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Tatiana Codreanu
Kadir Gunes
Mert Karakus


Cancer Biology Society

               About us


The Cancer Biology Society provides a platform for members to discover and critically analyse recent papers related to cancer research. During our meeting group members develop their presentation skills, critical thinking and learn innovative methods used in these cancer research. All of this will contribute to a detailed understanding into research methods therefore later applicable in their professional careers.


Also, we host events and bring in speakers who will inspire, and give a different perspective on coming up with a hypothesis. The members will gain insight on developing scientific research skills which they can use later on in the future. Furthermore, the society supplies information about webinars, conferences and events. In addition, our meetings are guided by the expert in the field Dr. Lauren Pecorino who inspire the members of the society.


Cancer Biology Society meets up once a week usually on Tuesdays  with the times confirmed from the previous meeting.












Cancer is a highly diverse collection of over 200 diseases found in nearly all cell types that share at least one commonality; unregulated cellular growth leading to abnormal proliferation of cells. Cancer cells in solid tumors can remain at the primary lesion site (in situ or localized cancer) or spread as locally-advanced or metastatic cancer. Cancer metastasis accounts for 90% of all cancer-related deaths and is the main determining factor between low-risk cancers, treatable by active surveillance, surgical removal or adjuvant therapy and high-risk cancers that require aggressive therapeutic treatment . Locally-advanced tumors spread externally from, but close to their primary organ site and include both low and high-risk cancers. Metastatic tumors spread to a distant location from their primary site and are high-risk cancers.


Carcinoma cells escaping from primary tumors can intravasate into the circulation, either as single circulating tumor cells (CTCs) or as multicellular CTC clusters. The bloodstream represents a hostile environment for CTCs, exposing them to rapid clearance by natural killer (NK) cells or fragmentation due to the physical stresses encountered in transit through the circulation. Carcinoma cells gain physical and immune protection through the actions of platelets, which coat CTCs shortly after intravasation. Neutrophils can provide protection from NK cell attacks as well, while also contributing to the physical entrapment and extravasation of CTCs. Once lodged in a capillary, activated platelets and carcinoma cells secrete a number of bioactive factors that can act on monocytes, endothelial cells, and the carcinoma cells themselves. The collective effects of these interactions promote the transendothelial migration (TEM) of carcinoma cells, which can be aided by metastasis-associated macrophages (MAMs) in the target parenchyma. In lieu of TEM, arrested carcinoma cells may also proliferate intraluminally (not shown) or induce necroptosis in endothelial cells.(Figure 1)



Figure. 1 Interactions in Transit.(Lambert, Pattabiraman and Weinberg, 2017)


Metastatic cancers are extremely difficult to treat, and account for the vast majority of cancer-related deaths. The dissemination of tumor cells to distant sites is highly dynamic, asynchronous, and involves both tumor and host intrinsic factors. Effective therapeutic targets to block metastasis will need to disrupt key pathways that are required for multiple stages of metastasis.


 The development of metastatic disease is a complex interplay of genetic and epigenetic factors from the host and cancer cells acting in a patient-specific manner. Inhibiting key driver traits of metastasis should yield survival benefit at any stage of the disease, and we look forward to the next generation of personalized medicines for cancer therapy that target cancer cell motility for increased therapeutic efficacy (Stoletov, Beatty and Lewis, 2020).



Figure. 2 . Overview of the metastatic disease process from the primary lesion to the formation of a secondary lesion at a distant site within the body. (Stoletov, Beatty and Lewis, 2020)




Further reading can be found on the link below:!ZSJzxIgR!75Xc9QrfCPelttEn-ZNmnw




Lambert, A., Pattabiraman, D. and Weinberg, R. (2017). Emerging Biological Principles of Metastasis.

Stoletov, K., Beatty, P. and Lewis, J. (2020). Novel therapeutic targets for cancer metastasis. Expert Review of Anticancer Therapy, 20(2), pp.97-109.





Extrachromosomal circular DNA.


Are geneticists ready for the circulome?

For decades biologists have known of mysterious rings of DNA in the nuclei of some human cells, interspersed among the linear chromosomes. Now, what were once curiosities are increasingly looking like key players in health and disease. The circulome, a term introduced at the Biology of Genomes meeting here, may turn out to be a new frontier in genetics. At the meeting, Massa Shoura, a biophysicist at Stanford University in Palo Alto, California, reported that she had adapted a biophysics technique to better survey human cells for so-called extrachromosomal circular DNA (eccDNA), finding diverse complements of independent loops in many kinds of cells. Other recent work suggests that by carrying multiple copies of specific genes, the rings can affect cells’ functions or boost the growth of cancers. One recent paper even proposes that by releasing such loops, cells can influence other, distant cells. This circular DNA is “going to turn out to be extremely important,” predicts Paul Mischel, a cancer biologist at the Ludwig Institute for Cancer Research at the University of California, San Diego (UCSD). Not to be confused with circular bacterial chromosomes or circular RNA— another newly recognized cellular actor (Science, 31 March, p. 1363)—these rings of DNA were first spotted in the nuclei of plant cells. Then other scientists, finding similar free-standing DNA loops in brain cancer cells, speculated that they might give tumors a genetic boost by carrying extra copies of cancer-related genes. This year, Mischel confirmed those suspicions. He and his colleagues revealed that very large DNA circles—up to 5 million base pairs—exist in half of all human cancers, but are rarely found in normal cells. “Levels can be sky high in some tumors,” Mischel says. The cancer cell rings carry many copies of the oncogenes driving the tumor growth, potentially churning out more cancerpromoting protein than chromosomebound copy alone could, he and his colleagues reported on 2 March in Nature.


When a cell divides, such DNA rings replicate as well, but—unlike chromosomal DNA—they may not be evenly apportioned between the daughter cells. They can pile up in one cell, greatly increasing the number of copies of the oncogene it contains. If the extra oncogenes give the cell a big growth boost, that cell type can take over the tumor cell population, Mischel says. The DNA rings may even transfer an oncogene back onto the cell’s linear DNA—his team has found oncogenes outside their normal chromosome locations in cells with the circular DNA. “It provides a different way of thinking about how cancers evolve,” Mischel says. Roel Verhaak, a cancer biologist at Jackson Laboratory for Genomic Medicine in Farmington, Connecticut, found similar evidence that eccDNA contributes to cancer growth. His group recently assessed gene activity in tumors from 13 glioblastoma patients and found DNA circles carrying the cancer-promoting gene MET boosted its activity in those cancer cells, as wellas in tumors that grew when the human cells were implanted in mice. (That work is unpublished but the data were posted in a preprint last year.) 


The team found that the circles varied widely in size and gene content, the largest being 16,000 bases. “That they exist in normal cells with such huge complexity is amazing,” says Anindya Dutta, a molecular biologist at the University of Virginia in Charlottesville, who with his colleagues did an earlier, more limited search for eccDNA in normal and cancer cells (Science, 6 April 2012, p. 82). As Shoura described at the meeting, the circular DNA repertoire varies from cell to cell, perhaps providing a handy way to distinguish cell types, she suggested. (A recent preprint on bioRxiv also details her team’s results.) Preliminary work suggests that each cell type’s complement of circles may also help it specialize. Heart muscle cells, for example, have eccDNA with lots of genes for a particular form of the muscle protein titin. “Extrachromosomal circular DNA is one way that the genome could have some plasticity in it,” notes Kelly Frazer, a genome scientist at UCSD. “It looks like this may be happening in normal development and other types of processes.” Dutta has recently found that DNA rings may help cells communicate, even over long distances. When human tumor cells are grafted into mice, human DNA circles soon appear in the rodent circulatory system, he and his colleagues report in the 26 May issue of Molecular Cancer Research.The shed DNA may transport gene fragments to other cells, although that hasn’t been shown yet. It could also form the basis of a cancer blood test, Dutta says. He further suggests that RNA transcribed from DNA circles could fine-tune gene activity and protein production. For now, the potential roles of these DNA circles are making biologists’ heads spin. “It basically opens a new field and a new way of thinking about DNA and about how dynamic the genome is,” Shoura says.


Further reading can be found on the link below:!kS4wESqZ!PTs5qWaNYxPqcnCEGfBpyQ



Nerves in cancer.




The contribution of nerves to the pathogenesis of malignancies has emerged as
an important component of the tumour microenvironment. Recent studies have shown that
peripheral nerves (sympathetic, parasympathetic and sensory) interact with tumour and
stromal cells to promote the initiation and progression of a variety of solid and haematological
malignancies. Furthermore, new evidence suggests that cancers may reactivate nerve-dependent
developmental and regenerative processes to promote their growth and survival. Here we review
emerging concepts and discuss the therapeutic implications of manipulating nerves and neural
signalling for the prevention and treatment of cancer.

Further reading can be found in the link below:!sHphVToS!OKqdqBilHR-O7Hcg60J6ng




Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels.

The process of angiogenesis is controlled by chemical signals in the body. Some of these signals, such as vascular endothelial growth factor (VEGF), bind to receptors on the surface of normal endothelial cells. When VEGF and other endothelial growth factors bind to their receptors on endothelial cells, signals within these cells are initiated that promote the growth and survival of new blood vessels. Other chemical signals, called angiogenesis inhibitors, interfere with blood vessel formation.

Angiogenesis plays a critical role in the growth of cancer because solid tumors need a blood supply if they are to grow beyond a few millimeters in size. Tumors can actually cause this blood supply to form by giving off chemical signals that stimulate angiogenesis. Tumors can also stimulate nearby normal cells to produce angiogenesis signaling molecules.

The resulting new blood vessels “feed” growing tumors with oxygen and nutrients, allowing the tumor to enlarge and the cancer cells to invade nearby tissue, to move throughout the body, and to form new colonies of cancer cells, called metastases.

Because tumors cannot grow beyond a certain size or spread without a blood supply, scientists have developed drugs called angiogenesis inhibitors, which block tumor angiogenesis. The goal of these drugs, also called antiangiogenic agents, is to prevent or slow the growth of cancer by starving it of its needed blood supply.

Angiogenesis inhibitors are unique cancer-fighting agents because they block the growth of blood vessels that support tumor growth rather than blocking the growth of tumor cells themselves.

Angiogenesis inhibitors interfere in several ways with various steps in blood vessel growth. Some are monoclonal antibodies that specifically recognize and bind to VEGF. When VEGF is attached to these drugs, it is unable to activate the VEGF receptor. Other angiogenesis inhibitors bind to VEGF and/or its receptor as well as to other receptors on the surface of endothelial cells or to other proteins in the downstream signaling pathways, blocking their activities. Some angiogenesis inhibitors are immunomodulatory drugs—agents that stimulate or suppress the immune system—that also have antiangiogenic properties.

In some cancers, angiogenesis inhibitors appear to be most effective when combined with additional therapies. Because angiogenesis inhibitors work by slowing or stopping tumor growth without killing cancer cells, they are given over a long period.



Further reading can be found on the link below:!dCpSWarK!nwWIkkCURSpMt2yW_8oZPQ


Cancer Immunotherapy


Immunotherapy (or immune-therapy) is now becoming a front-line treatment for many tumour types and recently highlighted by the award of the Nobel Prize to Prof. A. Allison and Prof. Honjo who pioneered this new approach to treatment.

At this point, the question arises:
Why is there a need for therapy if the bodies own immune cells can kill cancer cells?

There are several types of immunotherapy, including:


  • Monoclonal antibodies and tumor-agnostic therapies

  • Non-specific immunotherapies

  • Oncolytic virus therapy

  • T-cell therapy

  • Cancer vaccines


Further reading can be found on the link below:!EbwilQ6b!GkY-7pL3ZBd7dhBaz-furw





Cancer Immunotherapy

Mon 24 Feb 2020


Mon 24 Feb 2020

Nerves in cancer.

Mon 17 Feb 2020




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