Losses at chromosome 4q are associated with poor survival in operable ductal pancreatic adenocarcinoma

Luebke, Andreas M.; Baudis, Michael; Matthaei, Hanno; Vashist, Yogesh K.; Verde, Pablo Emilio; Hosch, Stefan B.; Erbersdobler, Andreas; Izbicki, Jakob R.; Knoefel, Wolfram Trudo; Stoecklein, NH

doi:10.1016/j.pan.2011.11.001

Cited by 9 publications

(8 citation statements)

References 44 publications

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“…25 A high number of chromosomal imbalances and losses of 4q are involved in the progression of multiple myeloma, 26 hepatocellular carcinoma, 27 and pancreatic adenocarcinoma. 28 Thus, the association of RASSF6 silencing with 4q loss warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

Liang

Zheng

et al. 2014

Cell Cycle

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Section: Discussionmentioning

confidence: 99%

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

Liang

Zheng

et al. 2014

Cell Cycle

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“…In parallel, several studies have found an association between specific cytogenetic profiles identified by interphase fluorescence in situ hybridization (iFISH) and/or high-density single-nucleotide polymorphism (SNP) arrays and prognostic features of PDAC [13,[38][39][40][41]. Thus, alterations of chromosomes 4, 7, 9q34 17q, and 20, in the absence of abnormalities involving chromosome 18q, including specific (numerical) alterations of chromosomes 4, 7, and 9q34 [11] and gains/amplification of chromosome 8q24, 17q, and 20q, have all been associated with more extended and disseminated disease at diagnosis and/or a poorer patient outcome [8,11,13,[41][42][43].…”

Section: Molecular Heterogeneity Of Pdac 21 Genomic Signatures Of Pdac Cells Associated With Patient Outcomementioning

confidence: 99%

Genomic Heterogeneity of Pancreatic Ductal Adenocarcinoma and Its Clinical Impact

Gutiérrez

Muñoz‐Bellvís

Órfão

2021

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer death due to limited advances in recent years in early diagnosis and personalized therapy capable of overcoming tumor resistance to chemotherapy. In the last decades, significant advances have been achieved in the identification of recurrent genetic and molecular alterations of PDAC including those involving the KRAS, CDKN2A, SMAD4, and TP53 driver genes. Despite these common genetic traits, PDAC are highly heterogeneous tumors at both the inter- and intra-tumoral genomic level, which might contribute to distinct tumor behavior and response to therapy, with variable patient outcomes. Despite this, genetic and genomic data on PDAC has had a limited impact on the clinical management of patients. Integration of genomic data for classification of PDAC into clinically defined entities—i.e., classical vs. squamous subtypes of PDAC—leading to different treatment approaches has the potential for significantly improving patient outcomes. In this review, we summarize current knowledge about the most relevant genomic subtypes of PDAC including the impact of distinct patterns of intra-tumoral genomic heterogeneity on the classification and clinical and therapeutic management of PDAC.

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“…HELQ gene is located in 4q where genetic alterations frequently happened in oral squamous cell carcinoma [94], hepatocellular carcinoma [95], ductal pancreatic adenocarcinoma [96], and gastric cancer [97]. In ovarian cancer, deletion of 4q21 is the most common genetic alteration, detected in 54% of ovarian carcinoma [98].…”

Section: Helq and Cancermentioning

confidence: 99%

HELQ in cancer and reproduction

Han¹,

Zhao²,

Li³

2016

neo

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Helicase POLQ-like (HELQ), an ATP-dependent 3'-5' DNA helicase, plays pivotal roles in DNA processing, such as DNA replication, recombination and repair. The recent discovery of HELQ in mouse model and human cancer cell reveal that genetic alteration of HELQ is involved in cancer susceptibility and subfertility. Here we review the origin, function and mechanisms of HELQ in maintaining genomic stability. Furthermore, we also summarize the known roles of HELQ in human carcinogenesis and reproduction. Importantly, we review that HELQ releases DNA replication block at interstrand cross-linking sites in cellular tolerance to cross-linking agents during DNA repair process. It may provide new avenues to develop novel therapies for enhancing efficacy of conventional chemotherapy.

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Losses at chromosome 4q are associated with poor survival in operable ductal pancreatic adenocarcinoma

Cited by 9 publications

References 44 publications

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

Genomic Heterogeneity of Pancreatic Ductal Adenocarcinoma and Its Clinical Impact

HELQ in cancer and reproduction

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Losses at chromosome 4q are associated with poor survival in operable ductal pancreatic adenocarcinoma

Cited by 9 publications

References 44 publications

RASSF6promotes p21Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

RASSF6promotes p21Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

Genomic Heterogeneity of Pancreatic Ductal Adenocarcinoma and Its Clinical Impact

HELQ in cancer and reproduction

Contact Info

Product

Resources

About

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma

RASSF6promotes p21^Cip1/Waf1-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma