Clonal Evolution
Clonal Evolution - Related Videos
15:07
VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
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Cited by 19 •
2015
This protocol describes an approach to interrogate the recombined immunoglobulin heavy chain VDJ regions of lymphomas by deep-sequencing and retrieve VDJ rearrangement and somatic hypermutation status to delineate clonal architecture of individual tumor. Comparing clonal architecture between paired diagnosis and relapse samples reveals lymphoma relapse clonal evolution modes.
12:02
Molecular Evolution of the Tre Recombinase
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Cited by 4 •
2008
Here we report the generation of Tre recombinase through directed, molecular evolution. Tre recombinase recognizes a pre-defined target sequence within the LTR sequences of the HIV-1 provirus, resulting in the excision and eradication of the provirus from infected human cells. While still in its infancy, directed molecular evolution will allow the creation of custom enzymes that will serve as tools of molecular surgery and molecular medicine.
10:32
Enumeration of Neural Stem Cells Using Clonal Assays
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Cited by 5 •
2016
Neural stem cells (NSCs) refer to cells which can self-renew and differentiate into the three neural lineages. Here, we describe a protocol to determine NSC frequency in a given cell population using neurosphere formation and differentiation under clonal conditions.
12:06
Isolation of CD133+ Liver Stem Cells for Clonal Expansion
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Cited by 22 •
2011
Here we describe the isolation of CD133 expressing liver stem cells and cancer stem cells from whole murine liver, a process that requires tissue digestion, cell enrichment, and flow cytometry isolation. We include methods for advanced single cell isolation and clonal expansion.
02:31
Synteny and Evolution
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2021
John H. Renwick first coined the term “synteny” in 1971, which refers to the genes present on the same chromosomes, even if they are not genetically linked. The species with common ancestry tend to show conserved syntenic regions. Therefore, the concept of synteny is nowadays used to describe the evolutionary relationship between species. Around 80 million years ago, the human and mice lineages diverged from the common ancestor. During the course of evolution, the ancestral chromosome underwent...
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New heritable alterations, including DNA mutations, can generate subclones with different traits from a common ancestor. If one subclone survives better or proliferates faster under local conditions, its frequency may increase. This does not require every cell to respond identically; divergent subclones can experience different selective advantages within the same tumor, helping explain changing tumor behavior.
Natural selection favors subclones whose inherited traits improve survival, proliferation, invasion, or resistance under particular conditions. Genetic drift changes subclone frequencies through chance rather than clear functional advantage. Both processes can operate together, while changing microenvironments alter which traits are beneficial. Distinguishing these influences helps researchers interpret why some populations expand and others decline.
Subclones compete within a tumor, and their relative success can change as local conditions change. This competition contributes to intratumoral heterogeneity, meaning that genetically distinct populations coexist in one tumor. The resulting diversity can influence progression because different subclones may differ in survival, proliferation, invasion, or treatment resistance, producing changing disease behavior over time.
Researchers can compare genetically distinct cell populations and examine how their frequencies change over time. Shared alterations can indicate descent from a common ancestor, whereas additional differences can distinguish later-emerging subclones. This evolutionary perspective helps organize tumor development as a history of branching populations rather than as a uniform process, clarifying how diversity arose.
Treatment creates a changing environment in which some subclones may be less affected than others. Populations with traits that support resistance can survive while more sensitive populations decline, allowing resistant cells to become more prominent. Studying these shifts helps researchers identify treatment-resistant populations and recognize that therapy may alter tumor composition rather than eliminate every subclone equally.
Clonal evolution provides a framework for interpreting recurrence as a consequence of tumor diversity and changing subclone frequencies. Resistant or surviving populations may contribute to disease returning after treatment. By accounting for intratumoral heterogeneity and ongoing evolutionary change, researchers can design therapeutic strategies that address diverse tumor populations instead of assuming that one treatment response represents the entire tumor.