Dermatoglyphic Peculiarities in Members of a High-Cancer-Risk Kindred

2015 ◽  
pp. 325-332 ◽  
Author(s):  
Henry T. Lynch ◽  
Arnold R. Kaplan ◽  
Austin Moorhouse ◽  
Anne J. Krush ◽  
George Clifford
Keyword(s):  
Cancer Risk ◽  
High Cancer Risk

scholarly journals Carcinogens and DNA damage

2018 ◽  
Vol 46 (5) ◽  
pp. 1213-1224 ◽  
Author(s):  
Jessica L. Barnes ◽  
Maria Zubair ◽  
Kaarthik John ◽  
Miriam C. Poirier ◽  
Francis L. Martin
Keyword(s):  
Dna Damage ◽  
Cancer Risk ◽  
Epidemiological Studies ◽  
Heterocyclic Aromatic Amines ◽  
Migrant Populations ◽  
Wide Range ◽  
High Cancer Risk ◽  
Polycyclic Aromatic ◽  
Exogenous Agents ◽  
Cross Links

Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens. DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA–DNA or DNA–protein cross-links. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.

Adipose tissue, obesity and adipokines: role in cancer promotion

2015 ◽  
Vol 21 (1) ◽  
Author(s):  
Andrea Booth ◽  
Aaron Magnuson ◽  
Josephine Fouts ◽  
Michelle Foster
Keyword(s):  
Adipose Tissue ◽  
Cancer Risk ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Epidemiological Studies ◽  
Normal Weight ◽  
Cell Progression ◽  
High Cancer Risk ◽  
Apoptosis Pathways ◽  
And Migration

AbstractAdipose tissue is a complex organ with endocrine, metabolic and immune regulatory roles. Adipose depots have been characterized to release several adipocytokines that work locally in an autocrine and paracrine fashion or peripherally in an endocrine fashion. Adipocyte hypertrophy and excessive adipose tissue accumulation, as occurs during obesity, dysregulates the microenvironment within adipose depots and systemically alters peripheral tissue metabolism. The term “adiposopathy” is used to describe this promotion of pathogenic adipocytes and associated adipose – elated disorders. Numerous epidemiological studies confirm an association between obesity and various cancer forms. Proposed mechanisms that link obesity/adiposity to high cancer risk and mortality include, but are not limited to, obesity-related insulin resistance, hyperinsulinemia, sustained hyperglycemia, glucose intolerance, oxidative stress, inflammation and/or adipocktokine production. Several epidemiological studies have demonstrated a relationship between specific circulating adipocytokines and cancer risk. The aim of this review is to define the function, in normal weight and obesity states, of well-characterized and novel adipokines including leptin, adiponectin, apelin, visfatin, resistin, chemerin, omentin, nesfatin and vaspin and summarize the data that relates their dysfunction, whether associated or direct effects, to specific cancer outcomes. Overall research suggests most adipokines promote cancer cell progression via enhancement of cell proliferation and migration, inflammation and anti-apoptosis pathways, which subsequently can prompt cancer metastasis. Further research and longitudinal studies are needed to define the specific independent and additive roles of adipokines in cancer progression and reoccurrence.

High Cholesterol = High Cancer Risk?

Science News ◽  
1987 ◽  
Vol 131 (1) ◽  
pp. 4
Author(s):  
J. Silberner
Keyword(s):  
Cancer Risk ◽  
High Cholesterol ◽  
High Cancer Risk

scholarly journals DNA Repair Gene Variants Associated with Benign Breast Disease in High Cancer Risk Women

2009 ◽  
Vol 18 (1) ◽  
pp. 346-350 ◽  
Author(s):  
Timothy J. Jorgensen ◽  
Kathy J. Helzlsouer ◽  
Sandra C. Clipp ◽  
Judy Hoffman Bolton ◽  
Rosa M. Crum ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cancer Risk ◽  
Benign Breast Disease ◽  
Breast Disease ◽  
Gene Variants ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
High Cancer Risk

The genetics of inherited cancers

2020 ◽  
pp. 456-470
Author(s):  
Rosalind A. Eeles
Keyword(s):  
Relative Risk ◽  
Cancer Risk ◽  
Cancer Genetics ◽  
Clinical Pathways ◽  
Cancer Predisposition ◽  
Cellular Growth ◽  
Increased Risk ◽  
Predisposition Genes ◽  
High Cancer Risk ◽  
Cancer Predisposition Gene

All cancer can be termed ‘genetic’ as the disease is caused by somatic cell mutations (alterations in the DNA code), which result in abnormal cellular growth and/or proliferation. Most of these mutations are sporadic (only occurring in the cancer cell), but some are due to the inheritance of a germline mutation in a cancer predisposition gene. Cancer predisposition genes can be rare and confer a high cancer risk (about 10-fold lifetime relative risk), or common and confer a low to moderately increased risk (from just over onefold, up to two- to threefold). They have been shown to be involved in causing some of most common cancers as well as some rare cancers. Cancer genetics will become part of mainstream clinical pathways for cancer care in the coming years and is likely to contribute to healthcare that is tailored to individual patients.

scholarly journals Reappraisal of main pancreatic duct in IPMN under surveillance: duct dilatation of 5 to 9 mm alone is not associated with high cancer risk

HPB ◽  
2018 ◽  
Vol 20 ◽  
pp. S294
Author(s):  
S. Andrianello ◽  
G. Marchegiani ◽  
G. Morbin ◽  
E. Secchettin ◽  
M. D'Onofrio ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Pancreatic Duct ◽  
Main Pancreatic Duct ◽  
Duct Dilatation ◽  
High Cancer Risk

Mammographic density is not a worthwhile examination to distinguish high cancer risk women in screening

2014 ◽  
Vol 24 (10) ◽  
pp. 2412-2416 ◽  
Author(s):  
Catherine Colin ◽  
Anne-Marie Schott ◽  
Pierre-Jean Valette
Keyword(s):  
Cancer Risk ◽  
Mammographic Density ◽  
High Cancer Risk

High cancer risk and increased mortality in patients with Peutz–Jeghers syndrome

Gut ◽  
2011 ◽  
Vol 61 (2) ◽  
pp. 322.2-322 ◽  
Author(s):  
Douglas L Riegert-Johnson ◽  
Wytske Westra ◽  
Maegan Roberts
Keyword(s):  
Cancer Risk ◽  
High Cancer Risk ◽  
Peutz Jeghers Syndrome
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