| 31. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Cytotoxic treatment of adrenocortical carcinoma.
- 2001
-
In: World journal of surgery. - : Springer Science and Business Media LLC. - 0364-2313 .- 1432-2323. ; 25:7, s. 927-33
-
Journal article (peer-reviewed)abstract
- Adrenocortical carcinoma (ACC) is a rare, aggressive tumor that is often detected in an advanced stage. Medical treatment with the adrenotoxic drug mitotane has been used for decades, but critical prospective trials on its role in residual disease or as an adjuvant agent after surgical resection are still lacking. The concept of a critical threshold plasma level of the drug must be confirmed in controlled studies. Because individual responsiveness cannot be predicted, the use mitotane is still advised for nonresectable disease. In case of cortisol or other steroid overproduction, several drugs (e.g., ketoconazole or aminoglutethimide) may be used. Chemotherapy with single agents (e.g., doxorubicin or cisplatin) have been disappointing, with low response rates (< 30%) and a short response duration. Part of this refractoriness may be explained by the fact that ACC tumors express the multidrug-resistance gene MDR-1. Chemotherapy with multiple agents has been tested in smaller series and has resulted in significant side effects. The best results were achieved by the combination of etoposide, doxorubicin, and cisplatin associated with mitotane, achieving a response rate of 54%, including individual complete responses. To be able to make progress in treating advanced ACC disease, adjuvant multicenter trials must be encouraged. When mitotane-based therapies are used, monitored drug levels are mandatory.
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| 32. |
- Ahlman, Håkan, 1947, et al.
(author)
-
En "ny" tumörmarkör.
- 1996
-
In: Klinisk Kemi i Norden, 8.. - Göteborg. ; , s. 45-52
-
Book chapter (other academic/artistic)
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| 33. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Growth regulation in carcinoid tumors.
- 1993
-
In: Endocrinology and metabolism clinics of North America. - 0889-8529. ; 22:4, s. 889-915
-
Research review (peer-reviewed)abstract
- In hormone-producing tumors such as the carcinoids, overproduction of certain hormones may activate proto-oncogenes. Hormones, or growth factors, thus can be of importance for growth regulation. Information is presented on some growth factors and their receptors in this respect and on the involvement of gastrin and its receptor on tumor development in the experimental Mastomys model. The relevance of differential expression of cell adhesion molecules in endocrine tumors is discussed also.
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| 34. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Interventional treatment of gastrointestinal neuroendocrine tumours.
- 2000
-
In: Digestion. - 0012-2823. ; 62 Suppl 1, s. 59-68
-
Journal article (peer-reviewed)abstract
- Neuroendocrine (NE) tumours of the gastrointestinal tract (carcinoids and endocrine pancreatic tumours) are rare diseases. In the presence of liver metastases these patients may suffer from disabling symptoms due to hormone overproduction. Patients with localized disease can be resected for cure and also patients with liver metastases can undergo potentially curative tumour resection. However, long-term follow-up of the latter cases indicates frequent recurrence of tumour. Using close biochemical monitoring of tumour markers combined with newer techniques for tumour visualization, these recurrences can often be diagnosed at an early stage so that repeat surgical procedures can be performed. During the last years very active surgery has been recommended for NE tumours, many of which have a relatively slow growth. Even in patients not amenable to curative liver surgery, debulking can be considered if the main tumour burden can be safely excised. The primary aim of this type of treatment is palliation of hormonal symptoms. An important question is whether the aggressive treatment actually prolongs survival. No prospective studies have been performed. Such studies are hampered by the lack of strict surgical programs running over long periods and the relative rarity of NE tumours. Liver transplantation may be another treatment modality in selected cases.
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| 35. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Interventional treatment of the carcinoid syndrome
- 2004
-
In: Neuroendocrinology. - 0028-3835. ; 80 Suppl 1, s. 67-73
-
Journal article (peer-reviewed)abstract
- Liver metastases imply a major problem in patients with carcinoid tumours and hormone overproduction. Patients with distant metastases can undergo resection for potential cure or for symptom palliation. In patients with bilobar liver metastases other interventions are at hand, e.g. local ablation or hepatic arterial embolization. In selected cases liver transplantation can be a treatment alternative. Prior to all interventions patients with midgut carcinoids are protected with somatostatin analogues to reduce hormone secretion. Patients with foregut carcinoids may present special problems with life-threatening release of histamine during interventions.
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| 36. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Liver transplantation for treatment of metastatic neuroendocrine tumors
- 2004
-
In: Annals of the New York Academy of Sciences. - 0077-8923. ; 1014, s. 265-9
-
Journal article (peer-reviewed)abstract
- Liver transplantation can be considered a therapeutic option for patients with neuroendocrine tumors only metastatic to the liver. Important selection criteria are well-differentiated tumors and a low proliferation rate (Ki67 <10%). In this series, orthopic liver transplantation offered good relief of symptoms and long disease-free intervals with initial survival of grafts and patients as in benign disease. The experience with multivisceral transplantation is still limited.
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| 37. |
|
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| 38. |
- Ahlman, Håkan, 1947, et al.
(author)
-
Neuroendocrine insights from the laboratory to the clinic.
- 1996
-
In: American journal of surgery. - 0002-9610. ; 172:1, s. 61-7
-
Journal article (peer-reviewed)abstract
- The interaction between adrenergic nerves and enterochromaffin (EC) cells was studied in health and disease using animal models and patients with the midgut carcinoid syndrome.
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| 39. |
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| 40. |
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