O Hessman

Publications (7)36.7 Total impact

• Article: Randomized clinical trial comparing open with video-assisted minimally invasive parathyroid surgery for primary hyperparathyroidism.

  O Hessman, J Westerdahl, N Al-Suliman, P Christiansen, P Hellman, A Bergenfelz
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  ABSTRACT: : Previous studies of video-assisted techniques for parathyroidectomy in patients with primary hyperparathyroidism have found similar or better results compared with bilateral neck exploration. The aim of the present study was to compare open minimally invasive parathyroidectomy with the video-assisted technique for primary hyperparathyroidism in a multicentre randomized trial. : Some 143 patients were randomized to open (n = 75) or video-assisted (n = 68) parathyroidectomy after positive sestamibi scintigraphy. There were no differences in preoperative data. The open operation was performed through a 15-mm incision. The video-assisted techniques used were minimally invasive video-assisted parathyroidectomy (MIVAP) or video-assisted parathyroidectomy using the lateral approach (VAPLA). Data were collected prospectively including postoperative pain scoring. : The procedure was significantly quicker for the open compared to the video assisted operations: mean(s.d.) 60(35) versus 84(47) min (P = 0.001). Both groups of patients had similar conversion rates and the same outcome, with comparable incision lengths, low scores for postoperative neck discomfort, high cosmetic satisfaction and low complication rates. : Open minimally invasive parathyroidectomy for primary hyperparathyroidism was quicker than either video-assisted technique. Registration number: NCT00877981 (http://www.clinicaltrials.gov)
  British Journal of Surgery 02/2010; 97(2):177-84. · 4.61 Impact Factor
• Article: Chromosome 18 deletions are common events in classical midgut carcinoid tumors.

  R M Löllgen, O Hessman, E Szabo, G Westin, G Akerström
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  ABSTRACT: Classical midgut carcinoids are rare intestinal neuroendocrine tumors that often present with metastases at diagnosis. In contrast to foregut carcinoids, midgut carcinoids are not related to the multiple endocrine neoplasia type 1 syndrome, and the mechanisms involved in their tumorigenesis are unknown. Eight classical midgut carcinoids were analyzed by genome-wide screening for loss of heterozygosity. Deletions on chromosome 18 were found in 88% of the tumors. DNA sequencing and immunohistochemical staining for Smad4/DPC4, which often is homozygously mutated in pancreatic and colon carcinomas, revealed no aberrations. In 1 tumor, a region telomeric to the Smad4/DPC4/DCC genes at 18q21 was deleted. Other chromosomes were affected in 3 lesions only. The high frequency of chromosome 18 deletions strongly indicates a genetic alteration of importance in classical midgut carcinoid tumorigenesis, apparently not involving the Smad4/DPC4 gene.
  International Journal of Cancer 07/2001; 92(6):812-5. · 5.44 Impact Factor
• Article: Multiple allelic deletions and intratumoral genetic heterogeneity in men1 pancreatic tumors.

  O Hessman, B Skogseid, G Westin, G Akerström
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  ABSTRACT: Multiple endocrine neoplasia type 1 (MEN1) is an inherited syndrome with multiple tumors of the endocrine pancreas, the parathyroid, the pituitary, and other tissues. The MEN1 gene at 11q13 is homozygously mutated in the majority of MEN1 tumors. Here we present a genome-wide loss of heterozygosity (LOH) screening of 23 pancreatic lesions, one duodenal tumor, and one thymic carcinoid from 13 MEN1 patients. Multiple allelic deletions were found. Fractional allelic loss varied from 6-75%, mean 31%. All pancreatic tumors displayed LOH on chromosome 11, whereas the frequency of losses for chromosomes 3, 6, 8, 10, 18, and 21 was over 30%. Different lesions from individual patients had discrepant patterns of LOH. Intratumoral heterogeneity was revealed, with chromosome 6 and 11 deletions in most tumor cells, whereas other chromosomal loci were deleted in portions of the analyzed tumor. Chromosome 6 deletions were mainly found in lesions from patients with malignant features. Fractional allelic loss did not correlate to malignancy or to tumor size. Our findings indicate that MEN1 pancreatic tumors fail to maintain DNA integrity and demonstrate signs of chromosomal instability.
  Journal of Clinical Endocrinology &amp Metabolism 04/2001; 86(3):1355-61. · 6.50 Impact Factor
• Article: Genetic alterations on 3p, 11q13, and 18q in nonfamilial and MEN 1-associated pancreatic endocrine tumors.

  O Hessman, D Lindberg, A Einarsson, P Lillhager, T Carling, L Grimelius, B Eriksson, G Akerström, G Westin, B Skogseid
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  ABSTRACT: Pancreatic endocrine tumors occur sporadically and as part of the multiple endocrine neoplasia type 1 (MEN 1) and von Hippel-Lindau (VHL) syndromes. The MEN1 locus on 11q13 and a candidate tumor suppressor locus on 3p are known to be hemi- or homozygously mutated in a subset of these tumors. Chromosome arm 18q harbors the SMAD4/DPC4 tumor suppressor gene that is frequently deleted and inactivated in tumors of the exocrine pancreas. We have analyzed 22 nonfamilial and 16 MEN 1-associated pancreatic endocrine tumors for loss of heterozygosity (LOH) at 3p, 11q13, and 18q. LOH at 3p was revealed in 45% and 36% of tumors from 31 patients with nonfamilial and MEN 1-associated disease, respectively. The corresponding proportions for 11q13 were 55% and 91%, and for 18q 27% and 25%, respectively. A striking relation between LOH at 11q13 and 3p and a malignant phenotype was found for the nonfamilial tumors. None of the six benign tumors (all of them insulinomas) had allelic loss at 3p or 11q13, whereas 92% (P < 0.01) of the malignant tumors (including malignant insulinomas) had such deletions. Besides the 11q13 abnormality, more than half of the MEN 1-associated tumors had additional genetic lesions affecting 3p or 18q. LOH analysis of several tumors from two MEN 1 patients suggested different clonal origin of the lesions. Sequencing of the SMAD4/DPC4 gene did not identify mutations in coding regions or at exon/intron boundaries in tumors with LOH at 18q. The data indicate involvement of tumor suppressor genes on 3p and 18q, in addition to the MEN1 gene at 11q13, in the tumorigenesis of both nonfamilial and MEN 1-associated pancreatic endocrine tumors.
  Genes Chromosomes and Cancer 12/1999; 26(3):258-64. · 3.31 Impact Factor
• Article: Parathyroid MEN1 gene mutations in relation to clinical characteristics of nonfamilial primary hyperparathyroidism.

  T Carling, P Correa, O Hessman, J Hedberg, B Skogseid, D Lindberg, J Rastad, G Westin, G Akerström
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  ABSTRACT: Biochemical signs and severity of symptoms of primary hyperparathyroidism (pHPT) differ among patients, and little is known of any coupling of clinical characteristics of nonfamilial pHPT to genetic abnormalities in the parathyroid tumors. Mutations in the recently identified MEN1 gene at chromosome 11q13 have been found in parathyroid tumors of nonfamilial pHPT. Using microsatellite analysis for loss of heterozygosity (LOH) at 11q13 and DNA sequencing of coding exons, the MEN1 gene was studied in 49 parathyroid lesions of patients with divergent symptoms, operative findings, histopathological diagnosis, and biochemical signs of nonfamilial pHPT. Allelic loss at 11q13 was detected in 13 tumors, and 6 of them demonstrated previously unrecognized somatic missense and frameshift deletion mutations of the MEN1 gene. Many of the detected mutations would most likely result in a nonfunctional menin protein, consistent with a tumor suppressor mechanism. Clinical and biochemical characteristics of HPT were apparently unrelated to the presence or absence of LOH and the MEN1 gene mutations. However, the demonstration of LOH at 11q13 and MEN1 gene mutations in small parathyroid adenomas of patients with slight hypercalcemia and normal serum PTH levels suggest that altered MEN1 gene function may also be important for the development of mild sporadic pHPT.
  Journal of Clinical Endocrinology &amp Metabolism 09/1998; 83(8):2960-3. · 6.50 Impact Factor
• Source

  Available from: Per Hellman

  Article: Mutation of the multiple endocrine neoplasia type 1 gene in nonfamilial, malignant tumors of the endocrine pancreas.

  O Hessman, D Lindberg, B Skogseid, T Carling, P Hellman, J Rastad, G Akerström, G Westin
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  ABSTRACT: Endocrine pancreatic tumors are rare neoplasms that occur sporadically or as part of a multiple endocrine neoplasia type 1 (MEN1) syndrome. Germ-line mutations of the MEN1 gene, located at 11q13, have been demonstrated in MEN1 kindreds, and loss of heterozygosity (LOH) on 11q13 together with somatic MEN1 mutations have been detected in 20% of nonfamilial parathyroid tumors. Here, we examine 11 non-MEN1 malignant tumors of the endocrine pancreas, 9 nonfunctioning tumors, and 2 glucagonomas. LOH of at least one informative locus on 11q13 was found in 70% of the tumors. Three tumors displayed somatic mutations of the MEN1 gene together with LOH on 11q13, whereas the corresponding germ-line DNA was normal. These findings support the hypothesis that MEN1 gene mutations contribute to the tumorigenesis of nonfamilial, malignant endocrine pancreatic tumors.
  Cancer Research 03/1998; 58(3):377-9. · 7.86 Impact Factor
• Article: Colorectal cancer in patients over 75 years of age--determinants of outcome.

  O Hessman, L Bergkvist, S Ström
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  ABSTRACT: Two hundred and two consecutive patients with colorectal cancer, aged 75 years or older, diagnosed between 1980 and 1990, were followed up from the date of diagnosis until their death or until October 1994. Of these, 194 underwent some type of surgery, in 151 cases elective and in 43 emergency. The peri-operative mortality rate was 10.8% and the overall 5-year survival rate 28%. The ASA score was a predictor for both peri-operative mortality and survival. Peri-operative mortality was significantly increased among patients who had palliative operations, and those with post-operative complications and blood transfusions. Overall survival was worse for patients with absence of blood in the stools or absence of anaemia, for patients who lived in institutions pre-operatively, and for patients with advanced tumour stages. We conclude that the survival rate in elderly patients with colorectal cancer is acceptable after surgery. Old age is not a risk factor per se for peri-operative mortality or poor prognosis, and should not disqualify a person from operation.
  European Journal of Surgical Oncology 03/1997; 23(1):13-9. · 2.50 Impact Factor