Foreword: Chemoradiation for GI cancers

2003 ◽  
Vol 21 (4) ◽  
pp. 221-222
Author(s):  
Tyvin A. Rich
Keyword(s):  
Gi Cancers

scholarly journals PD-4 A phase I trial of trifluridine/tipiracil in combination with nanoliposomal irinotecan in advanced GI cancers

2021 ◽  
Vol 32 ◽  
pp. S200
Author(s):  
O. Alese ◽  
W. Shaib ◽  
M. Akce ◽  
M. Diab ◽  
M. Issa-Boube ◽  
...  
Keyword(s):  
Phase I ◽  
Phase I Trial ◽  
Nanoliposomal Irinotecan ◽  
Gi Cancers

scholarly journals Lysyl Oxidase Mechanisms to Mediate Gastrointestinal Cancer Progression

2020 ◽  
pp. 1-10
Author(s):  
Ahmadshah Farhat ◽  
Gordon A. Ferns ◽  
Korosh Ashrafi ◽  
Mohammad-Hassan Arjmand
Keyword(s):  
Cancer Progression ◽  
Extracellular Enzymes ◽  
Lysyl Oxidase ◽  
Ecm Remodeling ◽  
Complex Process ◽  
High Prevalence ◽  
Different Types ◽  
Fibrotic Diseases ◽  
Gi Cancers ◽  
Improvement In Survival

<b><i>Background:</i></b> Malignancy is a complex process resulting from different changes such as extracellular matrix (ECM) remodeling and stiffness. One of the important enzymes that contribute to ECM remodeling is lysyl oxidase (Lox) that is overexpressed in different types of human cancers. Because of the high prevalence and poor survival of gastrointestinal (GI) malignancies in this review, we discuss the association between Lox activity and the progression of GI cancers. Lox proteins are a group of extracellular enzymes that catalyzed the cross-linking of collagen and elastin, so they have important roles in the control of structure and homeostasis of ECM. Abnormal activation and expression of the Lox family of proteins lead to changes in the ECM toward increased rigidity and fibrosis. Stiffness of ECM can contribute to the pathogenesis of cancers. <b><i>Summary:</i></b> Dysregulation of Lox expression is a factor in both fibrotic diseases and cancer. ECM stiffness by Lox overactivity creates a physical barrier against intratumoral concentration of chemotherapeutic drugs and facilitates cancer inflammation, angiogenesis, and metastasis. <b><i>Key Message:</i></b> Because of the roles of Lox in GI cancers, development targeting Lox protein isotypes may be an appropriate strategy for treatment of GI cancers and improvement in survival of patients.

scholarly journals Younger patients with GI cancers have better disease free survival

2017 ◽  
Vol 47 ◽  
pp. S92
Author(s):  
P.S. d-Safi ◽  
Yassar Qureshi ◽  
Konstantinos Fragkos ◽  
Borzoueh Mohammadi ◽  
Khaled Dawas
Keyword(s):  
Disease Free Survival ◽  
Free Survival ◽  
Younger Patients ◽  
Gi Cancers ◽  
Disease Free

scholarly journals Investigation of an Alternative Marker for Hypermutability Evaluation in Different Tumors

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 197
Author(s):  
Anqi Chen ◽  
Suhua Zhang ◽  
Lei Xiong ◽  
Shihan Xi ◽  
Ruiyang Tao ◽  
...  
Keyword(s):  
Tandem Repeats ◽  
Cell Cancer ◽  
Objective Response ◽  
Hepatocellular Cancer ◽  
The Status ◽  
Promising Treatment ◽  
Gi Cancers ◽  
Tumor Types ◽  
Potential Threshold ◽  
Short Tandem

A growing number of studies have shown immunotherapy to be a promising treatment strategy for several types of cancer. Short tandem repeats (STRs) have been proven to be alternative markers for the evaluation of hypermutability in gastrointestinal (GI) cancers. However, the status of STRs and microsatellite instability (MSI) in other tumors have not yet been investigated. To further compare STR and MSI alterations in different tumors, a total of 407 paired DNAs were analyzed from the following eight tumor types: breast cancer (BC), hepatocellular cancer (HCC), pancreatic cancer (PC), colorectal cancer (CRC), gastric cancer (GC), lung cancer (LC), esophageal cancer (EC), and renal cell cancer (RCC). The STR alteration frequencies varied in different tumors as expected. Interestingly, none of the patients possessed MSI-low (MSI-L) or MSI-high (MSI-H), except for the GI patients. The highest STR alteration was detected in EC (77.78%), followed by CRC (69.77%), HCC (63.33%), GC (54.55%), LC (48.00%), RCC (40.91%), BC (36.11%), and PC (25.71%). The potential cutoff for hypermutability was predicted using the published objective response rate (ORR), and the cutoff of LC and HCC was the same as that of GI cancers (26.32%). The cutoffs of 31.58% and 10.53% should be selected for BC and RCC, respectively. In summary, we compared MSI and STR status in eight tumor types, and predicted the potential threshold for hypermutability of BC, HCC, CRC, GC, LC, EC, and RCC.

Understanding relevant immune mechanisms in gastrointestinal oncology

2021 ◽  
pp. 107815522199286
Author(s):  
Bulent Cetin ◽  
Ozge Gumusay
Keyword(s):  
Checkpoint Inhibitors ◽  
Treatment Options ◽  
Checkpoint Inhibition ◽  
Immune Checkpoint Inhibition ◽  
Gastrointestinal Cancers ◽  
Therapeutic Approaches ◽  
Cancer Treatments ◽  
Multiple Treatment ◽  
Gi Cancers ◽  
The Many

Rapid and successful drug development has resulted in multiple treatment options for gastrointestinal cancer, requiring careful decision making for individual patients. The general theme in modern immunology is that the field is moving beyond establishing the fundamental principles of immune response mechanisms to applying these propositions to understand human diseases and develop new therapies. Immunotherapy has contributed enormously to cancer treatments with a virtual explosion in novel therapeutics including checkpoint inhibitors and other recently developed immunomodulators and the development of novel therapeutic approaches. Although the majority of gastrointestinal (GI) cancers are generally considered poorly immunogenic, clinical trials have revealed that some of the patients with various gastrointestinal cancers are highly responsive to immune checkpoint inhibition-based therapies. We paid special attention to the clinical relevance of immunology and emphasized how newly developed therapies work, including what their strengths and pitfalls are. This review aims to enhance the interest of practitioners in the many specialties and subspecialties that the discipline influences and to assist them in understanding this increasing complexity.

The Clinical Application of Circulating Tumor Cells and DNAs as Prognostic and Predictive Biomarkers in Gastrointestinal Cancer

2021 ◽  
Vol 21 ◽  
Author(s):  
Sara Memarpour ◽  
Ghazaleh Khalili-Tanha ◽  
Awa Alizadeh Ghannad ◽  
Masoud Sharifian Razavi ◽  
Mona Joudi ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Tumor Biology ◽  
Predictive Biomarkers ◽  
Invasive Approach ◽  
New Approach ◽  
Non Invasive ◽  
Gi Cancer ◽  
Gi Cancers ◽  
Tumor Dna

: Gastrointestinal (GI) cancer is one of the most common cancers globally. Genetic and epigenetic mechanisms are involved in its pathogenesis. The conventional methods for diagnosis and screening for GI cancers are often invasive and have other limitations. In the era of personalized medicine, a novel non-invasive approach called liquid biopsy has been introduced for the detection and management of GI cancers, which focuses on the analysis of circulating tumor cells (CTCs) and circulating cell-free tumor DNA (ctDNA). Several studies have shown that this new approach allows for an improved understanding of GI tumor biology and will lead to an improvement in clinical management. The aim of the current review is to explore the clinical applications of CTCs and ctDNA in patients with GI cancer.

scholarly journals KCNQ gene family members act as both tumor suppressors and oncogenes in gastrointestinal cancers

2020 ◽  
Author(s):  
David Shorthouse ◽  
Eric Rahrmann ◽  
Cassandra Kosmidou ◽  
Benedict Greenwood ◽  
Michael W J Hall ◽  
...  
Keyword(s):  
Tumor Suppressors ◽  
Copy Number ◽  
Copy Number Alteration ◽  
Human Cancer ◽  
Gastrointestinal Cancers ◽  
Alter Patient ◽  
Cancer Data ◽  
Gi Cancers ◽  
Patient Prognosis

We present evidence that KCNQ genes are drivers and suppressors of gastrointestinal (GI) cancer in humans. The KCNQ family of genes encode for subunits of a potassium channel complex involved in membrane polarisation and little is known about their role in cancer. We use human cancer data and a multidisciplinary computational-based approach including structural modelling and simulation, coupled with in vitro experiments to show that KCNQ1 is a tumor suppressor, and KCNQ3 and KCNQ5 are oncogenic across human GI cancers. We link the expression of KCNQ genes to WNT signalling, EMT, and survival and propose that mutation/copy number alteration of KCNQ genes can significantly alter patient prognosis in GI cancers.

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