The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Uwe Haberkorn - One of the best experts on this subject based on the ideXlab platform.
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Angiopoietin-2 Overexpression in Morris hepatoma Results in Increased Tumor Perfusion and Induction of Critical Angiogenesis-Promoting Genes
2013Co-Authors: Pierre Kunz, Johannes Hoffend, Annette Altmann, Dirk Koczan, Walter Mier, Michael Eisenhut, Antonia Dimitrakopoulou-strauss, Gabriel A. Bonaterra, Thomas J. Dengler, Uwe HaberkornAbstract:Monitoring of angiogenesis-relevant approaches with functional imaging and histomorphometric analyses is desirable to evaluate the biologic effects. In this study we wished to examine the complex effects of angiopoietin-2 (Ang-2) gene transfer in a rat hepatoma model. Methods: Using a bicistronic retroviral vector for Ang-2, Morris hepatoma (MH3924A) cell lines with Ang-2 expression were generated (Ang-2-MH3924A). In human umbilical vein endothelial cells (HUVECs) cocultured with Ang-2-MH3924A, the proliferative action with or without growth factors were determined. Furthermore, animal experiments were performed to measure effects on tumor growth and perfusion. Finally, tumors were examined by immunohistochemistry and DNA chip analysis. Results: Ang-22expressing MH3924A enhanced basic fibroblast growth factor2mediated endothelial cell proliferation. Perfusion, as measured by H
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Troponin I Overexpression Inhibits Tumor Growth, Perfusion, and Vascularization of Morris hepatoma
2013Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H 15 2 O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N9,N99,N999-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis
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troponin i overexpression inhibits tumor growth perfusion and vascularization of Morris hepatoma
The Journal of Nuclear Medicine, 2006Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H215O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N′,N′′,N′′′-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis, proliferation, and gene array analyses were performed. Results: Apoptosis of HUVECs was increased and proliferation was decreased after coculture with TnI-MH3924A cells. TnI-MH3924A tumors showed a significant inhibition of growth (90%) and a decreased perfusion (25%), whereas blood volume remained unchanged. MRI investigations demonstrated a significant decrease of the rate constant kep. Immunohistochemical analyses showed decreased microvessel density and proliferation and significant induction of apoptosis. Furthermore, TnI-expressing hepatomas demonstrated changes in the expression of genes related to angiogenesis, apoptosis, signal transduction, or stress. Conclusion: TnI regulates tumor growth by modulating vascularization including apoptosis induction and decrease of proliferation. In addition, changes in expression of genes associated with angiogenesis, apoptosis, signal transduction, or stress were found. The upregulation of angiogenesis and stress-related genes indicates a cross-talk of different mechanisms as part of the tumor9s reaction to TnI. Because the decrease of vascularization led to lower perfusion values as measured by PET and MRI, these noninvasive methods are promising tools for the monitoring of antiangiogenic gene therapy.
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Apoptosis and changes in glucose transport early after treatment of Morris hepatoma with gemcitabine
European Journal of Nuclear Medicine, 2001Co-Authors: Uwe Haberkorn, Annette Altmann, Matthias E. Bellemann, Gunnar Brix, Huse Kamencic, Iris Morr, Ulrike Traut, Josef Doll, Johannes Blatter, Ralf KinscherfAbstract:Apoptosis has been described as an energy-consuming process. This combined in vivo/in vitro study investigated the effects of the antineoplastic agent gemcitabine on tumour metabolism and on the induction of apoptosis. Dynamic positron emission tomography (PET) measurements of fluorine-18 fluorodeoxyglucose (FDG) uptake were done in rats bearing Morris hepatoma prior to and after therapy with 90 mg gemcitabine/kg b.w. Furthermore, thymidine (TdR) incorporation into the DNA of these tumours was determined. In vitro measurements of FDG and TdR uptake were performed immediately and 24 h after the end of gemcitabine treatment, and the amount of apoptotic cells was determined using the TUNEL reaction. In vivo an increase in FDG transport and phosphorylation occurred early after gemcitabine treatment, although TdR incorporation into the DNA of the tumours declined. In vitro, an enhanced glucose transport, an increase in TdR uptake in the cytoplasm and a decrease in TdR incorporation in the nucleic acid fraction early after treatment occurred. Inhibition of glucose transport caused an increase in the amount of apoptotic cells. The increase in glucose uptake and TdR metabolism early after therapy is interpreted as a stress reaction of the tumour cells, protecting the cells from apoptosis during this early period after exposure to cytotoxic drugs like gemcitabine.
Ralf Kinscherf - One of the best experts on this subject based on the ideXlab platform.
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Troponin I Overexpression Inhibits Tumor Growth, Perfusion, and Vascularization of Morris hepatoma
2013Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H 15 2 O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N9,N99,N999-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis
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troponin i overexpression inhibits tumor growth perfusion and vascularization of Morris hepatoma
The Journal of Nuclear Medicine, 2006Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H215O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N′,N′′,N′′′-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis, proliferation, and gene array analyses were performed. Results: Apoptosis of HUVECs was increased and proliferation was decreased after coculture with TnI-MH3924A cells. TnI-MH3924A tumors showed a significant inhibition of growth (90%) and a decreased perfusion (25%), whereas blood volume remained unchanged. MRI investigations demonstrated a significant decrease of the rate constant kep. Immunohistochemical analyses showed decreased microvessel density and proliferation and significant induction of apoptosis. Furthermore, TnI-expressing hepatomas demonstrated changes in the expression of genes related to angiogenesis, apoptosis, signal transduction, or stress. Conclusion: TnI regulates tumor growth by modulating vascularization including apoptosis induction and decrease of proliferation. In addition, changes in expression of genes associated with angiogenesis, apoptosis, signal transduction, or stress were found. The upregulation of angiogenesis and stress-related genes indicates a cross-talk of different mechanisms as part of the tumor9s reaction to TnI. Because the decrease of vascularization led to lower perfusion values as measured by PET and MRI, these noninvasive methods are promising tools for the monitoring of antiangiogenic gene therapy.
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Apoptosis and changes in glucose transport early after treatment of Morris hepatoma with gemcitabine
European Journal of Nuclear Medicine, 2001Co-Authors: Uwe Haberkorn, Annette Altmann, Matthias E. Bellemann, Gunnar Brix, Huse Kamencic, Iris Morr, Ulrike Traut, Josef Doll, Johannes Blatter, Ralf KinscherfAbstract:Apoptosis has been described as an energy-consuming process. This combined in vivo/in vitro study investigated the effects of the antineoplastic agent gemcitabine on tumour metabolism and on the induction of apoptosis. Dynamic positron emission tomography (PET) measurements of fluorine-18 fluorodeoxyglucose (FDG) uptake were done in rats bearing Morris hepatoma prior to and after therapy with 90 mg gemcitabine/kg b.w. Furthermore, thymidine (TdR) incorporation into the DNA of these tumours was determined. In vitro measurements of FDG and TdR uptake were performed immediately and 24 h after the end of gemcitabine treatment, and the amount of apoptotic cells was determined using the TUNEL reaction. In vivo an increase in FDG transport and phosphorylation occurred early after gemcitabine treatment, although TdR incorporation into the DNA of the tumours declined. In vitro, an enhanced glucose transport, an increase in TdR uptake in the cytoplasm and a decrease in TdR incorporation in the nucleic acid fraction early after treatment occurred. Inhibition of glucose transport caused an increase in the amount of apoptotic cells. The increase in glucose uptake and TdR metabolism early after therapy is interpreted as a stress reaction of the tumour cells, protecting the cells from apoptosis during this early period after exposure to cytotoxic drugs like gemcitabine.
Annette Altmann - One of the best experts on this subject based on the ideXlab platform.
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Angiopoietin-2 Overexpression in Morris hepatoma Results in Increased Tumor Perfusion and Induction of Critical Angiogenesis-Promoting Genes
2013Co-Authors: Pierre Kunz, Johannes Hoffend, Annette Altmann, Dirk Koczan, Walter Mier, Michael Eisenhut, Antonia Dimitrakopoulou-strauss, Gabriel A. Bonaterra, Thomas J. Dengler, Uwe HaberkornAbstract:Monitoring of angiogenesis-relevant approaches with functional imaging and histomorphometric analyses is desirable to evaluate the biologic effects. In this study we wished to examine the complex effects of angiopoietin-2 (Ang-2) gene transfer in a rat hepatoma model. Methods: Using a bicistronic retroviral vector for Ang-2, Morris hepatoma (MH3924A) cell lines with Ang-2 expression were generated (Ang-2-MH3924A). In human umbilical vein endothelial cells (HUVECs) cocultured with Ang-2-MH3924A, the proliferative action with or without growth factors were determined. Furthermore, animal experiments were performed to measure effects on tumor growth and perfusion. Finally, tumors were examined by immunohistochemistry and DNA chip analysis. Results: Ang-22expressing MH3924A enhanced basic fibroblast growth factor2mediated endothelial cell proliferation. Perfusion, as measured by H
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Troponin I Overexpression Inhibits Tumor Growth, Perfusion, and Vascularization of Morris hepatoma
2013Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H 15 2 O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N9,N99,N999-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis
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troponin i overexpression inhibits tumor growth perfusion and vascularization of Morris hepatoma
The Journal of Nuclear Medicine, 2006Co-Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Fabian Kiessling, Ludwig Strauss, Dirk Koczan, Walter Mier, Michael Eisenhut, Ralf Kinscherf, Uwe HaberkornAbstract:Antiangiogenic gene transfer inhibiting growth of new blood vessels is a promising approach in cancer therapy. Human troponin I (TnI) efficiently inhibits endothelial cell proliferation, migration, as well as angiogenesis and tumor growth in vivo. However, little is known about its effects on perfusion and tumor biology. Methods: Stable Morris hepatoma (MH3924A) cells overexpressing human TnI (TnI-MH3924A) were cocultured with human umbilical vein endothelial cells (HUVECs) followed by measurements of endothelial apoptosis and proliferation. Furthermore, tumor growth and perfusion were determined using H215O and 68Ga-DOTA-albumin (DOTA is 1,4,7,10-tetraazacyclododecane-N,N′,N′′,N′′′-tetraacetic acid) PET as well as functional MRI. Additionally, histologic measurements of vascularization, apoptosis, proliferation, and gene array analyses were performed. Results: Apoptosis of HUVECs was increased and proliferation was decreased after coculture with TnI-MH3924A cells. TnI-MH3924A tumors showed a significant inhibition of growth (90%) and a decreased perfusion (25%), whereas blood volume remained unchanged. MRI investigations demonstrated a significant decrease of the rate constant kep. Immunohistochemical analyses showed decreased microvessel density and proliferation and significant induction of apoptosis. Furthermore, TnI-expressing hepatomas demonstrated changes in the expression of genes related to angiogenesis, apoptosis, signal transduction, or stress. Conclusion: TnI regulates tumor growth by modulating vascularization including apoptosis induction and decrease of proliferation. In addition, changes in expression of genes associated with angiogenesis, apoptosis, signal transduction, or stress were found. The upregulation of angiogenesis and stress-related genes indicates a cross-talk of different mechanisms as part of the tumor9s reaction to TnI. Because the decrease of vascularization led to lower perfusion values as measured by PET and MRI, these noninvasive methods are promising tools for the monitoring of antiangiogenic gene therapy.
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Apoptosis and changes in glucose transport early after treatment of Morris hepatoma with gemcitabine
European Journal of Nuclear Medicine, 2001Co-Authors: Uwe Haberkorn, Annette Altmann, Matthias E. Bellemann, Gunnar Brix, Huse Kamencic, Iris Morr, Ulrike Traut, Josef Doll, Johannes Blatter, Ralf KinscherfAbstract:Apoptosis has been described as an energy-consuming process. This combined in vivo/in vitro study investigated the effects of the antineoplastic agent gemcitabine on tumour metabolism and on the induction of apoptosis. Dynamic positron emission tomography (PET) measurements of fluorine-18 fluorodeoxyglucose (FDG) uptake were done in rats bearing Morris hepatoma prior to and after therapy with 90 mg gemcitabine/kg b.w. Furthermore, thymidine (TdR) incorporation into the DNA of these tumours was determined. In vitro measurements of FDG and TdR uptake were performed immediately and 24 h after the end of gemcitabine treatment, and the amount of apoptotic cells was determined using the TUNEL reaction. In vivo an increase in FDG transport and phosphorylation occurred early after gemcitabine treatment, although TdR incorporation into the DNA of the tumours declined. In vitro, an enhanced glucose transport, an increase in TdR uptake in the cytoplasm and a decrease in TdR incorporation in the nucleic acid fraction early after treatment occurred. Inhibition of glucose transport caused an increase in the amount of apoptotic cells. The increase in glucose uptake and TdR metabolism early after therapy is interpreted as a stress reaction of the tumour cells, protecting the cells from apoptosis during this early period after exposure to cytotoxic drugs like gemcitabine.
Catherine J Field - One of the best experts on this subject based on the ideXlab platform.
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reduced splenocyte metabolism and immune function in rats implanted with the Morris hepatoma 7777
Metabolism-clinical and Experimental, 1996Co-Authors: Leann D Shewchuk, Vickie E Baracos, Catherine J FieldAbstract:Although the immune system is important in antitumor defense, little is known about the immune response during progressive tumor growth. Sprague-Dawley rats (171 ± 3 g) of the Buffalo strain were implanted with the Morris hepatoma 7777 ([MH 7777] a poorly differentiated, rapidly growing tumor) and killed either 2 (T2) or 3 (T3) weeks postimplantation when the tumor weighed 3.0 ± 0.4 and 14 ± 1 g, respectively. Splenocytes were isolated and their phenotypes, metabolism (metabolite production from glucose and glutamine), proliferative response ([3H]thymidine incorporation in response to polyclonal mitogens), and natural killer (NK) cytotoxicity (lysis of YAC-1 cells) were determined. Five rats were killed with the T2 group to serve as non-tumor-bearing controls (T0). Food intake and nontumor body weight decreased (P < .01) 14 days after tumor implantation. There was a progressive decrease (T3 < T2 < T0) in splenic mitogen responses (P < .05) and plasma essential and nonessential amino acid concentrations (P < .05). Compared with T0, NK cytotoxic activity was significantly (P < .05) lower at T2 and higher at T3. The presence of the tumor at both T2 and T3 resulted in lower production of metabolites from glucose and glutamine by splenocytes. The proportion of CD8+ cells was lower (P < .05) and the proportion of B cells and macrophages higher (P < .05) in spleens from tumor-bearing rats. In conclusion, the presence of even a small tumor burden (1.4% of body weight) significantly altered the host's immune function and metabolism. A larger tumor burden (6% of body weight) increased NK cytotoxic activity and further reduced cell-mediated immune function.
Djuro Josic - One of the best experts on this subject based on the ideXlab platform.
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mass spectrometry based analysis of rat liver and hepatocellular carcinoma Morris hepatoma 7777 plasma membrane proteome
Analytical Chemistry, 2013Co-Authors: Lulu Cao, Werner Reutter, James Clifton, Djuro JosicAbstract:The gel-based proteomic analysis of plasma membranes from rat liver and chemically induced, malignant hepatocellular carcinoma Morris hepatoma 7777 was systematically optimized to yield the maximum number of proteins containing transmembrane domains (TMDs). Incorporation of plasma membrane proteins into a polyacrylamide "tube gel" followed by in-gel digestion of "tube gel" pieces significantly improved detection by electrospray ionization-liquid chromatography-tandem mass spectrometry. Removal of less hydrophobic proteins by washing isolated plasma membranes with 0.1 M sodium carbonate enables detection of a higher number of hydrophobic proteins containing TMDs in both tissues. Subsequent treatment of plasma membranes by a proteolytic enzyme (trypsin) causes the loss of some of the proteins that are detected after washing with sodium carbonate, but it enables the detection of other hydrophobic proteins containing TMDs. Introduction of mass spectrometers with higher sensitivity, higher mass resolution and mass accuracy, and a faster scan rate significantly improved detection of membrane proteins, but the improved sample preparation is still useful and enables detection of additional hydrophobic proteins. Proteolytic predigestion of plasma membranes enables detection of additional hydrophobic proteins and better sequence coverage of TMD-containing proteins in plasma membranes from both tissues.
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Mass Spectrometry-Based Analysis of Rat Liver and Hepatocellular Carcinoma Morris hepatoma 7777 Plasma Membrane Proteome
2013Co-Authors: Lulu Cao, Werner Reutter, James G. Clifton, Djuro JosicAbstract:The gel-based proteomic analysis of plasma membranes from rat liver and chemically induced, malignant hepatocellular carcinoma Morris hepatoma 7777 was systematically optimized to yield the maximum number of proteins containing transmembrane domains (TMDs). Incorporation of plasma membrane proteins into a polyacrylamide “tube gel” followed by in-gel digestion of “tube gel” pieces significantly improved detection by electrospray ionization–liquid chromatography–tandem mass spectrometry. Removal of less hydrophobic proteins by washing isolated plasma membranes with 0.1 M sodium carbonate enables detection of a higher number of hydrophobic proteins containing TMDs in both tissues. Subsequent treatment of plasma membranes by a proteolytic enzyme (trypsin) causes the loss of some of the proteins that are detected after washing with sodium carbonate, but it enables the detection of other hydrophobic proteins containing TMDs. Introduction of mass spectrometers with higher sensitivity, higher mass resolution and mass accuracy, and a faster scan rate significantly improved detection of membrane proteins, but the improved sample preparation is still useful and enables detection of additional hydrophobic proteins. Proteolytic predigestion of plasma membranes enables detection of additional hydrophobic proteins and better sequence coverage of TMD-containing proteins in plasma membranes from both tissues
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Comparative proteomics of rat liver and Morris hepatoma 7777 plasma membranes.
Journal of Chromatography B, 2006Co-Authors: James Clifton, Werner Reutter, Douglas C. Hixson, Djuro JosicAbstract:Plasma membranes from normal rat liver and hepatocellular carcinoma Morris hepatoma 7777 were selectively solubilized by use of different reagents. After selective solubilization, proteins were identified by nano-HPLC-electrospray ionization tandem mass spectrometry (LC-ESI MS/MS). Using simple software, the patterns of proteins identified in membrane solubilizates from liver and hepatoma were compared. Proteins identified in Morris hepatoma 7777 and not in the corresponding membrane solubilizate from liver, mostly members of the annexin and heat shock protein families, are discussed as potential candidate markers for hepatocellular carcinomas.
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Identification of members of the annexin family in the detergent-insoluble fraction of rat Morris hepatoma plasma membranes.
Journal of chromatography. A, 2006Co-Authors: James Clifton, Werner Reutter, Douglas C. Hixson, Mari Kino Brown, Feilei Huang, Werner Hofmann, Djuro JosicAbstract:Abstract For proteomic analysis, plasma membranes of rat hepatocellular carcinoma Morris hepatoma 7777 were selectively solubilized according to the previously developed method [D. Josic, K. Zeilinger, Methods Enzymol. 271 (1996) 113–134]. If the Triton X100 insoluble pellet is subsequently extracted, several proteins can be solubilized. These proteins can be classified in two groups according to their molecular size. The proteins with apparent molecular weights in SDS-PAGE between 70 and 75 kDa belong to the first group. Smaller proteins, with apparent molecular weights between 30 and 45 kDa, are members of the second group. The main protein of higher molecular weight was also found in the Triton X100 insoluble extract from normal rat liver plasma membranes. This protein was identified as Annexin A6. The proteins from the second group are practically absent in the Triton X100 insoluble extract from rat liver. These proteins are present in relatively high concentrations in plasma membranes of Morris hepatoma 7777. Both groups of detergent-insoluble proteins from Morris hepatoma 7777 were further analyzed with SELDI-TOF and LC electrospray ionization mass spectrometry. From the first group, Annexin A6, together with two other integral plasma membrane proteins, was identified. In the second group of proteins with apparent molecular weights between 30 and 45 kDa, further members of the annexin family, Annexins A1, A2, A4, A5 and A7 were identified. The possible role of these low molecular size annexins as potential cancer biomarkers is discussed.