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Call for Papers
Special Issue on “Intra-Tumour Genetic Heterogeneity”

Guest Editors:

Luciano G. Martelotto
Monash University, Monash Health, Clayton, Victoria, Australia.
Research Field: Cancer genomics, single cell sequening
Email: (also,

Yi-Hong Zhou
University of California, Irvine, Irvine, California, USA.
Research Field: Brain tumor biology, cancer evolution, and cancer therapy


Tumour genetic heterogeneity has been documented in human cancers, and there is burgeoning evidence to demonstrate that a large proportion of cancers, at diagnosis, are composed of mosaics of genetically and phenotypically distinct tumor cell populations or "sub-clones". Recent investigations have illustrated the likely biological and clinical impact of intra-tumour heterogeneity on cancer progression, metastasis, and therapeutic response. The characterisation of tumour heterogeneity and sub-clonality is therefore important for furthering our understanding about cancer and for the development of improved and more precise therapeutics.
from Dr. Luciano G. Martelotto
Chromosome instability (CIN) and intra-tumoral heterogeneity (TH) are two hallmarks of cancer. Recent investigations have demonstrated the role of CIN, i.e. mis-segregation (MS) of a tumor-specific chromosome and mis-distribution of double minute chromosomes with oncogene amplifications, in controlling the phenotypic transition of cancer cells. This makes TH an inherited feature of both de novo (primary) and metastatic or recurrent tumors. CIN can readily and rapidly give rise to tumor cells with diverse genotypes, which leads to dramatic changes in transcriptional profiles, and thus affect the behavior and survivability of the progeny cells. Hence, CIN plays a critical role in cancer progression and resistance to conventional therapy. Paradoxically, on occasion, CIN interferes with cancer evolution by producing a large number of cells lacking oncogenic function and viability. In such cases, selection would be directed toward suppressing CIN in maintaining the functionally diverse tumor cell subpopulations. This leads to the ability to adjust the MS rate in proliferating tumor cells in accordance with extracellular cues in their microenvironment. Identifying inhibitor(s) of CIN and thereby disrupting the mechanisms maintaining the TH equilibrium needed for optimal tumor growth, would be an entirely new and exciting approach towards cancer treatment. This could lead to the development of powerful therapeutants that could not only treat existing cancer, but potentially prevent tumor recurrence after therapy.
from Prof. Yi-Hong Zhou


Intra-tumour genetic heterogeneity, single cell sequencing, clonality, bioinformatics, chromosome instability, intra-tumoral heterogeneity, inhibitor of CIN on chromosome mis-segregation/double minute mis-distribution, genetic, metabolic, and tumor-forming functional heterogeneities of tumor cell subpopulations.

Why submit to us:

• Rigorous mechanism in peer review: one manuscript must be reviewed by at least two relevant experts. We will endeavour to ensure high standards for the review process and subsequent publication by a team of efficient and professional reviewers and scientific editors.
• No publication fee: there would be absolutely no charge for publication.
• Open Access: As an author you will retain the copyright to your work. By licensing your work under the Creative Commons Attribution License, articles can be re-used and re-distributed without restriction, as long as the original work is correctly cited.
• Wide promotions: Published articles will be promoted at academic conferences, through social networks for scientists and relevant indexing services.

Deadline for Submissions:

31 March 2018


Please click here for Author Instructions.
Please click here to submit your paper.

For administrative support and general queries, please contact:
Carrie Wang, Assistant Editor,

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)


All published articles are preserved here permanently:


All published articles are preserved here permanently: