bluuebunny/crossref_metadata_2025_split huggingface dataset:
The first Triassic lungfish from South America (Santa Maria Formation, Paraná Basin) and its bearing on geological correlations within Pangaea
Authors: Richter M. , Toledo C. E. V. 
Published: June 2008

Abstract

The Triassic fish faunas of the Southern Hemisphere are only known from a few sedimentary basins and the most productive sites are those from the Karoo Supergroup, in South Africa and the Sydney Basin of Australia. A single lungfish tooth plate ascribed to
Ptychoceratodus
cf.
philippsi
was recovered from Late Triassic (Carnian) red beds of southern Brazil and is described herein. This find extends to South America the palaeogeographic distribution of the genus, which occurs in the Early Triassic of Australia and South Africa and the Middle/Late Triassic of Europe and Late Triassic of Madagascar and India. The presence of this dipnoan solely in the uppermost part of the Santa Maria Formation suggests that the migration of
Ptychoceratodus
towards the Paraná Basin began not before the late Induan/early Olenekian (late Early Triassic). At that time, more humid (monsoonal) conditions prevailed in what is now southern Brazil, compared to semi-arid/desert conditions that dominated the Late Permian and possibly the earliest Early Triassic (the latter presumably not represented in the Paraná Basin).
Diversity and biogeography patterns of Late Jurassic neoselachians (Chondrichthyes: Elasmobranchii)
Authors: Kriwet Jürgen , Klug Stefanie 
Published: June 2008

Abstract
The regional diversity and biogeographic patterns of Late Jurassic neoselachians at genus level in Europe were analysed based on samples and an extensive literature survey of about 40 localities ranging from the Oxfordian to Tithonian. The simple completeness metric (SCM) displays a quite good fossil record of neoselachians in the Late Jurassic with a peak in the Kimmeridgian. The origination, extinction, diversification and turnover rates were calculated for every stage and indicate that background origination occurred in the Oxfordian and Kimmeridgian with no disappearance of genera. In the Tithonian, background extinction is the main factor for neoselachian diversity decline. The decline in neoselachian diversity at the end of the Jurassic is most probably related to reduced habitats in the course of major regression events, establishment of physical barriers, and climatic changes. Faunal assemblages are quite uniform and mostly agree well with the contemporaneous palaeogeographic situation. Our analyses indicate that both vicariance and dispersal were important processes in the biogeographic pattern of Late Jurassic neoselachians.
The varasichthyid and other crossognathiform fishes, and the Break-up of Pangaea
Authors: Arratia Gloria 
Published: June 2008

Abstract

Crossognathiforms have been traditionally considered typical marine Cretaceous forms widely represented in the Northern Hemisphere and by a few members in Brazil. During the last 30 years they have been interpreted as Teleostei
incertae sedis
, clupeocephalans or a non-monophyletic group. New evidence indicates that the Oxfordian taxon
Chongichthys
(previously considered a Teleostei
incertae sedis
or a clupeocephalan), the Late Jurassic family Varasichthyidae (interpreted as basal teleosts), and the crossognathoids and pachyrhizodontoids form a clade here recognized as the Crossognathiformes. Varasichthyids are the sister group of a clade including
Chongichthys
(at the base) and crossognathoids+pachyrhizodontoids. The Crossognathiformes (including Varasichthyidae and
Chongichthys
) are basal teleosts placed between the Late Jurassic basal genera
Tharsis
and
Ascalabos
in one tree or between
Ascalabos
and the ichthyodectiforms in the second tree. The position of elopomorphs as the most basal extant teleosts is confirmed. A new interpretation of the phylogenetic position of the clade [
Humbertia
+[
Erichalcis
+[
Leptolepides
+
Orthogonikleithrum
]]], at the base of clupeocephalans, is suggested.

The presence of the Late Jurassic varasichthyids (e.g.
Domeykos
) in South America (Chile) and Central America (Cuba;
Luisichthys
), and
Chongichthys
(Chile), and of the Late Jurassic genera
Ascalabos
and
Tharsis
and the ichthyodectiforms (e.g.
Allothrissops
) in Europe (e.g. Germany) allows the proposal of a sister-area relationship between Chile and Cuba, which was the sister area of Germany during the Late Jurassic. The Late Jurassic connection between the Palaeopacific (Chilean region) and the Tethys Sea (southern Germany) was through the newly formed Central Atlantic Ocean (Cuban region) as a result of the break up of Pangaea and separation of North America, South America and Africa.
Hybodont sharks from the lower Cretaceous Khok Kruat Formation of Thailand, and hybodont diversity during the Early Cretaceous
Authors: Cuny G. , Suteethorn V. , Kamha S. , Buffetaut E. 
Published: June 2008

Abstract

Isolated teeth of five hybodont species are described from the Khok Kruat Formation (Aptian):
Hybodus aequitridentatus
nov. sp.,
Heteroptychodus steinmanni
,
Thaiodus ruchae, Khoratodus foreyi
nov. gen. et nov. sp., and
Acrorhizodus khoratensis
. A new family, Thaiodontidae is also erected for
Thaiodus
and
Khoratodus.
Two species are recognized inside the genus
Heteroptychodus, H. steinmanni
and
H. chuvalovi
nov. comb. These sharks show a wide range of diet and many of them appear to be restricted to a freshwater environment and thus are probably endemic to the Khorat Plateau. However,
Thaiodus
and
Heteroptychodus
are also found in deltaic and/or marine environments outside Thailand, but are nevertheless restricted to the Asian continent. It seems that the appearance of three different palaeobiogeographical provinces (Europe, Asia and Africa–South America) around the Tethys during the Early Cretaceous led to the highest diversity at the generic level in the history of hybodont sharks.
A new species of
Placidichthys
(Halecomorphi: Ionoscopiformes) from the Lower Cretaceous Marizal Formation, northeastern Brazil, with a review of the biogeographical distribution of the Ophiopsidae
Authors: Brito Paulo M. , Alvarado‐Ortega Jesús 
Published: June 2008

Abstract

A new halecomorph fish is described from the Early Cretaceous Marizal Formation of Tucano Basin. This new material is identified as a new species of
Placidichthys, P. tucanensis
sp. nov. based on the absence of an anal fin, the lower number of flank scales in the caudal region, the slender shape of the body, and body proportions.
Placidichthys tucanensis
sp. nov. increases the distribution and diversity of ophiopsids in the western part of the Tethys Sea, being distributed along the epicontinental seas of Gondwana.

Placidichthys
is considered the sister-taxon of the exclusively Cretaceous taxa
Teoichthys
+
Macrepistius
from the western Tethys. These groups show a discernible geographical distribution pattern with
Placidichthys
known only from the Southern margin of the Tethys region (South America), whilst
Teoichthys
and
Macrepistius
are known only from North America and possibly Europe.
Cancer Suppression at Old Age
Authors: Harding Charles , Pompei Francesco , Lee Ellen E. , Wilson Richard 
Published: June 2008

Abstract
Increased age is regularly linked with heightened cancer risk, but recent research suggests a flattening around age 80. We report that, independent of cancer site or time period, most incidence rates decrease in the more elderly and drop to or toward zero near the ceiling of human life span. For all major organ sites, male and female, we use 1979 to 2003 Surveillance, Epidemiology, and End Results registry records (8–26% of the U.S. population) to construct three sequential cross-sections at 10-year intervals, totaling 129 sets of age-specific cancer data. To compute incidence rates, we estimate older populations at risk with census counts and NIH life tables. This article provides both a minimal and a more comprehensive extension of Surveillance, Epidemiology, and End Results cancer rates to those above 85. Almost all cancers peak at age ∼80. Generally, it seems that centenarians are asymptomatic or untargeted by cancers. We suggest that the best available justification for this pattern of incidence is a link between increased senescence and decreased proliferative potential among cancers. Then, thus far, as senescence may be a carcinogen, it might also be considered an anticarcinogen in the elderly. We model rising and falling incidence rates with a β curve obtained by appending a linearly decreasing factor to the well-known Armitage-Doll multistage model of cancer. Taken at face value, the β model implies that medical, diet, or lifestyle interventions restricting carcinogenesis ought to be examined for possible effects on longevity. [Cancer Res 2008;68(11):4465–78]
The Roles of Human Sucrose Nonfermenting Protein 2 Homologue in the Tumor-Promoting Functions of Rsf-1
Authors: Sheu Jim Jinn-Chyuan , Choi Jung Hye , Yildiz Isil , Tsai Fuu-Jen , Shaul Yosef , Wang Tian-Li , Shih Ie-Ming 
Published: June 2008

Abstract
Rsf-1 interacts with human sucrose nonfermenting protein 2 homologue (hSNF2H) to form a chromatin remodeling complex that participates in several biological processes. We have previously shown that Rsf-1 gene amplification was associated with the most aggressive type of ovarian cancer and cancer cells with Rsf-1 overexpression depended on Rsf-1 to survive. In this report, we determine if formation of the Rsf-1/hSNF2H complex could be one of the mechanisms contributing to tumor cell survival and growth in ovarian carcinomas. Based on immunohistochemistry, we found that Rsf-1 and hSNF2H were co-upregulated in ovarian cancer tissues. Ectopic expression of Rsf-1 in SKOV3 ovarian cancer cells with undetectable endogenous Rsf-1 expression enhanced hSNF2H protein levels and promoted SKOV3 tumor growth in a mouse xenograft model. Our studies also indicated that induction of Rsf-1 expression affected the molecular partnership of hSNF2H and translocated hSNF2H into nuclei where it colocalized with Rsf-1. Furthermore, analysis of Rsf-1 deletion mutants showed that the Rsf-D4 fragment contained the hSNF2H binding site based on coimmunoprecipitation and in vitro competition assays. As compared with other truncated mutants, expression of Rsf-D4 resulted in remarkable growth inhibition in ovarian cancer cells with Rsf-1 gene amplification and overexpression, but not in those without detectable Rsf-1 expression. The above findings suggest that interaction between Rsf-1 and hSNF2H may define a survival signal in those tumors overexpressing Rsf-1. [Cancer Res 2008;68(11):4050–7]
Unraveling the Mystery of Erythropoietin-Stimulating Agents in Cancer Promotion
Authors: May Kelly A. , Khuri Fadlo R. 
Published: June 2008

Abstract
Erythropoietin-stimulating agents (ESA) are approved for use in treating chemotherapy-induced anemia in patients with nonmyeloid malignancies. However, recent clinical trials have shown evidence of inferior overall survival and/or locoregional control of tumors in patients receiving ESAs. Given these concerning data, current studies are focused on elucidating the biological mechanisms by which ESAs may contribute to cancer promotion. Evidence suggests that ESAs activate several signaling pathways that are important in altering tumor behavior and response to treatment. Although further research is needed to more precisely elucidate these mechanisms, caution should be exercised in the use of ESAs beyond their approved indication in cancer patients. [Cancer Res 2008;68(11):4013–7]
Inhibition of STAT3Tyr705 Phosphorylation by Smad4 Suppresses Transforming Growth Factor β–Mediated Invasion and Metastasis in Pancreatic Cancer Cells
Authors: Zhao Shujie , Venkatasubbarao Kolaparthi , Lazor Jillian W. , Sperry Jane , Jin Changqing , Cao Lin , Freeman James W. 
Published: June 2008

Abstract
The role of Smad4 in transforming growth factor β (TGFβ)–mediated epithelial-mesenchymal transition (EMT), invasion, and metastasis was investigated using isogenically matched pancreatic cancer cell lines that differed only in expression of Smad4. Cells expressing Smad4 showed an enhanced TGFβ-mediated EMT as determined by increased expression of vimentin and decreased expression of β-catenin and E-cadherin. TGFβ-mediated invasion was suppressed in Smad4-intact cells as determined by in vitro assays, and these cells showed a reduced metastasis in an orthotopic model of pancreatic cancer. Interestingly, TGFβ inhibited STAT3Tyr705 phosphorylation in Smad4-intact cells. The decrease in STAT3Tyr705 phosphorylation was linked to a TGFβ/Smad4-dependent and enhanced activation of extracellular signal-regulated kinases, which caused an increase in serine phosphorylation of STAT3Ser727. Down-regulating signal transducer and activator of transcription 3 (STAT3) expression by short hairpin RNA in Smad4-deficient cells prevented TGFβ-induced invasion. Conversely, expressing a constitutively activated form of STAT3 (STAT3-C) in Smad4-intact cells enhanced invasion. This study indicates the requirement of STAT3 activity for TGFβ-induced invasion in pancreatic cancer cells and implicates Smad4-dependent signaling in regulating STAT3 activity. These findings further suggest that loss of Smad4, leading to aberrant activation of STAT3, contributes to the switch of TGFβ from a tumor-suppressive to a tumor-promoting pathway in pancreatic cancer. [Cancer Res 2008;68(11):4221–8]
Retinoblastoma Function Is Essential for Establishing Lung Epithelial Quiescence after Injury
Authors: Mason-Richie Nicole A. , Mistry Meenakshi J. , Gettler Caitlin A. , Elayyadi Asmaa , Wikenheiser-Brokamp Kathryn A. 
Published: June 2008

AbstractThe retinoblastoma gene product (RB) regulates cell cycle, quiescence, and survival in a cell type–dependent and environment-dependent manner. RB function is critical in the pulmonary epithelium, as evidenced by nearly universal RB inactivation in lung cancer and increased lung cancer risk in persons with germline RB gene mutations. Lung carcinomas occur in the context of epithelial remodeling induced by cytotoxic damage. Whereas the role of RB in development and normal organ homeostasis has been extensively studied, RB function in the context of cellular injury and repair has remained largely unexplored. In the current studies, the RB gene was selectively deleted in the respiratory epithelium of the mouse. Although RB was not required for establishing or maintaining quiescence during lung homeostasis, RB was essential for establishing quiescence during epithelial repair after injury. Notably, aberrant cell cycle progression was sustained for 9 months after injury in RB-deficient lungs. Prenatal and postnatal RB ablation had similar effects, providing evidence that timing of RB loss was not critical to the outcome and that the injury-induced phenotype was not secondary to compensatory alterations occurring during development. These data show that RB is essential for repair of the respiratory epithelium after cytotoxic damage and support a critical unique role for RB in the context of epithelial remodeling after injury. Because human cancers are associated with chronic cellular damage, these findings have important new implications for RB-mediated tumor suppression. [Cancer Res 2008;68(11):4068–76]
MetMAb, the One-Armed 5D5 Anti-c-Met Antibody, Inhibits Orthotopic Pancreatic Tumor Growth and Improves Survival
Authors: Jin Hongkui , Yang Renhui , Zheng Zhong , Romero Mally , Ross Jed , Bou-Reslan Hani , Carano Richard A.D. , Kasman Ian , Mai Elaine , Young Judy , Zha Jiping , Zhang Zemin , Ross Sarajane , Schwall Ralph , Colbern Gail , Merchant Mark 
Published: June 2008

Abstract
The hepatocyte growth factor (HGF) and its receptor, c-Met, have been implicated in driving proliferation, invasion, and poor prognosis in pancreatic cancer. Here, we investigated the expression of HGF and c-Met in primary pancreatic cancers and described in vitro and in vivo models in which MetMAb, a monovalent antibody against c-Met, was evaluated. First, expression of HGF and MET mRNA was analyzed in 59 primary pancreatic cancers and 51 normal samples, showing that both factors are highly expressed in pancreatic cancer. We next examined HGF responsiveness in pancreatic cancer lines to select lines that proliferate in response to HGF. Based on these studies, two lines were selected for further in vivo model development: BxPC-3 (c-Met+, HGF−) and KP4 (c-Met+, HGF+) cells. As BxPC-3 cells are responsive to exogenous HGF, s.c. tumor xenografts were grown in a paracrine manner with purified human HGF provided by osmotic pumps, wherein MetMAb treatment significantly inhibited tumor growth. KP4 cells are autocrine for HGF and c-Met, and MetMAb strongly inhibited s.c. tumor growth. To better model pancreatic cancer and to enable long-term survival studies, an orthotopic model of KP4 was established. MetMAb significantly inhibited orthotopic KP4 tumor growth in 4-week studies monitored by ultrasound and also improved survival in 90-day studies. MetMAb significantly reduced c-Met phosphorylation in orthotopic KP4 tumors with a concomitant decrease in Ki-67 staining. These data suggest that the HGF/c-Met axis plays an important role in the progression of pancreatic cancer and that targeting c-Met therein may have therapeutic value. [Cancer Res 2008;68(11):4360–8]
Dual-Specificity Phosphatase 1 Ubiquitination in Extracellular Signal-Regulated Kinase–Mediated Control of Growth in Human Hepatocellular Carcinoma
Authors: Calvisi Diego F. , Pinna Federico , Meloni Floriana , Ladu Sara , Pellegrino Rossella , Sini Marcella , Daino Lucia , Simile Maria M. , De Miglio Maria R. , Virdis Patrizia , Frau Maddalena , Tomasi Maria L. , Seddaiu Maria A. , Muroni Maria R. , Feo Francesco , Pascale Rosa M. 
Published: June 2008

Abstract
Sustained activation of extracellular signal-regulated kinase (ERK) has been detected previously in numerous tumors in the absence of RAS-activating mutations. However, the molecular mechanisms responsible for ERK-unrestrained activity independent of RAS mutations remain unknown. Here, we evaluated the effects of the functional interactions of ERK proteins with dual-specificity phosphatase 1 (DUSP1), a specific inhibitor of ERK, and S-phase kinase-associated protein 2 (SKP2)/CDC28 protein kinase 1b (CKS1) ubiquitin ligase complex in human hepatocellular carcinoma (HCC). Levels of DUSP1, as assessed by real-time reverse transcription–PCR and Western blot analysis, were significantly higher in tumors with better prognosis (as defined by the length of patients' survival) when compared with both normal and nontumorous surrounding livers, whereas DUSP1 protein expression sharply declined in all HCC with poorer prognosis. In the latter HCC subtype, DUSP1 inactivation was due to either ERK/SKP2/CKS1-dependent ubiquitination or promoter hypermethylation associated with loss of heterozygosity at the DUSP1 locus. Noticeably, expression levels of DUSP1 inversely correlated with those of activated ERK, as well as with proliferation index and microvessel density, and directly with apoptosis and survival rate. Subsequent functional studies revealed that DUSP1 reactivation led to suppression of ERK, CKS1, and SKP2 activity, inhibition of proliferation and induction of apoptosis in human hepatoma cell lines. Taken together, the present data indicate that ERK achieves unrestrained activity during HCC progression by triggering ubiquitin-mediated proteolysis of its specific inhibitor DUSP1. Thus, DUSP1 may represent a valuable prognostic marker and ERK, CKS1, or SKP2 potential therapeutic targets for human HCC. [Cancer Res 2008;68(11):4192–200]
Polo-like Kinase 3 Functions as a Tumor Suppressor and Is a Negative Regulator of Hypoxia-Inducible Factor-1α under Hypoxic Conditions
Authors: Yang Yali , Bai Jingxiang , Shen Rulong , Brown Sharron A.N. , Komissarova Elena , Huang Ying , Jiang Ning , Alberts Gregory F. , Costa Max , Lu Luo , Winkles Jeffrey A. , Dai Wei 
Published: June 2008

Abstract
Polo-like kinase 3 (Plk3) is an important mediator of the cellular responses to genotoxic stresses. In this study, we examined the physiologic function of Plk3 by generating Plk3-deficient mice. Plk3−/− mice displayed an increase in weight and developed tumors in various organs at advanced age. Many tumors in Plk3−/− mice were large in size, exhibiting enhanced angiogenesis. Plk3−/− mouse embryonic fibroblasts were hypersensitive to the induction of hypoxia-inducible factor-1α (HIF-1α) under hypoxic conditions or by nickel and cobalt ion treatments. Ectopic expression of the Plk3-kinase domain (Plk3-KD), but not its Polo-box domain or a Plk3-KD mutant, suppressed the nuclear accumulation of HIF-1α induced by nickel or cobalt ions. Moreover, hypoxia-induced HIF-1α expression was tightly associated with a significant down-regulation of Plk3 expression in HeLa cells. Given the importance of HIF-1α in mediating the activation of the “survival machinery” in cancer cells, these studies strongly suggest that enhanced tumorigenesis in Plk3-null mice is at least partially mediated by a deregulated HIF-1 pathway. [Cancer Res 2008;68(11):4077–85]
Laforin Confers Cancer Resistance to Energy Deprivation–Induced Apoptosis
Authors: Wang Yin , Liu Yan , Wu Cindy , McNally Beth , Liu Yang , Zheng Pan 
Published: June 2008

Abstract
A long-standing but poorly understood observation in experimental cancer therapy is the heterogeneity in cancer susceptibility to energy deprivation. Here, we show that the hexose kinase inhibitor 2-deoxyglucose (2-dG) preferentially kills cancer cells with defective laforin expression and significantly increases the survival of mice with aggressive lymphoma due to a genetic defect of the laforin-encoding Epm2a gene. Normal cells from Epm2a−/− mice also had greatly increased susceptibility to 2-dG. Thus, laforin is a novel regulator for cellular response to energy deprivation and its defects in cancer cells may be targeted for cancer therapy. [Cancer Res 2008;68(11):4039–43]
Identification of 6-Benzylthioinosine as a Myeloid Leukemia Differentiation–Inducing Compound
Authors: Wald David N. , Vermaat Hanna M. , Zang Shaolei , Lavik Andrew , Kang Zizhen , Peleg Gil , Gerson Stanton L. , Bunting Kevin D. , Agarwal Munna L. , Roth Bryan L. , Tse William 
Published: June 2008

Abstract
As the pathophysiology of acute myelogenous leukemia (AML) involves a block of myeloid maturation, a desirable therapeutic strategy is to induce leukemic cell maturation to increase the efficacy and to avoid the side effects of traditional chemotherapeutics. Through a compound library screen, 6-benzylthioinosine (6BT) was identified as a promising differentiation-inducing agent. 6BT induces monocytic differentiation of myeloid leukemia cell lines such as HL-60 and OCI-AML3, as well as primary patient samples as evidenced by morphology, immunophenotyping, and nitroblue tetrazolium reduction. Not only can 6BT induce differentiation but a subset of AML cell lines such as MV4-11 and HNT34 instead undergo 6BT-mediated cell death. Despite inducing cell death in some leukemic cells, 6BT exhibits extremely low toxicity on several nonmalignant cells such as fibroblasts, normal bone marrow, and endothelial cells. This toxicity profile may relate to the function of 6BT as an inhibitor of the nucleoside transporter, ent1, which is thought to prevent it from entering many cell types. In contrast, 6BT likely enters at least some leukemic cell lines as shown by its requirement for phosphorylation for its differentiation activity. 6BT is also able to synergize with currently used myeloid differentiation agents such as ATRA and decitabine. Early studies indicate that the mechanism of action of this compound may involve ATP depletion that leads to growth inhibition and subsequent differentiation. Besides in vitro activity, 6BT also shows the ability to impair HL-60 and MV4-11 tumor growth in nude mice. 6BT is a promising new monocytic differentiation agent with apparent leukemic cell–specific activity. [Cancer Res 2008;68(11):4369–76]