Interaction of cancer cells with normal cells SlideShare

Cancer cell - SlideShar

  1. Normal Cell VS Cancer Cell 19. Normal Cell VS Cancer Cell 20. Normal Cell VS Cancer Cell . Cells anchor to dish surface and divide (anchorage dependent). When cells have formed a complete single layer, they stop dividing (density-dependent inhibition). If some cells are scraped away, the remaining cells divide to fill the dish with a single.
  2. Cancer Biology. 1. 1 Cancer Biology • Cancer is a group of disease in which cells are aggressive (grow and divide without respect to normal limits), invasive (invade and destroy adjacent tissues), and sometimes metastatic (spread to other locations in the body). • These three malignant properties of cancers differentiate them from benign.
  3. Hallmarks of cancer 1. HALLMARKS OF CANCER By Dr. N. Sreekanth DNB-RT, BIACH&RI 2. What is Normal? Dependence on growth factors -Cell and tissue specific signals -Loss of these signals leads to apoptosis Anchorage dependent proliferation -Requires interaction of transmembrane proteins (integrins) with components of the ECM Contact inhibition -Contact with other cells inhibits.
  4. Oncology Nursing Ma. Tosca Cybil A. Torres, R

An Introduction to Cancer Biology Geoff Mitchell April 24, 2007 Learning Objectives The students will be able to: Identify the 3 most prevalent cancers for a person of their gender Define cancer Explain why cancer is a genetic disease even though its heritability is rather low Compare the functions of oncogenes and tumor suppressor genes Explain why tumor suppressors are often the 1st genes. The process by which normal cells become progressively transformed to malignancy is now known to require the sequential acquisition of mutations which arise as a consequence of damage to the genome. This damage can be the result of endogenous processes such as errors in replication of DNA, the intri

Cancer cells don't interact with other cells as normal cells do. Normal cells respond to signals sent from other nearby cells that say, essentially, you've reached your boundary.. When normal cells hear these signals they stop growing. Cancer cells do not respond to these signals Some of the other characteristics of cancer cells include: Altered cellular differentiation. They can evade the immune system that would otherwise destroy them. The protein that checks for gene damage (p53) in normal cells (thus initiating repair or cell damage) is defective in cancer cells which prevents their death The functional capabilities of normal stem cells and tumorigenic cancer cells are conceptually similar in that both cell types are able to proliferate extensively. Indeed, mechanisms that regulate the defining property of normal stem cells - self-renewal - also frequently mediate oncogenesis. These

The cancer stem cell (CSC) theory is gaining increasing attention from researchers and has become an important focus of cancer research. According to the theory, a minority population of cancer cells is capable of self-renewal and generation of differentiated progeny, termed cancer stem cells (CSCs) This is the essence of cancer. Normal Cell Division . The outer layer of skin (epidermis) is about 12 cells thick. Cells in the basal layer (bottom row) divide just fast enough to replenish cells that are shed. When a basal cell divides, it produces two cells. One remains in the basal layer and retains the capacity to divide Normal cells have a cytoskeleton which consists of microtubules and microfilaments. But the cytoskeleton of cancer cells undergo de-polymerisation and the microtubules disaggregate. (x) Chromosomal Change: Normal cell contains normal chromosome num­ber, e.g., normal cells of human beings contain 46 or 23 pairs chromosomes The key difference between cancer cells and normal cells is that the cancer cells divide uncontrollably while normal cells divide in an orderly manner.. Normal cells divide in an orderly way to produce more cells only when the body needs them. Thus, it is a normal process of cell division that is essential for the growth, development and repair of the body Normal versus Cancer Cells (National Cancer Institute, 2015) Normal Cells. Cancer Cells. Growth Factor Proteins. Stop growing and dividing when they stop producing growth factors, when they have reached their limit, or grown to their maximum. May produce their own growth factors that stimulate reproduction and are less dependent on growth.

T cells comprise one of the major components of the adaptive immune response. In the context of cancer, there are two antagonistic classes of T cells that have important roles in the fight against cancer — cytotoxic CD8 + T cells and CD4 + regulatory T cells (i.e. Tregs). 2.4.1. Cytotoxic CD8 + T cells The interactions of extracellular materials with the cell surface are important facets of the regulation of cell morphology and metabolism. Although it is not simple to unravel the complex actions and interrelationships of these molecules comprising the extracellular microenvironment of cells, their importance is now documented by a rapidly. #1. What we know:\rNormal cell: Mature, adult cells CANNOT renewably proliferate\r.\rWhat is new \(research\):\rCancer stem cells may be a precursor and the true origin of cancer\r- cause still controversial and debated. Oncogenic transformation:\r- Each round gains a genetic mutation\r- Each color is a different round #2

Cancer Biology - SlideShar

  1. Cancer cells in general are not as efficient as normal cells in repairing the damage caused by radiation treatment resulting in differential cancer cell killing . Radiation can be given with the intent of cure as well as being used as a very effective modality of palliative treatment to relieve patients from symptoms caused by the cancer
  2. e whether such dependence on cell density is a general property of ferroptosis, we tested a panel of human epithelial cancer cell lines (Fig. 1c).Most tested cell lines showed cell.
  3. The doubling time of cancer cells (~1-2 days) is orders of magnitude faster than the doubling time of tumours (~60-200 days) 10, implying that the vast majority of cancer cells die before they can divide 11. Thus, natural selection in tumours, like selection among organisms, often takes place through severe competition for space and resources
  4. In further study of the high-CD47 expressing cancer stem cells in a culture dish, researchers added an antibody that blocks the interaction of the cancer cells with macrophages — essentially.
  5. 1. How p53 Works. The p53 protein is normally bound to an active Mdm2 protein. To enable cell cycle checkpoints, p53-Mdm2 must separate and be kept separate to allow p53 time to act. In dividing cells, physical stress or chemical stress such as DNA damage during cell growth can activate an ATM kinase.ATM kinase in turn, phosphorylates Mdm2, causing it to dissociate from p53
  6. ent role in sustaining cell viability in cancer cells with defects in apoptosis 19, 20, 22, 23 (FIG. 1c)
  7. Cancer results when one or all of these processes go wrong, which leads to inconsistency in cancer cells that can successfully be exploited for treatment. Another critical aspect of cancer biology is studies related to protein function and interactions on a systems-wide scale to identify how signaling pathways are restructured in cancer cells.

Hallmarks of cancer - SlideShar

However, whereas the normal cells were only transiently arrested, G 2 /M arrest in the malignant breast cancer cells was permanent and was accompanied by a massive cell death. In accordance. 1. Cell heterogeneity (due to genetic variation, mixture of different cell types including normal cells, transdifferentiation, etc.) is responsible for cancer heterogeneity. Therefore the optimal determination of cancer subtypes necessitates the detection of the many forms of cell heterogeneity on a per-cell basis, which requires careful evaluation of appropriate biomarkers Stromal-Epithelial Interactions: A History. Grobstein's seminal work in the 1950s on the role of mesenchyme in the development of the submandibular gland laid the foundation for a proper understanding of organogenesis (Grobstein, 1953).Soon it was discovered by Le Douarin that the endodermal germ layer was the source of inductive mesenchyme in multiple digestive tissues and that this tissue.

Effects on Cell Physiology: The interaction of virus with the cell membrane and/or subsequent events, (for example, de novo synthesized viral proteins) may change the physiological parameters of infected cells, including movement of ions, formation of secondary messengers, and activation cascades leading to altered cellular activities A striking difference in the cell-cell interactions displayed by normal cells and those of cancer cells is illustrated by the phenomenon of contact inhibition (Figure 15.10). Normal fibroblasts migrate across the surface of a culture dish until they make contact with a neighboring cell Cancer cell migration seems to involve 'leader' and 'follower' cells. The leader cells guide the way and normal barriers are destroyed. Cancer cells can invade blood (and lymphatic) vessels. Once in vessels, cancer cells can move through the body. Cancer cells can be taken to distant areas, where they can form new tumors Cancer Stem Cells • Not all the cells within a tumor can maintain tumor growth, most cancers are not clonal. • Several long-known oncogenic pathways are pivotal to the maintenance of normal stem cell self-renewal. • Techniques used in the stem cell field have identified self-renewing cells. •By identifying the stem cells in tumors, it.

Direct interactions between mesenchymal stroma/stem cells and cancer cells. a Notch signaling: A prominent example for direct cell-to-cell interaction is represented by Notch signaling. DAPT, a Notch signaling inhibitor, was shown to decrease functional alterations of breast cancer cells after co-culture with MSC underlining the involvement of Notch signaling in MSC-cancer cell interactions mary cause of cancer, and the pathogenesis of cancer is seen as a process of transformation of a normal cell into a tumor cell, as evidenced by deep fundamental research of the pathogenesis of cancer, which is held exclusively at the cellular, molecular and genetic levels of the organism [1] [2]. Such a vector of the scientific researc Healthy normal tissues and cells have the inherent ability to avoid the self-elimination of macrophages by expressing anti-phagocytosis molecules, but cancer cells rely even more on similar mechanisms to escape the eradication of immune-mediated (97-100) Some cancer treatments use parts of the immune system to help treat cancer. Immunotherapy. Immunotherapy is a treatment for some types of cancer. It uses the immune system to find and kill cancer cells. They are helpful in cancer treatment because cancer cells are different from normal cells. And the immune system can recognise and kill.

Cancer - SlideShar

Some cancer cells in the tumour become too clever and immune cells can't adapt fast enough to keep them at bay. Escaping the immune system. Immune cells recognise danger through a group of molecules found on the surface of all cells in the body. This helps them inspect potential problems closely and decide whether to attack Stromal interaction with metastatic cells is vital to the proliferation of metastatic cells. For example breast cancer cells produce cytokines such as parathyroid hormone-related peptide (PTHrP) and interleukin-11 which favour osteoclast differentiation through the RANK-RANK ligand (RANKL) system, producing characteristic metastatic osteolytic. The T cell is the primary cell responsible for direct recognition and killing of tumor cells. T cells carry out immunologic surveillance, then proliferate and destroy newly transformed tumor cells after recognizing TAAs. The T-cell response to tumors is modulated by other cells of the immune system; some cells require the presence of humoral antibodies directed against the tumor cells.

This weakness has been exploited to specifically kill the tumor cells while sparing the normal ones, a concept known as 'synthetic lethality'. Recent efforts in the design of cancer therapies are directed towards exploiting synthetic lethal interactions with cancer-associated mutations in the DDR Cancer stem cell markers for several human cancers are listed in Table 1. Cancer stem cells markers have functional attributes such as adhesion, cell invasion (CD44) and interactions with GLI1 and focal adhesion kinase (FAK) (CD24) (58). Table 1. Biomarkers for Human Cancer Stem Cells Cancer Type Markers Breast CD44+CD24_/low Ovar

Cancer stem cells have been created in research laboratories from skin cells10 The researchers used a virus to activate specific pathways and give the target cell stem cell-like qualities. The research proves that a normal cell can become a stem cell with the right set of mutations 1. How p53 Works. The p53 protein is normally bound to an active Mdm2 protein. To enable cell cycle checkpoints, p53-Mdm2 must separate and be kept separate to allow p53 time to act. In dividing cells, physical stress or chemical stress such as DNA damage during cell growth can activate an ATM kinase.ATM kinase in turn, phosphorylates Mdm2, causing it to dissociate from p53 Like stem cells, fetal cells are pluripotent, which means they can grow into many kinds of tissue. Once in the mother's blood, these cells circulate in the body and lodge themselves in tissue

Cancer cells can alter the steady-state activity of all myeloid cells present in the tumor microenvironment by secreting factors such as interleukin (IL)-6 or granulocyte-macrophage colony-stimulating factor (GM-CSF), that induce the recruitment of immature myeloid cells to tumor cells, as well as cell proliferation Recent insights in the fields of cell cycle regulation and cancer would each alone have provided prime examples of research at the Frontiers of Science. However, some of the most revealing information about both topics has derived from the intersection of the two fields. The intent of this summary is to introduce the basics of the cell cycle, cancer, and their overlap, and then to.

• Cell cycle • Cell survival curves • Radiobiological damage: oxygenation, fractionation, and 4 R's of radiobiology • Cell and tissue radiosensitivity Radiation biology • Radiation biology is the study of the action of ionizing radiation on living organisms • The action is very complex, involving physics, chemistry, and biolog Metastasis is the primary cause of cancer morbidity and mortality. The process involves a complex interplay between intrinsic tumor cell properties as well as interactions between cancer cells and multiple microenvironments. The outcome is the development of a nearby or distant discontiguous secondary mass. To successfully disseminate, metastatic cells acquire properties in addition to those.

The molecular biology of cancer - PubMe

Any damage done to a cancer is passed on to descendent cancer cells as proliferation continues. If this damage is severe enough, it will induce cells to undergo apoptosis. Risks. A drawback of treatment is that many genotoxic drugs are effective on cancerous cells and normal cells alike. Selectivity of a particular drug's action is based on the. Cancer cells are normal cells that have acquired numerous hallmark abilities that allow them to become malignant; 4 thus, they are essentially self—part of the host. In spite of this, they. Immunotherapy is a type of cancer treatment that helps your immune system fight cancer. The immune system helps your body fight infections and other diseases. It is made up of white blood cells and organs and tissues of the lymph system.. Immunotherapy is a type of biological therapy.Biological therapy is a type of treatment that uses substances made from living organisms to treat cancer

Cancer Cells vs. Normal Cells: How Are They Different

Cancer cells (HeLa, HT1080) and normal fibroblasts expressing an introduced hTERT cDNA express high levels of telomerase protein (Fig. 2), but this protein is not detected in normal cells (Fig. 2). Cells with telomerase activity have positive nuclear signals whereas cells without telomerase activity do not ( 132 ) Many new therapies are currently being used to treat cancer. Among these new methods, chemotherapy based on peptides has been of great interest due to the unique advantages of peptides, such as a low molecular weight, the ability to specifically target tumor cells, and low toxicity in normal tissues. In treating cancer, peptide-based chemotherapy can be mainly divided into three types, peptide. cell-cell interaction, molecules that play a role in the localization and binding of activated B cells . B cell activation • Two major types: T cell dependent (TD) and T cell independent (TI) • TD: involves protein antigens and CD4+ helper T cells Tumor cells absorb light of different wavelengths (or colors) than normal cells do. So, tumor cells can be targeted by selecting the proper wavelength of the laser. Laser therapy is a type of local treatment, which means it treats a specific part of your body

Cancer Cells - Characteristics, Vs normal cells, Types and

  1. ate cancer. Immunotherapy can: Educate the immune system to recognize and attack specific cancer cells. Boost immune cells to help them eli
  2. Cancer/testis (CT) antigens are a group of proteins united by their importance in development and in cancer immunotherapy.In general, expression of these proteins is restricted to male germ cells in the adult animal. However, in cancer these developmental antigens are often re-expressed and can serve as a locus of immune activation
  3. Most chemotherapeutics elevate intracellular levels of reactive oxygen species (ROS), and many can alter redox-homeostasis of cancer cells. It is widely accepted that the anticancer effect of these chemotherapeutics is due to the induction of oxidative stress and ROS-mediated cell injury in cancer. However, various new therapeutic approaches targeting intracellular ROS levels have yielded.
  4. Cancer is a mass of abnormal and detrimental cells in a given part of the body. The main elucidated cause is the uncontrolled growth and proliferation of those cells after the corruption of the physiological processes responsible for normal development and functioning. The advantage of adjuvant therapy, therapy done after surgery, is to prevent the occurring of symptoms and not necessarily to.
  5. The interaction between high-mobility group box 1 protein (HMGB1) and receptor for advanced glycation end products (RAGE) is important for tumor cell growth. We investigated the tumor biological effects of HMGB1 and RAGE interaction. Previously, we identified an inhibitor of HMGB1/RAGE interaction, papaverine (a non-narcotic opium alkaloid), using a unique drug design system and drug.

Our body's immune system recognizes cancer cells as foreign or abnormal. Unlike normal cells, cancer cells have unique proteins (antigens) on their outer surface. Antibodies are proteins produced by the immune system. They latch onto the cancer cells' antigens. In this way, they label or tag the abnormal cells. Ideally, special cells in the. Gene therapy is the treatment of disease by replacing, altering, or supplementing a gene that is absent or abnormal and whose absence or abnormality is responsible for the disease. Gene therapy may use the genetic material, DNA, itself as the means of treatment. DNA or deoxyribonucleic acid is the very long molecule that encodes the genetic. Cervical cancer happens when the cells of your cervix change. The cancer might invade other tissues and organs. Learn more about the causes, symptoms, diagnosis, treatment, prevention, and outlook. Western blot analysis of siRNA-transfected cells was performed as follows: Cancer cell lines (1.0-1.3×10 5) infected with adenovirus (MOI 30) were incubated with T3 for 12 h and then 50 nm of siRNA was transfected into the cells by using Lipofectamine 2000 (Life Technologies) according to the manufacturer's instructions

Normal stem cells and cancer stem cells: similar and

Regarding the cell - cell interaction proteins, CDH1 is connected to Computation 2021 , 9 , 81 12 of 26 BCAR1 via PIK3R1 in MCF7 cells ( upper picture ), while CDH2 forms a complex with TNS1 an Researchers have known that cancer cells interact extensively with the surrounding microenvironment of the tumor, added Dinah Singer, Ph.D., director of NCI's Division of Cancer Biology. What's novel here is the suggestion that the interactions extend beyond that to tissue that appears to be pathologically normal These delivering agents are introduced into the body through intravenous infusion. These delivering agents highlights the infected areas (tumor cells). The low energy radiations interact with B-10 in the tumor cells to produce B-11 isotope. B-11 through fission reaction produce 2.31Mev energy Delivering agents 14 Once the metastatic cells gain mobility, they push their way out of their native tumor and through other layers of tough cells and molecules until they reach a blood vessel or the lymph system. Here, too, cancer hijacks healthy cells to help do its dirty work. Tumor-associated macrophages come along for the ride, as do other normal cells It supplies structure to cells and acts as a scaffolding for the attachment of many organelles. It is responsible for the ability of cells to move. It is required for the proper division of cells during cellular reproduction. As we will see, changes in the cytoskeleton are observed in cancer cells

Cancer. Cancer cells often resist cell death, even after anti-cancer treatment. Autoimmunity e.g. Lupus, type 1 diabetes. Immune cells that attack the body's own tissues normally die. If this cell death does not occur it can cause diseases such as lupus or type 1 diabetes. Viral infection. Viruses need to keep a cell alive in order to reproduce Targeting the cell cycle checkpoints in cancer. a Chk1/2 or ATR inhibitors in combination with DNA damaging drugs forces cancer cells with DNA damage to bypass the S and G2/M checkpoint arrest and enter mitosis, leading to cell death.b Wee1 inhibitors in combination with DNA damaging drugs forces cancer cells with DNA damage to bypass the G2/M checkpoint arrest and progress into mitosis. include substances that are either produced by cancer cells themselves or by other cells in response to cancer.36, 37 Protein biomarkers are primarily found in the blood and, sometimes, urine.38 Most protein biomarkers related to cancer serve multiple clinical purposes during early or late diseas cancer cell lines derived from earlier stage tumours and the original tumour tissues showed good concordance in several parameters, including the state of P53 (100%) and ERBB2 (93%) [4]. This shows that this type of cells are more representative of the original tumour [4], reflecting more accurately the events that occur in cancer cells in vivo. Immortalized cells are a population of cells from a multicellular organism due to mutation, which can escape normal cellular senescence and keep undergoing division. Thus, this kind of cells can grow in vitro for prolonged periods. The mutations required for immortality can occur naturally or be intentionally induced for experimental purposes

Cancer stem cells: therapeutic implications and

Evidence indicates that lung cancer development is a complex process that involves interactions between tumor cells, stromal fibroblasts, and immune cells. Cancer Cell . 17, 121-134 (2010. Cancer is the uncontrolled growth of abnormal ce lls anywhere in the bod y. These abnormal cells. are termed cancer cells, malignant cells, or tumor cells. Th ese cells can i nfiltrate normal body. Cancer Research: Since both normal cells and cancer cells can be grown in culture, the basic differences between them can be closely studied. In addition, it is possible, by the use of chemicals, viruses and radiation, to convert normal cultured cells to cancer causing cells. Thus, the mechanisms that cause the change can be studied

Normal Cell Division: Growth & Replacemen

Mutation and Cancer. It seems the transition from a normal, healthy cell to a cancer cell is a stepwise progression. Cancer development requires genetic changes in several different oncogenes and tumor suppressors. All cancers have to overcome the same spectrum of regulatory functions in order to grow and progress, but the genes involved may. Monoclonal origin to a mass of extremely heterogeneous constituent cells: Hallmarks of Cancer Fundamental changes in cell physiology which together comprise the malignant phenotype Self-Sufficiency in Growth Signals Physiologic cell proliferation (Figure not in book) 1. Binding of growth factor to its specific receptor on cell membrane 2 Targeted cancer therapies are drugs or other substances that block the growth and spread of cancer by interfering with specific molecules (molecular targets) that are involved in the growth, progression, and spread of cancer.Targeted cancer therapies are sometimes called molecularly targeted drugs, molecularly targeted therapies, precision medicines, or similar names

LC3s (MAP1-LC3A, B and C) are structural proteins of autophagosomal membranes, widely used as biomarkers of autophagy. Whether these three LC3 proteins have a similar biological role in autophagy remains obscure. We examine in parallel the subcellular expression patterns of the three LC3 proteins in a panel of human cancer cell lines, as well as in normal MRC5 fibroblasts and HUVEC, using. Oncogenes: These genes regulate the normal growth of cells. Scientists commonly describe oncogenes as similar to a cancer switch that most people have in their bodies. What flips the switch to make these oncogenes suddenly become unable to control the normal growth of cells and allowing abnormal cancer cells to begin to grow, is unknown NK cells mediate regulatory functions of other cell types including myeloid [DC (246, 287-290), monocytes (291-293), and macrophages (246, 294-296)] or lymphoid [T (297, 298) and B (299-301) cells] via cytokines production or through direct cell-cell contact in a receptor-ligand interaction-dependent manner. As part of the innate. INtERAcT (Interaction Network infErence from vectoR representATions of words) is a novel approach to extract information on protein-protein interactions from scientific papers in a completely unsupervised way. Normally, the way proteins interact is well-regulated. In diseases like cancer, however, disturbed biological processes are reflected in.

Study Notes on Cancer - Biology Discussio

Paramutation (interaction between alleles at a single locus, e.g. maize) 5. Bookmarking (transmitting cellular pattern of expression during mitosis to the daughter cell) 6. Reprogramming 7. Transvection (interaction of alleles on diff. homologous chromosomes) 8. Maternal effects 9. Progress of carcinogenesis 10 The interaction of B-lymphocytes with this bound antigen can have important effects on B-lymphocyte responses. Cell # 7. Mast Cells: Mast cell precursors originate in the bone marrow and are released into the blood as undifferentiated cells. Mast cells are not differentiated from their precursors until the latter leave the blood and enter the. Cancer treatment vaccines are a type of immunotherapy that treats cancer by strengthening the body's natural defenses against the cancer. Unlike cancer prevention vaccines, cancer treatment vaccines are designed to be used in people who already have cancer—they work against cancer cells, not against something that causes cancer Nickel is a known carcinogen. NDRG1 protein is expressed at low levels in normal tissues, but, in a variety of cancers, it is over-expressed. This differential expression in cancer cells compared with normal cells makes the NDRG1 gene an important cancer marker ( 72)

Difference Between Cancer Cells and Normal Cells Compare

Explore MAPK Understanding the MAPK pathway as it relates to oncology. The mitogen-activated protein kinase (MAPK) pathway plays a role in the regulation of gene expression, cellular growth, and survival. 1 Abnormal MAPK signaling may lead to increased or uncontrolled cell proliferation and resistance to apoptosis. 2 Research into the MAPK pathway has shown it to be important in some cancers. Doru Paul, MD. on June 05, 2020. Tumor suppressor genes make proteins that regulate the growth of cells, and they play an important role in preventing the development of cancer cells . When tumor suppressor genes are altered or inactivated due to a mutation (either one that is present at birth or one that occurs later in life), they make. Cancer cells grow more rapidly than normal cells, so they are more affected by the drug. In people with sickle cell disease, this drug changes the shape of red blood cells. This makes it less. Some mutations don't have a noticeable effect, but others may lead to a disease. For example, a certain mutation in the gene for hemoglobin causes the disease sickle cell anemia. Cells become cancer cells largely because of mutations in their genes. Often many mutations are needed before a cell becomes a cancer cell The key difference between cell proliferation and differentiation is that cell proliferation is the process of increasing the cell number while cell differentiation is the process of forming a variety of cell types that have specific functions.. Fertilization is the act that produces a diploid zygote from the fusion of male gamete with a female gamete during sexual reproduction Dendritic cells (DCs) are essential in immunity owing to their role in activating T cells, thereby promoting antitumor responses. Tumor cells, however, hijack the immune system, causing T cell exhaustion and DC dysfunction. Tumor-induced T cell exhaustion may be reversed through immune checkpoint blockade (ICB); however, this treatment fails to show clinical benefit in many patients