Howard L. Kaufman - Melanoma
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Melanoma is one of the most types of cancer. When melanoma is detected at an early stage, treatment is highly successful, but outcomes can be poor when the disease is advanced. There has been significant progress in our understanding of the molecular biology, genetics, and immunology of melanoma over the past decade. This has been accompanied by rapid advances in therapeutic strategies for patients with melanoma. This book provides the clinician and the researcher with a broad understanding of the molecular and cellular pathogenesis of melanoma, explores the clinical characteristics and criteria for clinical and pathological staging of the disease, and provides an overview of current and evolving treatment strategies in the adjuvant, metastatic, and preventive settings. The treatment of special populations and rare variants of melanoma that often present particular clinical challenges is also covered. Authored by international experts in melanoma biology and clinical management, this volume concisely explains how to diagnose, treat, and prevent melanoma while reviewing advances in basic science and providing an overview of innovative approaches still under development.
Howard L. Kaufman: author's other books
Who wrote Melanoma? Find out the surname, the name of the author of the book and a list of all author's works by series.
Howard L. Kaufman
Steven Q. Wang
Claudia Cornwall
Chamberlain Daniel MD
Kishwer S. Nehal
Raymond L. Barnhill
Dr. Murad Alam MD (editor)
Michael J. Murphy (editor)
Adam I. Riker
Theodora Ross MD
John M. Kirkwood
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Springer International Publishing Switzerland 2016
Howard L. Kaufman and Janice M. Mehnert (eds.) Melanoma Cancer Treatment and Research 10.1007/978-3-319-22539-5_1Heterogeneity in Melanoma
Batool Shannan 1, Michela Perego 1, Rajasekharan Somasundaram 1 and Meenhard Herlyn 1
(1)
Molecular and Cellular Oncogenesis Program, Melanoma Research Center, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA
Meenhard Herlyn
Email:
Abstract
Melanoma is among the most aggressive and therapy-resistant human cancers. While great strides in therapy have generated enthusiasm, many challenges remain. Heterogeneity is the most pressing issue for all types of therapy. This chapter summarizes the clinical classification of melanoma, of which the research community now adds additional layers of classifications for better diagnosis and prediction of therapy response. As the search for new biomarkers increases, we expect that biomarker analyses will be essential for all clinical trials to better select patient populations for optimal therapy. While individualized therapy that is based on extensive biomarker analyses is an option, we expect in the future genetic and biologic biomarkers will allow grouping of melanomas in such a way that we can predict therapy outcome. At this time, tumor heterogeneity continues to be the major challenge leading inevitably to relapse. To address heterogeneity therapeutically, we need to develop complex therapies that eliminate the bulk of the tumor and, at the same time, the critical subpopulations.
Keywords
Melanoma Heterogeneity TherapyAbbreviations
ABCB5
ATP-binding cassette subfamily B5
AKT
V-akt murine thymoma viral oncogene homolog
ALCAM
Activated leukocyte cell adhesion molecule
ALDH1
Aldehyde dehydrogenase 1
ARID1A
AT-rich interactive domain-containing protein 1A
BRAF
V-raf murine sarcoma viral oncogene homolog B1
CD
Cluster differentiation
CDK
Cyclin-dependent Kinase
CDKN2A
Cyclin-dependent kinase inhibitor 2A
ERK
Extracellular signal-regulated kinase
Fbxw-7
F-box/WD repeat-containing protein 7
gp100
Glycoprotein 100
HGF
Hepatocyte growth factor
IGF
Insulin-like growth factor
JARID1B
Jumonji/ARID1 (JARID1) histone 3 K4 (H3K4) demethylases
Kit
C-kit tyrosine kinase receptor
MAPK
Mitogen-activated protein kinase
MART-1/Melan-A
Melanoma antigen recognized by T cells-1/melanoma antigen A
MCAM
Melanoma cell adhesion molecule
MEK
MAPK/ERK Kinase
MITF
Microphthalmia-associated transcription factor
mTOR
Mammalian target of Rapamycin
NF
Neurofibromatosis
NGF
Nerve growth factor
NGFR
Nerve growth factor receptor
NRAS
Neuroblastoma RAS viral (v-ras) oncogene homolog
PI3K
Phosphoinositide-3 Kinase
PTEN
Phosphatase and tensin homolog
Rac1
Ras-related C3 botulinum toxin substrate-1
RAF
RAS viral (v-raf) oncogene homolog
RAS
RAS viral (v-ras) oncogene homolog
SCF
Stem cell factor
SEER
Surveillance, epidemiology, end results
TGF-
Transforming growth factor beta
TICs
Tumor-initiating cells
TME
Tumor microenvironment
TNF
Tumor necrosis factor
TP53
Tumor protein p53
UV
Ultraviolet
Batool Shannan and Michela Perego have equally contributed.
Introduction
Melanoma is the most aggressive form of skin cancer and incidences continue to rise worldwide. According to the American Cancer Society, an estimated 76,100 new cases of melanoma will be diagnosed in the USA and 9710 people are expected to die of metastatic disease [].
Efforts are underway to understand the biology of melanoma heterogeneity to better design strategies for more precise choices for targeting. In this chapter, we review clinical and genetic profiles in melanoma and discuss heterogeneity as one of the most significant causes for cancer therapy resistance.
Clinical and Molecular Classification of Melanoma
Clinical and histological classifications of melanoma have been extensively described (Fig. ] suggesting a fluid transition from one state of cellular differentiation to the other, making it very difficult to trace the origin of melanomas. As tumors become more aggressive, they often lose their pigmentation markers and dedifferentiate acquiring stem cell features, which make them more resistant to therapy. 
Fig. 1
Clinical grouping of melanoma. There are distinct patterns of clinical appearances of melanoma that led to the distinction of the histogenetic types in the first classification system in 1973. a Melanomas arising from epithelium-associated melanocytes. The relationship between sun exposure and melanoma has been established for decades (high UV melanoma); however, it was later discovered that melanomas can also occur in areas that are well-protected from UV exposure (low UV, mucosal, and palm/sole/nail melanomas). b Melanomas arising from non-epithelium-associated melanocytes. These melanomas fall into the categories of intradermal melanocytic neoplasms (blue nevi, uveal melanoma). These types of melanoma harbor mutations of G protein alpha subunits of Gq family. These mutations are virtually absent from epithelium-associated melanocytes. Melanocytomas are neoplasms of the central nervous system and they closely resemble blue nevi. However, they can pose differential problems to melanoma metastases diagnosis. CSD chronic sun damage. Adapted from Bastian []
The clinical classifications are the results of long-standing observations. They have been critical in making therapy decisions, although their usefulness as guides has been controversial. For practicing oncologists, a distinction between benign and malignant has been most critical, with intermediate stages generating controversial discussions, some of which have been ongoing for decades without a clear resolution. One major reason for this is that any suspected lesion is surgically removed for extensive diagnostic evaluation. Thus, follow-up of existing lesions has rarely been done, leading to considerable variations in risk estimates for dysplastic nevi, as well as biologically early melanomas that progress to aggressive tumors. Genetic analyses of melanocytic lesions have for the first time allowed a more detailed classification, but such new classifications are at an early stage as we know of very few drivers in the disease. Still, the first genetic analyses are becoming routine in making clinical decisions for melanoma therapy.
It is important to discuss the major mutations in melanoma and their affected pathways, while acknowledging that of all human cancers, melanomas carry the most mutations, generally more than 10 per Mb with lung cancer following as the second most non-euploid tumor [). Thus, codrivers can be oncogenes (CDK4, Cyclin D1) or inactivation of tumor suppressor genes (phosphatase and tensin homolog [PTEN]). Likely, cells carry more than one codriver, but their real number remains uncertain and will only be better understood in years to come. Gaining this knowledge is important because each codriver will likely constitutively activate additional pathways, which will require specific targeting for therapy.
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