vendredi 28 juin 2013

Press Review (June 29, 2013) – Revue de presse (29 juin 2013)

Heart Failure Patients May Face Higher Cancer Risk
Doctors may want to keep an even closer eye on their patients who have experienced heart failure, a condition where not enough blood is able to be pumped by the heart to other parts of the body. A new study shows they face a higher risk of cancer.
In Huffington Post

Many cancer patients expect palliative care to cure
In a survey of patients with terminal lung cancer, nearly two-thirds did not understand that radiation treatments intended only to ease their symptoms would not cure their disease.
By Kathryn Doyle. In Reuters                            

Cancer: An acidic link
Obese people are at higher risk of multiple types of cancer, but why? One explanation could be that obesity enhances the production of pro-inflammatory, and carcinogenic, bile acids by gut microorganisms.
By Suzanne Devkota & Peter. J. Turnbaugh. In         

Cancer Clinics Closing: Community Oncology 'Near Crisis'
The community cancer care landscape in the United States continues to evolve, and not for the better, according to a report released by the Community Oncology Alliance (COA). Since their previous report, issued in April 2012, there has been a 20% increase in clinic closings and in consolidation into hospitals.
By Roxanne Nelson. In Medscape                    

Lifestyle cancers increase by 40% due to 'bad habits' and changes in fashion
Cancers caused by smoking, drinking and excessive sunbathing have soared in the past decade, official statistics have revealed.
By Richard Gray. In The Telegraph

Cancer : le rat-taupe nu fait renaître l'espoir
Aucun cancer n'a jamais été détecté chez ce petit rongeur appelé le rat-taupe "nu" ou "glabre". L'animal produirait lui-même son propre anti-cancéreux, l'acide hyaluronique.
Dans Le Nouvel Observateur

Cancers héréditaires : les malades obligés de prévenir leur entourage
Les personnes à risque de développer un cancer héréditaire seront désormais contraintes de prévenir leur entourage. En cas de refus, c'est le médecin qui en avertira la famille par courrier.
Dans Le Nouvel Observateur

jeudi 27 juin 2013

FDA approves Xgeva to treat giant cell tumor of the bone

The U.S. Food and Drug Administration recently expanded the approved use of Xgeva (denosumab) to treat adults and some adolescents with giant cell tumor of the bone (GCTB), a rare and usually non-cancerous tumor.

GCTB generally occurs in adults between the ages of 20 and 40 years. In most cases, GCTB does not spread to other parts of the body but destroys normal bone as it grows, causing pain, limited range of motion and bone fractures. Rarely, GCTB can transform into a cancerous tumor and spread to the lungs.

Xgeva is a monoclonal antibody that binds to RANKL, a protein essential for maintenance of healthy bone. RANKL is also present in GCTB. Xgeva is intended for patients whose GCTB cannot be surgically removed or when surgery is likely to result in severe morbidity, such as loss of limbs or joint removal. It should only be used in adolescents whose bones have matured.

Xgeva was approved in 2010 to prevent fractures when cancer has spread to the bones.

vendredi 21 juin 2013

Press Review (June 22, 2013) – Revue de presse (22 juin 2013)

A Homely Rodent May Hold Cancer-Fighting Clues
The laboratory of Vera Gorbunova and Andrei Seluanov, a husband-and-wife team of biologists at the University of Rochester, has the feel of a petting zoo. They maintain colonies of several species of rodents — some familiar, like mice and guinea pigs, and some much more exotic, like blind mole rats from Israel and naked mole rats from East Africa.
By Carl Zimmer. In New York Times

Pluripotent Stem Cells Made from Pancreatic Cancer Cells Are First Human Model of the Cancer's Progression
Pancreatic cancer carries a dismal prognosis. According to the National Cancer Institute, the overall five-year relative survival for 2003-2009 was 6 percent.
In Science Daily (blog)                                      

Red Meat and Cancer: What's the Beef?
Large European and American studies are the most recent to examine the link between red meat and cancer. Medscape talked to the study authors and reviewed other evidence to determine whether there is reason to have a beef about eating beef.
By Laura A. Stokowski. In Medscape Oncology     

Cancer in numbers - infographic
Some key statistics on current and projected cancer diagnoses.
By Samantha Jones. In The Guardian              

Herding cancer cells to their death
Researchers report a therapeutic strategy that appears to destroy drug resistant melanomas and suppress metastasis.
In EurekAlert (press release)

Les produits laitiers ne favorisent pas le cancer (à une exception près)
La consommation régulière de produits laitiers, encouragée par les autorités, ne favorise pas le cancer et aurait même dans certains cas un effet protecteur. Mais elle augmenterait légèrement le risque de cancer de la prostate, selon des spécialistes réunis jeudi à Paris.
Dans Huffington Post

Le secret du rat-taupe nu contre le cancer
Ce petit animal est laid. Mais il a une propriété qui pourrait bien tous nous intéresser.

lundi 17 juin 2013

FDA approves two drugs, companion diagnostic test for advanced skin cancer

The U.S. Food and Drug Administration recently approved two new drugs, Tafinlar (dabrafenib) and Mekinist (trametinib), for patients with advanced or unresectable melanoma,.

Tafinlar, a BRAF inhibitor, is approved to treat patients with melanoma whose tumors express the BRAF V600E gene mutation. Mekinist, a MEK inhibitor, is approved to treat patients whose tumors express the BRAF V600E or V600K gene mutations. Approximately half of melanomas arising in the skin have a BRAF gene mutation. Tafinlar and Mekinist are being approved as single agents, not as a combination treatment.

The FDA approved Tafinlar and Mekinist with a genetic test called the THxID BRAF test, a companion diagnostic that will help determine if a patient’s melanoma cells have the V600E or V600K mutation in the BRAF gene.

“Advancements in our understanding of the biological pathways of a disease have allowed for the development of Tafinlar and Mekinist, the third and fourth drugs the FDA has approved for treating metastatic melanoma in the past two years,” said Richard Pazdur, M.D., director of the Office of Hematology and Oncology Products in the FDA’s Center for Drug Evaluation and Research.

Zelboraf (vemurafenib) and Yervoy (ipilimumab) were approved in 2011 for the treatment of metastatic or unresectable melanoma.

The FDA’s approval of the THxID BRAF test is based on data from clinical studies that support the Tafinlar and Mekinist approvals. Samples of patients’ melanoma tissue were collected to test for the mutation.

vendredi 14 juin 2013

Press Review (June 15, 2013) – Revue de presse (15 juin 2013)

Oral Cancer Sneaks Up
The actor Michael Douglas has done for throat cancer what Rock Hudson did for AIDS and Angelina Jolie did for prophylactic mastectomy. By asserting last week that his cancer was caused by a virus transmitted during oral sex, Mr. Douglas pushed the disease onto the front pages and made millions of Americans worry about it for the first time.

More women removing ovaries to prevent cancer
There are risks and benefits to the procedure.
By Andrea K. Walker. In Baltimore Sun (blog)  

Curing cancer with finance
JUST back from an inspirational talk by Andrew Lo of MIT Sloan at a seminar in the furthest reaches of Canary Wharf. The Economist has mentioned his idea before but the maths is compelling when he spells it out in person (here is a link to a video presentation). While biotechnology had made some great breakthroughs in the last 10 years, the returns to investors have been lousy; money is now being withdrawn from the sector. So there is clearly a problem that needs to be solved if we want more cures to be developed.
By Buttonwood. In The Economist                    

Childhood Cancer Survivors Have Significant Chronic Disease
A study of over 1,700 childhood cancer survivors found that 98% of the participants had at least one chronic disease such as new cancers, heart disease or abnormal lung function
By Alexandra Sifferlin. In TIME (blog)               

'Master protocol' aims to revamp cancer trials        
Pilot project will bring drug companies together to test targeted lung-cancer therapies.
By Heidi Ledford. In

Des nanodiamants pour améliorer les traitements du cancer?
Un des enjeux actuels de la médecine est le développement de nouveaux traitements du cancer, qui est aujourd'hui une cause majeure de mortalité dans le monde. D'après les dernières estimations de l'OMS, la mortalité liée au cancer continue d'augmenter et pourrait dépasser 13 millions de décès en 2030. Des progrès significatifs au niveau des traitements disponibles ont pourtant été observés ces dernières années, notamment grâce à une meilleure compréhension des mécanismes biologiques à l'origine des cancers.
Par Tristan Petit. Dans Huffington Post

L'Homme de Néandertal était aussi atteint par le cancer
L'évolution est une chose fascinante qui attise toujours la curiosité des chercheurs. La cause de l'extinction de l'homme de Néandertal reste encore inconnue à l'homme moderne. Toutefois, une anomalie a été décelée dans un fossile d'un individu néandertalien vieux de 120 000 ans. Le cancer de l'os touchait déjà l'homme de Neandertal, alors que les scientifiques pensaient que ce dérèglement des cellules était plus récent.

vendredi 7 juin 2013

Press Review (June 8, 2013) – Revue de presse (8 juin 2013)

Komen Breast Cancer Charity Cancels Races in 7 Cities
The Susan G. Komen for the Cure foundation has canceled half of its “3-Day” fund-raising races around the country next year as it struggles to regain support nearly 18 months after its 2012 decision to withdraw funding for breast cancer screening at some Planned Parenthood affiliates.
By Jennifer Preston. In New York Times (blog)

Nontoxic cancer therapy proves effective against metastatic cancer
A combination of nontoxic dietary and hyperbaric oxygen therapies effectively increased survival time in a mouse model of aggressive metastatic cancer, a research team from the Hyperbaric Biomedical Research Laboratory at the University of South Florida has found.
In Science Daily                                                

Cancer treatments still caught in sequestration politics
The Obama administration says it does not have the power to ease the cuts, leaving it to Congress to act.
By Katie McDonough. In Salon                          

Genetic Testing of Rare Blood Cancer Reveals New Mutation
A recent article in the New England Journal of Medicine describes genetic testing of a rare blood cancer called atypical chronic neutrophilic leukemia (CNL) that revealed a new mutation present in most patients with the disease. The mutation also serves as an Achilles heel, allowing doctors at the University of Colorado Cancer Center to prescribe a never-before-used, targeted treatment. The first patient treated describes his best snowboarding season ever.
In Science Daily                                                

World’s Oldest Cancer Found in Bone of 120,000 Year-Old Neanderthal
The world's oldest known human tumour has been found in the rib bone of a Neanderthal who lived more than 120,000 years ago.

The bone was evacuated from a site in Krapina, Croatia more than 100 years ago and has been found to have contracted the fibrous dysplasia  tumour, a cancer which is common among modern-day humans.
By Ewan Palmer. In International Business Times 

Une nouvelle arme contre le cancer du col de l'utérus ?
Des chercheurs viennent de mettre au point une stratégie pour stopper le développement du cancer du col de l’utérus, causé par certains papillomavirus. Cette méthode est basée sur l’utilisation d’une molécule d’ARN synthétique qui bloque l’action d’une protéine virale.
Par Agnès Roux. Dans Futura-Sciences

Le rôle de l'oestrogène mieux compris dans le cancer colorectal
Le cancer colorectal touche surtout les personnes de plus de 50 ans, un peu plus d'hommes que de femmes. C'est un cancer qui se développe sur plusieurs années – parfois même sur 20 ans – et qui reste discret très longtemps. En 2012 au Québec, on estime qu'il y a eu quelque 6200 nouveaux cas diagnostiqués et environ 2400 décès. Les facteurs de risque peuvent varier: polypes colorectaux, antécédents familiaux, mauvaises habitudes alimentaires (trop de viande rouge, pas assez de fruits et légumes), manque d'exercice physique et obésité. L'importance de la recherche sur le cancer colorectal est donc implicite.

jeudi 6 juin 2013


Author: Marc Lacroix (InTextoResearch, Baelen, Wallonia, Belgium)
Nova Sciences Publishers
ISBN: 978-1-62257-817-7    
(also available as e-book - ISBN: 978-1-62618-780-1)

Book Description:

Cancer is characterized by uncontrolled cell division and the potential of the cells to invade surrounding tissues and spread around the body. Most of these changes in cellular behavior are the result of alterations in the function or levels of the proteins that control these processes. And these alterations are, in turn, usually caused by modifications at the DNA level. Indeed, cancer is now recognized as being essentially a disease caused by mutation, or dysregulated expression, of genes. Of the estimated 30,000 genes in the human genome, currently more than 250 are known to play an important role in the development of cancer, either sporadic or familial. In some cases, their effects result from gene fusion, due to translocation for instance, or from amplification of a chromosomal region. During the last years, attention has largely shifted from the identification of rare high-risk genetic mutations to a hunt for lower risk gene polymorphisms, many of which are likely to be common within the population. Another increasingly investigated field is epigenetics, which relates to abnormal and prolonged changes in the mechanisms that alter gene expression and activity, without involving changes in genetic sequence.

Table of Contents:

Chapter 1: A Detailed List of Major Cancer Genes
Chapter 2: Gene Fusions in Cancer
Chapter 3: Gene Amplification in Cancer
Chapter 4: Low Penetrance Sites in Cancer: Candidate Genes
Chapter 5: Familial Cancer Syndromes
Chapter 6: Epigenetics and Cancer

The Author:

Born in 1963, Marc Lacroix has been working on breast cancer in several academic institutions and at InTextoResearch, an agency devoted to scientific information on cancer. He authored four books: “Tumor Suppressor Genes in Breast Cancer” (2008), “Molecular Therapy of Breast Cancer: Classicism meets Modernity” (2009), “MicroRNAs in Breast Cancer” (2010) and “A Concise History of Breast Cancer” (2011 & 2013)


Chapter 1

ABL1 (v-abl Abelson murine leukemia viral oncogene homolog 1)
AKT1 (RAC-alpha serine/threonine-protein kinase)
AKT2 (v-akt murine thymoma viral oncogene homolog 2)
ALK (Anaplastic lymphoma receptor tyrosine kinase)
APC (Adenomatous polyposis coli)
ARID1A (AT rich interactive domain 1A)
ARID1B (AT rich interactive domain 1B)
ARID2 (AT rich interactive domain 2)
ASXL1 (Additional sex combs like 1)
ATM (Ataxia telangiectasia mutated)
BAP1 (BRCA1 associated protein-1)
BLM (Bloom syndrome, RecQ helicase-like)
BMPR1A (Bone morphogenetic protein receptor, type IA)
BRAF (v-raf murine sarcoma viral oncogene homolog B1)
BRCA1 (Breast cancer 1, early onset)
BRCA2 (Breast cancer 2, early onset)
BRIP1 (BRCA1 interacting protein C-terminal helicase 1)
BUB1B (Budding uninhibited by benzimidazoles 1 homolog beta)
CASP8 (Caspase 8, apoptosis-related cysteine peptidase)
CBFB (Core-binding factor, beta subunit)
CBL (Cas-Br-M (murine) ecotropic retroviral transforming sequence)
CDH1 (Cadherin 1, type 1, E-cadherin)
CDK4 (Cyclin-dependent kinase 4)
CDKN1B (Cyclin-dependent kinase inhibitor 1B)
CDKN2A (Cyclin-dependent kinase inhibitor 2A)
CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha)
CHEK2 (CHK2 checkpoint homolog)
CTNNB1 (Catenin (cadherin-associated protein), beta 1, 88kDa)
CYLD (Cylindromatosis)
DDB2 (also known as XPE) (Damage-specific DNA binding protein 2)
DNMT3A (DNA (cytosine-5-)-methyltransferase 3 alpha)
EGFR (Epidermal growth factor receptor)
ERBB2 (v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/glioblastoma derived oncogene homolog)
ERCC2 (also known as XPD) (Excision repair cross-complementing rodent repair deficiency, complementation group 2)
ERCC3 (also known as XPB) (Excision repair cross-complementing rodent repair deficiency, complementation group 3)
ERCC4 (also known as XPF) (Excision repair cross-complementing rodent repair deficiency, complementation group 4)
ERCC5 (also known as XPG) (Excision repair cross-complementing rodent repair deficiency, complementation group 5)

EXT1 (Exostosin-1)
EXT2 (Exostosin-2)
EZH2 (Enhancer of zeste homolog 2)
FAM123B (Family with sequence similarity 123B)
Fanconi Anemia pathway
FANCA (Fanconi anemia, complementation group A)
FANCB (Fanconi anemia, complementation group B)
FANCC (Fanconi anemia, complementation group C)
FANCD1 (also known as BRCA2) (Fanconi anemia, complementation group D1)
FANCD2 (Fanconi anemia, complementation group D2)
FANCE (Fanconi anemia, complementation group E)
FANCF (Fanconi anemia, complementation group F)
FANCG (Fanconi anemia, complementation group G)
FANCI (Fanconi anemia, complementation group I)
FANCJ (also known as BRIP1) (Fanconi anemia, complementation group J)
FANCL (Fanconi anemia, complementation group L)
FANCM (Fanconi anemia, complementation group M)
FBXW7 (F-box and WD repeat domain containing 7)
FGFR3 (Fibroblast growth factor receptor 3)
FH (Fumarate hydratase )
FLCN (Folliculin)
FLT3 (Fms-related tyrosine kinase 3)
FOXL2 (Forkhead box L2)
GATA1 (GATA binding protein 1)
GATA3 (GATA binding protein 3)
GNAQ (Guanine nucleotide binding protein (G protein), q polypeptide)
GNAS (GNAS complex locus)
HNF1A (HNF1 homeobox A)
HRAS (v-Ha-ras Harvey rat sarcoma viral oncogene homolog)
IDH1 (Isocitrate dehydrogenase 1)
IDH2 (Isocitrate dehydrogenase 2)
JAK2 (Janus kinase 2)
KIT (v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog)
KLF6 (Kruppel-like factor 6)
KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog)
MAP2K4 (Mitogen-activated protein kinase kinase 4)
MAP3K1 (Mitogen-activated protein kinase kinase kinase 1, E3 ubiquitin protein ligase)
MAP3K13 (Mitogen-activated protein kinase kinase kinase 13)
MEN1 (Multiple endocrine neoplasia I)
MLH1 (MutL homolog 1, colon cancer, nonpolyposis type 2)
MSH2 (MutS homolog 2, colon cancer, nonpolyposis type 1)
MSH6 (MutS homolog 6)
MPL (Myeloproliferative leukemia virus oncogene)
MUTYH (MutY homolog)
MYC (v-myc myelocytomatosis viral oncogene homolog)
NCOR1 (Nuclear receptor corepressor 1)
NF1 (Neurofibromin 1) & NF2 (Neurofibromin 2)
NOTCH1 (Notch 1)
NPM1 (Nucleophosmin 1)
NRAS (Neuroblastoma RAS viral (v-ras) oncogene homolog)
NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3)
PALB2 (also known as FANCN) (Fanconi anemia, complementation group N)
PBRM1 (Polybromo 1)
PDGFRA (Platelet-derived growth factor receptor, alpha polypeptide)
PHOX2B (Paired-like homeobox 2b)
PIK3CA (Phosphoinositide-3-kinase, catalytic, alpha polypeptide)
PMS1 (PMS1 postmeiotic segregation increased 1)
PMS2 (PMS2 postmeiotic segregation increased 2)
POLH (also known as XPV) (Polymerase (DNA directed), eta)
Polycomb group (PcG) proteins
PPP2R1A (protein phosphatase 2, regulatory subunit A, α)
PRKAR1A (Protein kinase, cAMP-dependent, regulatory, type I, α)
PTCH1 (Patched 1)
PTEN (Phosphatase and tensin homolog)
PTPN11 (Protein tyrosine phosphatase, non-receptor type 11)
RAD51C (RAD51 homolog C)
RAD51C (also known as FANCO) (Fanconi anemia, complementation group O)
RB1 (Retinoblastoma 1)
RECQL4 (RecQ protein-like 4)
RET (Ret proto-oncogene)
RUNX1 (Runt-related transcription factor 1)
SDHA (Succinate dehydrogenase complex, subunit A, flavoprotein variant)
SDHAF2 (Succinate dehydrogenase complex assembly factor 2)
SDHB (Succinate dehydrogenase complex, subunit B, iron sulfur)
SDHC (Succinate dehydrogenase complex, subunit C, integral membrane protein, 15kDa)
SDHD (Succinate dehydrogenase complex, subunit D, integral membrane protein)
SETD2 (SET domain containing 2)
SF3B1  (Splicing factor 3b, subunit 1, 155kDa)
SMAD4 (SMAD family member 4)
SMO (Smoothened homolog)
SOCS1 (Suppressor of cytokine signaling 1)
STK11 (Serine/threonine kinase 11)
SUFU (Suppressor of fused homolog)
SWI/SNF complex components
SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4)
SMARCB1 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1) are the most frequently mutated.
TBX3 (T-box 3)
TET2 (Tet (ten-eleven-translocation) oncogene family member 2)
TMEM127 (Transmembrane protein 127)
TNFAIP3 (Tumor necrosis factor, alpha-induced protein 3)
TP53 (Tumor protein p53)
TSC1 (Tuberous sclerosis 1) & TSC2 (Tuberous sclerosis 2)
TSHR (Thyroid stimulating hormone receptor)
XPA (Xeroderma pigmentosum, complementation group A)
XPC (Xeroderma pigmentosum, complementation group C)
WRN (Werner syndrome, RecQ helicase-like)
WT1 (Wilms tumor 1)

Chapter 2

Balanced translocations and gene fusions
Deletions and gene fusions
Dicentric aberrations and gene fusions
Insertions and gene fusions
Inversions and gene fusions
Non-reciprocal translocations and gene fusions
Ring chromosome and gene fusions

Chapter 3

AKT2 (V-akt murine thymoma viral oncogene homolog 2)
AR (Androgen receptor)
ARPC1A (Actin related protein 2/3 complex, subunit 1A, 41kDa)
AURKA (Aurora kinase A)
BCL2L2 (BCL2-like 2)
CACNA1E (Calcium channel, voltage-dependent, R type, alpha 1E subunit)
CCND1 (Cyclin D1)
CCNE1 (Cyclin E1)
CDK4 (Cyclin-dependent kinase 4)
CDK6 (Cyclin-dependent kinase 6)
CHD1L (Chromodomain helicase DNA binding protein 1-like)
CKS1B (CDC28 protein kinase regulatory subunit 1B)
DCUN1D1 (DCN1, defective in cullin neddylation 1, domain containing 1)
DYRK2 (Dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 2)
E2F3  (E2F transcription factor 3)
EGFR (Epidermal growth factor receptor)
EIF5A2 (Eukaryotic translation initiation factor 5A2)
ERBB2 (V-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/glioblastoma derived oncogene homolog)
FADD (Fas (TNFRSF6)-associated via death domain)
FGFR1 (Fibroblast growth factor receptor 1)
GATA6 (GATA binding protein 6)
GPC5 (Glypican 5)
GRB7 (Growth factor receptor-bound protein 7)
JUN (Jun proto-oncogene)
KIT (V-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog)
MAP3K5 (Mitogen-activated protein kinase kinase kinase 5)
MDM2 (Mdm2, p53 E3 ubiquitin protein ligase homolog)
MDM4 (Mdm4 p53 binding protein homolog)
MED29 (Mediator complex subunit 29)
MET (Met proto-oncogene)
MITF (Microphthalmia-associated transcription factor)
MTDH (Metadherin)
MYC (V-myc myelocytomatosis viral oncogene homolog)
MYCL1 (V-myc myelocytomatosis viral oncogene homolog 1, lung carcinoma derived)
MYCN (V-myc myelocytomatosis viral related oncogene, neuroblastoma derived)
NCOA3 (Nuclear receptor coactivator 3)
NKX2-1 (NK2 homeobox 1)
NKX2-8 (NK2 homeobox 8)
PAK1 (P21 protein (Cdc42/Rac)-activated kinase 1)
PAX9 (Paired box 9)
PIK3CA (Phosphoinositide-3-kinase alpha polypeptide)
PPM1D (Protein phosphatase, Mg2+/Mn2+ dependent, 1D)
PRKCI            (Protein kinase C, iota)
RAB25 (RAB25, member RAS oncogene family)
REL (V-rel reticuloendotheliosis viral oncogene homolog)
RPS6KB1 (Ribosomal protein S6 kinase, 70kDa, polypeptide 1)
SKP2 (S-phase kinase-associated protein 2, E3 ubiquitin protein ligase)
SMURF1 (SMAD specific E3 ubiquitin protein ligase 1)
STARD3 (StAR-related lipid transfer (START) domain containing 3)
TSPAN31 (Tetraspanin 31)
WHSC1L1 (Wolf-Hirschhorn syndrome candidate 1-like 1)
YWHAB (Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide)           
YWHAQ (Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, theta polypeptide)
YWHAZ (Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide)
ZNF217 (Zinc finger protein 217)
ZNF639 (Zinc finger protein 639)

Chapter 4

GWAS in bladder cancer
GWAS in breast cancer (BC)
GWAS in colorectal cancer (CRC)
GWAS in lung cancer (LC)
GWAS in cancer types other than bladder, breast, colorectal, esophageal, lung, prostate, and upper aerodigestive
GWAS in prostate cancer (PC)
GWAS in upper aerodigestive and esophageal cancers

Chapter 5

Ataxia Telangiectasia
Basal Cell Nevus Syndrome
Beckwith–Wiedemann Syndrome
Birt–Hogg–Dubé Syndrome
Bloom Syndrome
Carney Complex, Types I and II
Cowden Syndrome
Dyskeratosis Congenita
Familial Adenomatous Polyposis
Familial platelet disorder with predisposition to acute myelogenous leukemia
Fanconi Anemia
Hereditary Breast/Ovarian Cancer
Hereditary Diffuse Gastric Cancer
Hereditary Leiomyomatosis and Renal Cell Cancer
Hereditary Multiple Exostosis
Hereditary Nonpolyposis Colon Cancer
Hereditary Papillary Renal Cell Carcinoma
Hereditary paraganglioma-pheochromocytoma syndrome
Li–Fraumeni Syndrome, including Li-Fraumeni-Like Syndrome
Multiple Endocrine Neoplasia Type 1
Multiple Endocrine Neoplasia Type 2A, 2B
MYH-Associated Polyposis
Neurofibromatosis Type 1
Neurofibromatosis Type 2
Nijmegen Breakage Syndrome
Peutz–Jeghers Syndrome
Polyposis, Familial Juvenile
Retinoblastoma, Hereditary
Rhabdoid Tumor Predisposition Syndrome
Rothmund–Thomson Syndrome
Shwachman-Bodian-Diamond Syndrome
Simpson–Golabi–Behmel Syndrome
Tuberous Sclerosis Complex
Variegated Aneuploidy, Mosaic
Von Hippel–Lindau Syndrome
Werner Syndrome
Wilms Tumor, Familial
Xeroderma Pigmentosum

Chapter 6

Cancer mutations in histone genes
Chromatin remodelers
DNA Hydroxy-Methylation and Its Oxidation Derivatives
DNA Methylation:
Histone acetylation
Histone acetylation readers
Histone demethylation
Histone desacetylation
Histone methylation
Histone methylation readers
Histone modifications
Histone phosphorylation
Noncoding RNAs