV RNA was found in 7 (88%) of 8 TNB specimens and 6 (86%) of 7 LNB specimens. The detection of HCV RNA did not seem to be affected by storage of the paraffin blocks, the presence of advanced fibrosis and cirrhosis, or fragmentation of the core cylinder. TNB yields enough qualitative suitable material to detect HCV RNA by RT-PCR.

Adult↗
PubMed2003

Comparative genomic hybridization. Synchronous occurrence of focal nodular hyperplasia and hepatocellular carcinoma in the same liver is not based on common chromosomal aberrations.

Occasionally hepatocellular carcinomas (HCCs) occur synchronously with or within focal nodular hyperplasias (FNHs), raising the question of a putative causal relationship. In the present study, we used comparative genomic hybridization to investigate the occurrence of genomic aberrations in FNHs, which might lead to hepatocarcinogenesis. Tissue samples from FNHs and nonlesional liver tissue were obtained from 7 women. None of the patients had a chronic diffuse liver disease. A synchronous HCC not spatially related to FNH was present in 1 patient. Two patients had received oral contraceptives. Genomic aberrations were found in only 1 FNH. No aberration was found in the FNH occurring synchronously with HCC, but the HCC included gains at chromosomes 1q, 5, 12, and 19q and losses at 4p, 7q22-q35, 9p, 17p, 21q, and 22q. No aberrations were found in nonneoplastic liver tissues. Our findings support the notion that FNH is not a preneoplastic lesion for the occurrence of HCC in humans and that the synchronous occurrence of FNH and HCC is coincidental in our case.

Adult↗
PubMed2003

HSP90 is a key for telomerase activation and malignant transition in pheochromocytoma.

Recent studies on a limited number of pheochromocytomas (PCs) revealed a potential role of telomerase in the malignant transition of these tumors. Telomerase is a ribonucleoprotein complex that includes the telomerase RNA component (hTR), the telomerase-associated protein (TP1), the telomerase catalytic subunit (hTERT), and the heat-shock protein 90 (HSP90). The interactions between these subunits and the activation machinery of telomerase are still unclear. To test whether the expression and regulation of telomerase subunits are reflected in the malignant transition of PCs, we determined their mRNA and/or protein expression in 28 benign and 9 malignant PCs and compared the results with telomerase activity. Reverse transcriptase polymerase chain reaction analysis revealed that TP1 was ubiquitously expressed. hTR was found in all malignant (100%) and in 13/28 (46%) benign PCs. By contrast, hTERT was clearly associated with aggressive biologic behavior. All the malignant (100%) but only 2/28 benign (7%) PCs expressed hTERT. HSP90 was increased in malignant PCs but was also expressed at a lower level in benign tumors. High telomerase activity was measurable in only hTERT-positive tissues. Our data indicate that hTERT, HSP90, and telomerase activity are upregulated in malignant cells of the adrenal medulla. Overexpression of HSP90 is an important factor in the activation of telomerase via hTERT. The common expression of hTERT and telomerase activity thus represents an additional prognostic marker that may identify more aggressive tumors.

Adult↗
PubMed2003

Thymic hyperplasia following successful treatment for nodular-sclerosing Hodgkin's disease.

A young female patient showed up with mediastinal bulky disease and lymph node swelling in her left supraclavicular region. Clinical and histological investigations proved nodular-sclerosing Hodgkin's lymphoma. The patient received combined modality treatment according to the protocols of the German Hodgkin's Disease Study Group and achieved complete remission. Six months later the chest X-ray and thoracic CT-scan showed mediastinal tumor masses suggesting relapsed Hodgkin's disease. Surprisingly, the histological investigation showed thymic hyperplasia as well as the absence of any signs of Hodgkin lymphoma. Thymic hyperplasia is well known as a potential differential diagnosis of mediastinal space-occupying lesions and also as a long-term complication in patients cured of Hodgkin's disease. A detailed case report and a complete review of literature are provided.

Adult↗