Abstract
In this issue of Cancer Research, Almassalha and colleagues have proposed a new concept of the development of malignancy, that of the greater genomic landscape. They propose a stressor related exploration of intracellular genomic sites as a response mechanism. This process can express sites with beneficial or deleterious effects, among them those that promote cell proliferation. They point out that their conception is broader, although certainly inclusive, of the process of gene induction. The authors view the physical process of chromatin reorganization as central to the exploration of the genomic landscape. Accordingly, they advocate the development of agents to limit chromatin structural modification as a chemotherapeutic approach in cancer. We found their theory relevant to understand the phenotypic heterogeneity of malignancy, particularly in familial cancer syndromes. For example, the familial atypical multiple mole melanoma (FAMMM) syndrome, related to a gene mutation, is characterized by a diversity of melanocytic lesions, only some of which become malignant melanoma. This new conceptualization can do much to increase understanding of the diversity of malignancy in families with hereditary cancer.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 5602-5604 |
| Number of pages | 3 |
| Journal | Cancer Research |
| Volume | 76 |
| Issue number | 19 |
| DOIs | |
| State | Published - Oct 1 2016 |
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All Science Journal Classification (ASJC) codes
- Oncology
- Cancer Research
Cite this
Commentary on Almassalha et al., "the greater genomic landscape : The heterogeneous evolution of cancer. / Lynch, Henry T.; Rendell, Marc; Shaw, Trudy G.; Silberstein, Peter T.; Ngo, Binh T.
In: Cancer Research, Vol. 76, No. 19, 01.10.2016, p. 5602-5604.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Commentary on Almassalha et al., "the greater genomic landscape
T2 - The heterogeneous evolution of cancer
AU - Lynch, Henry T.
AU - Rendell, Marc
AU - Shaw, Trudy G.
AU - Silberstein, Peter T.
AU - Ngo, Binh T.
PY - 2016/10/1
Y1 - 2016/10/1
N2 - In this issue of Cancer Research, Almassalha and colleagues have proposed a new concept of the development of malignancy, that of the greater genomic landscape. They propose a stressor related exploration of intracellular genomic sites as a response mechanism. This process can express sites with beneficial or deleterious effects, among them those that promote cell proliferation. They point out that their conception is broader, although certainly inclusive, of the process of gene induction. The authors view the physical process of chromatin reorganization as central to the exploration of the genomic landscape. Accordingly, they advocate the development of agents to limit chromatin structural modification as a chemotherapeutic approach in cancer. We found their theory relevant to understand the phenotypic heterogeneity of malignancy, particularly in familial cancer syndromes. For example, the familial atypical multiple mole melanoma (FAMMM) syndrome, related to a gene mutation, is characterized by a diversity of melanocytic lesions, only some of which become malignant melanoma. This new conceptualization can do much to increase understanding of the diversity of malignancy in families with hereditary cancer.
AB - In this issue of Cancer Research, Almassalha and colleagues have proposed a new concept of the development of malignancy, that of the greater genomic landscape. They propose a stressor related exploration of intracellular genomic sites as a response mechanism. This process can express sites with beneficial or deleterious effects, among them those that promote cell proliferation. They point out that their conception is broader, although certainly inclusive, of the process of gene induction. The authors view the physical process of chromatin reorganization as central to the exploration of the genomic landscape. Accordingly, they advocate the development of agents to limit chromatin structural modification as a chemotherapeutic approach in cancer. We found their theory relevant to understand the phenotypic heterogeneity of malignancy, particularly in familial cancer syndromes. For example, the familial atypical multiple mole melanoma (FAMMM) syndrome, related to a gene mutation, is characterized by a diversity of melanocytic lesions, only some of which become malignant melanoma. This new conceptualization can do much to increase understanding of the diversity of malignancy in families with hereditary cancer.
UR - http://www.scopus.com/inward/record.url?scp=84989902153&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84989902153&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-16-2319
DO - 10.1158/0008-5472.CAN-16-2319
M3 - Review article
C2 - 27638875
AN - SCOPUS:84989902153
VL - 76
SP - 5602
EP - 5604
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0099-7013
IS - 19
ER -