Albumin and alpha-fetoprotein gene expression in various nonhepatic rat tissues.

Nahon, Jean‐Louis; Tratner, Isabelle; Poliard, Anne; Presse, Françoise; Poiret, Maryse; Gál, A.; Sala‐Trepat, José M.; Legrès, Luc; Feldmann, Gérard; Bernuau, Dominique

doi:10.1016/s0021-9258(18)37976-6

Cited by 71 publications

(8 citation statements)

References 45 publications

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“…We confirmed by histology and CK-19/Hep Par 1 IHC that the pulmonary lesions were primary lung adenocarcinomas, not metastatic HCC (Supplementary Figure S4). Notably, low levels of albumin expression exist in the alveolar cells of adult lungs per the Human Protein Atlas and are also well reported in fetal lung tissues [63]. Therefore, the observed lung lesions likely represent breakthrough Cre expression in this organ.…”

Section: Kras G12d Activation In Combination With Homozygous Bap1 Deletion Results In Development Of Iccmentioning

confidence: 72%

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

Marcus

Ferri-Borgogno

Hosein

et al. 2021

Cancers

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Intrahepatic cholangiocarcinoma (ICC) is a primary biliary malignancy that harbors a dismal prognosis. Oncogenic mutations of KRAS and loss-of-function mutations of BRCA1-associated protein 1 (BAP1) have been identified as recurrent somatic alterations in ICC. However, an autochthonous genetically engineered mouse model of ICC that genocopies the co-occurrence of these mutations has never been developed. By crossing Albumin-Cre mice bearing conditional alleles of mutant Kras and/or floxed Bap1, Cre-mediated recombination within the liver was induced. Mice with hepatic expression of mutant KrasG12D alone (KA), bi-allelic loss of hepatic Bap1 (BhomoA), and heterozygous loss of Bap1 in conjunction with mutant KrasG12D expression (BhetKA) developed primary hepatocellular carcinoma (HCC), but no discernible ICC. In contrast, mice with homozygous loss of Bap1 in conjunction with mutant KrasG12D expression (BhomoKA) developed discrete foci of HCC and ICC. Further, the median survival of BhomoKA mice was significantly shorter at 24 weeks when compared to the median survival of ≥40 weeks in BhetKA mice and approximately 50 weeks in BhomoA and KA mice (p < 0.001). Microarray analysis performed on liver tissue from KA and BhomoKA mice identified differentially expressed genes in the setting of BAP1 loss and suggests that deregulation of ferroptosis might be one mechanism by which loss of BAP1 cooperates with oncogenic Ras in hepato-biliary carcinogenesis. Our autochthonous model provides an in vivo platform to further study this lethal class of neoplasm.

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Section: Kras G12d Activation In Combination With Homozygous Bap1 Deletion Results In Development Of Iccmentioning

confidence: 72%

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

Marcus

Ferri-Borgogno

Hosein

et al. 2021

Cancers

View full text Add to dashboard Cite

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“…Tissue hypoxia and activation of anaerobic glycolysis induce acidosis and release Cu 2+ ions from copper-containing proteins, such as ceruloplasmin (1). In the presence of reducing agents, e.g., ascorbic acid, Cu 2+ is reduced to Cu + (2), followed by the formation of superoxide anion O − 2 (3)(4). Superoxide dismutase (SOD) catalyzes the dismutation of superoxide O − 2 to hydrogen peroxide H 2 O 2 (5), which, in the presence of Cu 2+ , undergoes the Fenton reaction with the formation of hydroxyl radicals ⋅ OH (6).…”

Section: Methods For Measuring імаmentioning

confidence: 99%

“…Albumin is synthesized in the liver at a rate of 10-12 g/day, accounting for about 25% of total proteins [3]. In addition, smaller amounts of albumin can be produced in extrahepatic tissues, such as kidneys, pancreas, intestines, lymph, mammary glands, reproductive tissues, and brain [4][5][6]. This multifunctional globular protein has a molecular weight of approximately 66-69,000 Dа, with minor variations among species.…”

Section: Introductionmentioning

confidence: 99%

Ischemia-Modified Albumin: Origins and Clinical Implications

et al. 2021

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Albumin is one of the most abundant proteins in the body of mammals: about 40% of its pool is located in the intravascular space and the remainder is found in the interstitial space. The content of this multifunctional protein in blood is about 60-65% of total plasma proteins. A decrease in its synthesis or changes of functional activity can destabilize oncotic blood pressure, cause a violation of transporting hormones, fatty acids, metals, and drugs. Albumin properties change under ischemic attacks associated with oxidative stress, production of reactive oxygen species, and acidosis. Under these conditions, ischemia-modified albumin (IMA) is generated that has a reduced metal-binding capacity, especially for transition metals, such as copper, nickel, and cobalt. The method of determining the cobalt-binding capability of HSA was initially proposed to evaluate IMA level and then licensed as an ACB test for routine clinical analysis for myocardial ischemia. Subsequent studies have shown the viability of the ACB test in diagnosing other diseases associated with the development of oxidative stress. This review examines recent data on IMA generation mechanisms, describes principles, advantages, and limitations of methods for evaluation of IMA levels, and provides detailed analysis of its use in diagnostic and monitoring therapeutic efficacy in different diseases.

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“…The copyright holder for this preprint this version posted October 13, 2021. ; https://doi.org/10.1101/2021.10.12.464103 doi: bioRxiv preprint confirmed by histology and CK-19 / Hep Par 1 IHC that the pulmonary lesions were primary lung adenocarcinomas, not metastatic HCC (Supplementary Figure 4). Notably, low levels of Albumin expression exists in the alveolar cells of adult lung per the Human Protein Atlas, and is also well reported in fetal lung tissues [58]. Therefore, the observed lung lesions likely represent breakthrough Cre expression in this organ.…”

Section: Genotypementioning

confidence: 73%

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

Marcus

Ferri-Borgogno

Hosein

et al. 2021

Preprint

View full text Add to dashboard Cite

Intrahepatic cholangiocarcinoma (ICC) is a primary biliary malignancy that harbors a dismal prognosis. Oncogenic mutations of KRAS and loss of function mutations of BRCA1-associated protein 1 (BAP1) have been identified as recurrent somatic alterations in ICC. However, an autochthonous genetically engineered mouse model of ICC that genocopies the co-occurrence of these mutations has never been developed. By crossing Albumin-Cre mice bearing conditional alleles of mutant Kras and/or floxed Bap1, Cre-mediated recombination within the liver was induced. Mice with hepatic expression of mutant KrasG12D alone (KA), bi-allelic loss of hepatic Bap1 (BhomoA), and heterozygous loss of Bap1 in conjunction with mutant KrasG12D expression (BhetKA) developed primary hepatocellular carcinoma (HCC), but no discernible ICC. In contrast, mice with homozygous loss of Bap1 in conjunction with mutant KrasG12D expression (BhomoKA) devel-oped discrete foci of HCC and ICC. Further, the median survival of BhomoKA mice was significantly shorter at 24 weeks, when compared to median survival of ≥40 weeks in BhetKA mice and approximately 50 weeks in BhomoA and KA mice (p <0.001). Microarray analysis performed on liver tissue from KA and BhomoKA mice identified differentially expressed genes in the setting of BAP1 loss and suggests that deregulation of ferroptosis might be one mechanism by which loss of BAP1 cooperates with oncogenic Ras in hepato-biliary carcinogenesis. Our autochthonous model provides an in vivo platform to further study this lethal class of neoplasm.

show abstract

Albumin and alpha-fetoprotein gene expression in various nonhepatic rat tissues.

Cited by 71 publications

References 45 publications

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

Ischemia-Modified Albumin: Origins and Clinical Implications

Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma

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