scholarly journals Copy number variations alter methylation and parallel IGF2 overexpression in adrenal tumors

2015 ◽  
Vol 22 (6) ◽  
pp. 953-967 ◽  
Author(s):  
Helene Myrtue Nielsen ◽  
Alexandre How-Kit ◽  
Carole Guerin ◽  
Frederic Castinetti ◽  
Hans Kristian Moen Vollan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Copy Number ◽  
Methylation Status ◽  
Uniparental Disomy ◽  
Copy Number Variations ◽  
Conclusive Evidence ◽  
Adrenal Tumors ◽  
Benign Tumors ◽  
Parental Origin ◽  
Adrenocortical Carcinomas

Overexpression of insulin growth factor 2 (IGF2) is a hallmark of adrenocortical carcinomas and pheochromocytomas. Previous studies investigating the IGF2/H19 locus have mainly focused on a single molecular level such as genomic alterations or altered DNA methylation levels and the causal changes underlying IGF2 overexpression are still not fully established. In the current study, we analyzed 62 tumors of the adrenal gland from patients with Conn's adenoma (CA, n=12), pheochromocytomas (PCC, n=10), adrenocortical benign tumors (ACBT, n=20), and adrenocortical carcinomas (ACC, n=20). Gene expression, somatic copy number variation of chr11p15.5, and DNA methylation status of three differential methylated regions of the IGF2/H19 locus including the H19 imprinting control region were integratively analyzed. IGF2 overexpression was found in 85% of the ACCs and 100% of the PCCs compared to 23% observed in CAs and ACBTs. Copy number aberrations of chr11p15.5 were abundant in both PCCs and ACCs but while PCCs retained a diploid state, ACCs were frequently tetraploid (7/19). Loss of either a single allele or loss of two alleles of the same parental origin in tetraploid samples resulted in a uniparental disomy-like genotype. These copy number changes correlated with hypermethylation of the H19 ICR suggesting that the lost alleles were the unmethylated maternal alleles. Our data provide conclusive evidence that loss of the maternal allele correlates with IGF2 overexpression in adrenal tumors and that hypermethylation of the H19 ICR is a consequence thereof.

scholarly journals DNA Methylation Status of SHOX-Flanking CpG Islands in Healthy Individuals and Short Stature Patients with Pseudoautosomal Copy Number Variations

2019 ◽  
Vol 158 (2) ◽  
pp. 56-62 ◽  
Author(s):  
Kenichiro Ogushi ◽  
Atsushi Hattori ◽  
Erina Suzuki ◽  
Hirohito Shima ◽  
Masako Izawa ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Short Stature ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Copy Number ◽  
Methylation Status ◽  
Cpg Islands ◽  
Copy Number Variations ◽  
Peripheral Blood Cells ◽  
Healthy Individuals

SHOX resides in the short arm pseudoautosomal region (PAR1) of the sex chromosomes and escapes X inactivation. SHOX haploinsufficiency underlies idiopathic short stature (ISS) and Leri-Weill dyschondrosteosis (LWD). A substantial percentage of cases with SHOX haploinsufficiency arise from pseudoautosomal copy number variations (CNVs) involving putative enhancer regions of SHOX. Our previous study using peripheral blood samples showed that some CpG dinucleotides adjacent to SHOX exon 1 were hypomethylated in a healthy woman and methylated in a woman with gross X chromosomal rearrangements. However, it remains unknown whether submicroscopic pseudoautosomal CNVs cause aberrant DNA methylation of SHOX-flanking CpG islands. In this study, we examined the DNA methylation status of SHOX-flanking CpG islands in 50 healthy individuals and 10 ISS/LWD patients with pseudoautosomal CNVs. In silico analysis detected 3 CpG islands within the 20-kb region from the translation start site of SHOX. Pyrosequencing and bisulfite sequencing of genomic DNA samples revealed that these CpG islands were barely methylated in peripheral blood cells and cultured chondrocytes of healthy individuals, as well as in peripheral blood cells of ISS/LWD patients with pseudoautosomal CNVs. These results, in conjunction with our previous findings, indicate that the DNA methylation status of SHOX-flanking CpG islands can be affected by gross X-chromosomal abnormalities, but not by submicroscopic CNVs in PAR1. Such CNVs likely disturb SHOX expression through DNA methylation-independent mechanisms, which need to be determined in future studies.

scholarly journals A novel decision tree model based on chromosome imbalances in cell-free DNA and CA-125 in the differential diagnosis of ovarian cancer

2021 ◽  
pp. 172460082199235
Author(s):  
Weina Zhang ◽  
Yu-min Zhang ◽  
Yuan Gao ◽  
Shengmiao Zhang ◽  
Weixin Chu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Differential Diagnosis ◽  
Decision Tree ◽  
Copy Number ◽  
Malignant Tumors ◽  
Copy Number Variations ◽  
Ca 125 ◽  
Benign Tumors ◽  
Cell Free Dna ◽  
Free Dna

Objective: CA-125 is widely used as biomarker of ovarian cancer. However, CA-125 suffers low accuracy. We developed a hybrid analytical model, the Ovarian Cancer Decision Tree (OCDT), employing a two-layer decision tree, which considers genetic alteration information from cell-free DNA along with CA-125 value to distinguish malignant tumors from benign tumors. Methods: We consider major copy number alterations at whole chromosome and chromosome-arm level as the main feature of our detection model. Fifty-eight patients diagnosed with malignant tumors, 66 with borderline tumors, and 10 with benign tumors were enrolled. Results: Genetic analysis revealed significant arm-level imbalances in most malignant tumors, especially in high-grade serous cancers in which 12 chromosome arms with significant aneuploidy ( P<0.01) were identified, including 7 arms with significant gains and 5 with significant losses. The area under receiver operating characteristic curve (AUC) was 0.8985 for copy number variations analysis, compared to 0.8751 of CA125. The OCDT was generated with a cancerous score (CScore) threshold of 5.18 for the first level, and a CA-125 value of 103.1 for the second level. Our most optimized OCDT model achieved an AUC of 0.975. Conclusions: The results suggested that genetic variations extracted from cfDNA can be combined with CA-125, and together improved the differential diagnosis of malignant from benign ovarian tumors. The model would aid in the pre-operative assessment of women with adnexal masses. Future clinical trials need to be conducted to further evaluate the value of CScore in clinical settings and search for the optimal threshold for malignancy detection.

PATH-39. INTEGRATED MOLECULAR-MORPHOLOGICAL MENINGIOMA CLASSIFICATION: A MULTICENTER RETROSPECTIVE ANALYSIS, RETRO- AND PROSPECTIVELY VALIDATED

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi123-vi124
Author(s):  
Sybren Maas ◽  
Damian Stichel ◽  
Thomas Hielscher ◽  
Philipp Sievers ◽  
Anna Berghoff ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Copy Number ◽  
Retrospective Cohort ◽  
Clinical Decision Making ◽  
Clinical Decision ◽  
Molecular Data ◽  
Copy Number Variations ◽  
Who Grade ◽  
Risk Of Progression ◽  
The Individual

Abstract PURPOSE Meningiomas are the most frequent primary intracranial tumors. Patient outcome varies widely from cases with benign to highly aggressive, ultimately fatal courses. Reliable identification of risk of progression for the individual patient is of pivotal importance in clinical management. However, only biomarkers for highly aggressive tumors are established at present (CDKN2A/B and TERT), while no molecularly-based stratification exists for the broad spectrum of low- and intermediate-risk meningioma patients. PATIENTS AND METHODS DNA methylation data and copy-number information were generated for 3,031 meningiomas of 2,868 individual patients, with mutation data for 858 samples. DNA methylation subgroups, copy-number variations (CNV), mutations and WHO grading were comparatively analyzed. Prediction power for outcome of these parameters was assessed in an initial retrospective cohort of 514 patients, and validated on a retrospective cohort of 184, and on a prospective cohort of 287 multi-center cases, respectively. RESULTS Both CNV and methylation family- (MF)-based subgrouping independently resulted in an increase in prediction accuracy of risk of recurrence compared to the WHO classification (c-indexes WHO 2016, CNV, and MF 0.699, 0.706 and 0.721, respectively). Merging all independently powerful risk stratification approaches into an integrated molecular-morphological score resulted in a further, substantial increase in accuracy (c-index 0.744). This integrated score consistently provided superior accuracy in all three cohorts, significantly outperforming WHO grading (c-index difference p=0.005). Besides the overall stratification advantage, the integrated score separates more precisely for risk of progression at the diagnostically challenging interface of WHO grade 1 and grade 2 tumors (HR 4.56 [2.97;7.00], 4.34 [2.48;7.57] and 3.34 [1.28; 8.72] for discovery, retrospective, and prospective validation cohort, respectively). CONCLUSIONS Merging these layers of histological and molecular data into an integrated, three-tiered score significantly improves the precision in meningioma stratification. Implementation into diagnostic routine informs clinical decision-making for meningioma patients on the basis of robust outcome prediction.

scholarly journals Identification of prognostic values defined by copy number variation, mRNA and protein expression of LANCL2 and EGFR in IDH1/2-wild-type glioblastoma

2021 ◽  
Author(s):  
Hua-fu Zhao ◽  
Xiu-ming Zhou ◽  
Jing Wang ◽  
Fan-fan Chen ◽  
Chang-peng Wu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Copy Number ◽  
Intracellular Localization ◽  
Methylation Status ◽  
Growth Factor Receptor ◽  
Copy Number Variations ◽  
Wild Type ◽  
Number Variation ◽  
Newly Diagnosed Glioblastoma ◽  
Mrna And Protein Expression

Abstract Background Epidermal growth factor receptor (EGFR) and lanthionine synthetase C-like 2 (LanCL2) genes locate in the same amplicon, and co-amplification of EGFR and LANCL2 is frequent in glioblastoma. However, the prognostic value of LANCL2 and EGFR co-amplification, and their mRNA and protein expression in glioblastoma remain unclear yet. Methods This study analyzed the prognostic values of the copy number variations (CNVs), mRNA and protein expression of LANCL2 and EGFR in glioblastoma specimens from TCGA database or our tumor banks. Results The amplification of LANCL2 or EGFR, and their co-amplification were frequent in glioblastoma of TCGA database and our tumor banks. CNVs of LANCL2 or EGFR were significantly correlated with IDH1/2 mutation but not MGMT promoter methylation status. LANCL2 or EGFR amplification, and their co-amplification were significantly associated with reduced overall survival (OS) of glioblastoma patients, rather than IDH1/2-wild-type glioblastoma patients. mRNA and protein overexpression of LANCL2 and EGFR was also frequently found in glioblastoma. LANCL2, rather than EGFR, was overexpressed in relapsing glioblastoma, compared with newly diagnosed glioblastoma. However, mRNA or protein expression of EGFR and LANCL2 was not significantly correlated with OS of glioblastoma patients. In addition, the intracellular localization of LanCL2, not EGFR, was associated with the grade of gliomas. Conclusions Taken together, amplification and mRNA overexpression of LANCL2 and EGFR, and their co-amplification and co-expression were frequent in glioblastoma patients. Our findings suggest that CNVs of LANCL2 and EGFR were the independent diagnostic and prognostic biomarkers for histological glioblastoma patients, but not for IDH1/2-wild-type glioblastoma patients.

scholarly journals MPC-08 CLINICOPATHOLOGICAL ANALYSIS OF 12P GAIN IN INTRACRANIAL GERM CELL TUMORS

2019 ◽  
Vol 1 (Supplement_2) ◽  
pp. ii23-ii23
Author(s):  
Kaishi Satomi ◽  
Hirokazu Takami ◽  
Shintaro Fukushima ◽  
Yoichi Nakazato ◽  
Shota Tanaka ◽  
...  
Keyword(s):  
Germ Cell ◽  
Germ Cell Tumor ◽  
Copy Number ◽  
Mature Teratoma ◽  
Methylation Status ◽  
Germ Cell Tumors ◽  
Copy Number Variations ◽  
Cell Tumor ◽  
Testicular Germ Cell ◽  
Intracranial Germ Cell Tumor

Abstract BACKGROUND Gain of short arm of chromosome 12 (12p) is commonly observed in testicular germ cell tumors (tGCTs). 12p gain is also frequently seen in intracranial GCTs (iGCTs). However, little is known about the clinical significance of 12p gain in iGCTs. MATERIALS AND METHODS We have collected over 200 fresh frozen tissue samples of iGCTs through the Intracranial Germ Cell Tumor Genome Analysis Consortium in Japan. Firstly, we analyzed DNA methylation status in 83 iGCTs, 3 seminomas and 6 normal control samples using Infinium Human Methylation 450K BeadChip array (Illumina, CA). Idat files were processed using R (Version 3.5.3) and minfi package (1.30.0) to generate copy number variations. Compared with average genome-wide copy number level, 12p gain was determined. Then, 58 iGCTs with clinicopathological information were analyzed for progression-free survival (PFS) and overall survival (OS). Those tumors that consist of only either germinoma and/or mature teratoma components were classified as Favorable Histology (FH) and all the others that contains malignant histological components were classified as Unfavorable Histology (UFH). RESULT 12p gain was observed in 100% (3/3) of seminoma, 13.6% (3/22) of germinoma, 16.7% (1/6) of mature teratoma, 25% (1/4) of immature teratoma, 55% (11/20) of mixed germ cell tumor, 100% (4/4) of yolk sac tumor, 100% (1/1) of embryonal carcinoma, and 100% (1/1) of choriocarcinoma. In total, 44.6% (37/83) of iGCT showed 12p gain. Regarding histological classification, the 12p gain rate in UFH (72%, 18/25) was significantly higher than that in FH (12.1%, 4/33, P&lt;0.01). Both PFS and OS were significantly worse in iGCTs with 12p gain (PFS: P=0.027, OS: P=0.0012). DISCUSSION 12p gain can be a molecular marker to predict prognosis and histological malignancy in iGCTs.

UTX, a Histone Demethylase, Is Inactivated through Homozygous Deletion, Mutation, and DNA Methylation in Multiple Myeloma.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1798-1798
Author(s):  
Brian A Walker ◽  
Paola E. Leone ◽  
Nicholas J Dickens ◽  
Kevin D Boyd ◽  
David Gonzalez ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cell Lines ◽  
Copy Number ◽  
Conflicts Of Interest ◽  
Cpg Island ◽  
Chromatin Condensation ◽  
Methylation Status ◽  
Significant Proportion ◽  
Histone Demethylase ◽  
Homozygous Deletions

Abstract Abstract 1798 Poster Board I-824 Histone modifications are known to mediate transcriptional regulation through changes in chromatin condensation and as such can lead to aberrant transcriptional patterns resulting in malignant transformation. Modulation of chromatin structure via histone modification is becoming recognised as an important pathogenic mechanism in myeloma and has been suggested by the over-expression of MMSET, a histone methyltransferase, by the t(4;14) chromosomal rearrangement. More recently inactivation of UTX, a histone demethylase, has also been suggested to have a role in myeloma pathogenesis and both UTX and MMSET are mediators of transcriptional repression. UTX is inactivated in a number of different cancer cell lines but importantly, mutations and deletions have been detected in myeloma cell lines and we wished to follow up on this observation in uniformly treated clinical cases. UTX is a large gene found on the X chromosome covering 240 kb of genomic DNA and consists of 29 exons encoding a protein with both JmjC-domains and tricopeptide repeats responsible for histone demethylation and polycomb protein interactions. Inactivation of UTX occurs through deletions of individual exons through to large whole gene deletions as well as by mutations scattered throughout the 29 exons. A further mechanism of UTX inactivation which has not been looked for to date is via DNA methylation of the CpG island upstream of the transcriptional start site. We set out to determine the status of UTX in our dataset which includes expression, mapping, and methylation array data from presenting myeloma samples entered into the MRC Myeloma IX clinical trial. The gene expression of UTX was measured on 272 samples using Affymetrix U133 Plus 2.0 arrays and showed that 80% of samples do not express UTX transcripts but using expression quartile analysis we could not detect an effect on overall survival. The mechanism underlying the abrogation of expression was investigated further using the Affymetrix 500K SNP mapping array on a subset of 114 samples to detect copy number alterations. UTX was hemizygously deleted in 21 (42%) female samples and was completely deleted in 1 male sample, at the resolution of the arrays. In order to determine if individual exons were deleted, at a resolution below that detectable by mapping arrays, we performed quantitative PCR coupled with high resolution melting (HRM) analysis using the Rotor-gene Q real-time cycler (Qiagen). Exons were amplified, over 40 cycles, to obtain products of ∼200 bp using LC Green Plus mastermix (Idaho Technologies) in a 10 μl reaction on the Rotor-gene Q with a final HRM step from 72-95 °C with increments of 0.1 °C. Amplification plots combined with the HRM step allows us to identify both homozygous deletions and mutations within the exons. We screened all 114 samples for micro-deletions and mutations and found homozygous deletions in ∼7% of samples and identified a significant proportion of mutations using the HRM method which accounted for a total of ∼10% of gene inactivation. In order to determine if methylation could be responsible for inactivation of the remaining allele we used the Illumina Infinium humanmethylation27 array to study the methylation status at the UTX locus. This array interrogates 27,578 highly informative CpG sites per sample at the single-nucleotide resolution using bisulfite converted DNA. The results of this analysis are presented as an average beta-score where 1.0 is fully methylated and 0 is fully unmethylated. Samples were analyzed using Illumina GenomeStudio and the custom differential methylation algorithm. In samples with a diploid copy number of UTX the methylation signals covered 2 ranges: hemi-methylated (0.35-0.55, n=7) and hyper-methylated (0.73-0.89, n=14). In samples with 1 copy of UTX, which includes all males, there were 3 ranges: hypomethylated (0.08-0.21, n=5), hemi-methylated (0.35-0.51, n=3), and hypermethylated (0.66-0.88, n=48). All of the hypomethylated samples with a single copy of UTX were male, and at least 1 of these samples contained an inactivating exonic deletion resulting in complete loss of function. These data indicate that methylation of the residual allele contributes significantly to the inactivation of UTX along with interstitial deletions and mutations. We will go on to present data on the interaction of UTX with variation at the UTY locus and how this modulates behaviour of the myeloma clone. Disclosures No relevant conflicts of interest to declare.

Quantitation of DNA methylation and copy number variations by targeted sequencing of retrotransposon.

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. e23139-e23139
Author(s):  
Jeffrey Buis ◽  
Tom Goodman ◽  
Julie Kim ◽  
Adele Kruger ◽  
Brendan Tarrier ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Copy Number ◽  
Copy Number Variations ◽  
Targeted Sequencing

Rapid Diagnosis of Imprinting Disorders Involving Copy Number Variation and Uniparental Disomy Using Genome-Wide SNP Microarrays

2015 ◽  
Vol 146 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Weiqiang Liu ◽  
Rui Zhang ◽  
Jun Wei ◽  
Huimin Zhang ◽  
Guojiu Yu ◽  
...  
Keyword(s):  
Copy Number ◽  
Snp Array ◽  
Uniparental Disomy ◽  
Copy Number Variations ◽  
Chromosomal Microarray ◽  
Chromosomal Microarray Analysis ◽  
Imprinting Disorders ◽  
Genome Wide ◽  
Number Variation ◽  
Efficient Alternative

Imprinting disorders, such as Beckwith-Wiedemann syndrome (BWS), Prader-Willi syndrome (PWS) and Angelman syndrome (AS), can be detected via methylation analysis, methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA), or other methods. In this study, we applied single nucleotide polymorphism (SNP)-based chromosomal microarray analysis to detect copy number variations (CNVs) and uniparental disomy (UPD) events in patients with suspected imprinting disorders. Of 4 patients, 2 had a 5.25-Mb microdeletion in the 15q11.2q13.2 region, 1 had a 38.4-Mb mosaic UPD in the 11p15.4 region, and 1 had a 60-Mb detectable UPD between regions 14q13.2 and 14q32.13. Although the 14q32.2 region was classified as normal by SNP array for the 14q13 UPD patient, it turned out to be a heterodisomic UPD by short tandem repeat marker analysis. MS-MLPA analysis was performed to validate the variations. In conclusion, SNP-based microarray is an efficient alternative method for quickly and precisely diagnosing PWS, AS, BWS, and other imprinted gene-associated disorders when considering aberrations due to CNVs and most types of UPD.

scholarly journals GENE-22. GENOME-WIDE METHYLATION PROFILING OF GLIOBLASTOMA EXTRACELLULAR VESICLE DNA ALLOWS TUMOR CLASSIFICATION

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi102-vi102
Author(s):  
Franz Ricklefs ◽  
Cecile Maire ◽  
Katharina Kolbe ◽  
Mareike Holz ◽  
Manfred Westphal ◽  
...  
Keyword(s):  
Copy Number ◽  
Methylation Status ◽  
Extracellular Vesicle ◽  
Copy Number Variations ◽  
Tumor Classification ◽  
Cns Tumors ◽  
Original Tumor ◽  
Genome Wide ◽  
Potential Biomarker ◽  
Methylation Profiling

Abstract BACKGROUND Genome-wide methylation profiling has recently been developed into a tool that allows subtype tumor classification in central nervous system (CNS) tumors. Extracellular vesicles (EVs) are released by CNS tumor cells and contain high molecular weight tumor DNA, rendering EVs a potential biomarker source to identify tumor subgroups, stratify patients and monitor therapy by liquid biopsy. We investigated whether the DNA in glioma-derived EVs reflects genome-wide tumor methylation profiles and allows tumor subtype classification. METHODS DNA was isolated from EVs secreted by cultured glioma stem-like cells (GSC) as well as from the cells of origin and from the original tumor samples (n=3 patients). EVs were classified by nanoparticle analysis (NTA), immunoblotting, imaging flow cytometry (IFCM), multiplex EV assays and electron microscopy. Genome-wide DNA methylation profiling was performed using an 850k Illumina EPIC array and results were classified according to the DKFZ brain tumor classifier. RESULTS The size range of GSC-derived EVs was 120–150 nm, as measured by NTA. The majority of secreted EVs exhibited high expression of common EV markers (i.e. CD9, CD63 and CD81), as characterized by IFCM and multiplex EV assays. Genome-wide methylation profiling of GSC-derived EVs correctly identified the methylation class of the original tumor, including information on the IDH mutation status and subclass classification (RTK1, RTK2). In addition, copy number alterations and the MGMT metyhlation status matched the pattern of the parental GSCs and original tumor samples. CONCLUSION EV DNA faithfully reflects the tumor methylation class as well as the MGMT methylation status and copy number variations present in the parental cells and the original tumor. Methylation profiling of circulating tumor EV DNA could become a useful tool to detect and classify CNS tumors.

scholarly journals Laparoscopic Adrenalectomy for Potentially Malignant Adrenal Tumors Greater than 5 Centimeters

2006 ◽  
Vol 91 (8) ◽  
pp. 3080-3083 ◽  
Author(s):  
Chun-Hou Liao ◽  
Shih-Chieh Chueh ◽  
Ming-Kuen Lai ◽  
Po-Jen Hsiao ◽  
Jun Chen
Keyword(s):  
Tumor Size ◽  
Laparoscopic Adrenalectomy ◽  
Malignant Tumors ◽  
Adrenal Tumors ◽  
Benign Tumors ◽  
Conversion To Open Surgery ◽  
Open Conversion ◽  
Potentially Malignant ◽  
Adrenocortical Carcinomas

Abstract Purpose: Laparoscopic adrenalectomy (LA) is controversial for large, potentially malignant tumors. We report a series of LA or hand-assisted LA for large (&gt;5 cm) adrenal tumors. Patients and Methods: Among 210 LAs performed in 6 yr, 39 patients had potentially malignant tumors greater than 5 cm in diameter. Their perioperative and follow-up data were retrospectively analyzed. Results: All 39 patients had successful LAs without perioperative mortality, conversion to open surgery, or capsular disruption during dissection. The mean tumor size was 6.2 cm (range, 5–12 cm), operative time 207 min (115–315 min), and blood loss 75 ml (minimal–1400 ml). Complications included one intraoperative diaphragmatic perforation, three mild wound infections, and one pneumonia. Preoperatively there were 27 nonfunctioning tumors, seven pheochromocytomas, three cortisol-secreting tumors, and two virilizing tumors. Final pathology revealed eight malignant (four adrenocortical carcinomas and four metastatic carcinomas) and 31 benign tumors (14 cortical adenomas, eight pheochromocytomas, six myelolipomas, and three ganglioneuromas). Median follow-up was 39 months. Four patients (two adrenocortical carcinomas, one metastatic hepatoma, and one lymphoma) died 24, 10, 9, and 3 months after surgery, respectively. A hand-assisted device was used in 10 patients. Only the tumor size was larger and length of postoperative hospital stay longer for those in the hand-assisted group. Conclusions: LA is a reasonable option for selected large adrenal tumors when complete resection is technically feasible and there is no evidence of local invasion. Hand-assisted LA is a good alternative to open conversion if a difficult dissection is encountered intraoperatively.

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