Tumor microenvironment

528: 520: 536: 377: 226: 22: 318: 496:, sustained angiogenesis, limitless replication potential, and tissue invasion. In cancer, changes in the ECM dynamics lead to changes in composition, density, and mechanical properties, affecting tumor aggressiveness and response to therapy. Research suggests that both pro- and anti-tumorigenic effects occurs during ECM remodeling. In early tumor formation, stromal cells produce excess ECM proteins, causing the tissue around the tumor to stiffen. Some of the contributing factors to tumor stiffness is increased 173:, where new blood vessels emerge from pre-existing vasculature. The blood vessel formed in the tumor environment often does not mature properly, and as a result the vasculature formed in the tumor microenvironment differs from that of normal tissue. The blood vessels formed are often "leaky" and tortuous, with a compromised blood flow. As tumors cannot grow large without proper vasculature, sustained angiogenesis is therefore considered one of the hallmarks of cancer. 485: 57:. Mutual interaction between cancer cells and the different components of the tumor microenvironment support its growth and invasion in healthy tissues which correlates with tumor resistance to current treatments and poor prognosis. The tumor microenvironment is in constant change because of the tumor's ability to influence the microenvironment by releasing extracellular signals, promoting 632:

block metastasis, as natural killer cells are most efficient at killing cancer cells outside of the tumor microenvironment. Tumor-infiltrating lymphocytes have been used in therapeutic treatments, where lab-amplificated immune cells are transferred to cancer patients to help their immune system fight the cancer. This treatment has seen success in solid tumors such as melanoma.

328:(CAFs) are a heterogenous group of activated fibroblasts central to the reactive stroma within the tumor microenvironment. The precise definition of CAFs remains challenging due to variations in cellular origins and expression markers. However, evidence suggests CAFs originate from activated resident fibroblasts, bone marrow-derived 671:(IL-2), and by cross-presenting tumor antigens. Tregs are, as opposed to CD8+, tumor promoting. They secrete tumor growth factors, and indirectly support cancer survival by interacting with endothelial cells and carcinoma associated fibroblasts. Tregs also have immunosuppressive mechanisms that can make CD8+ cells less effective. 355:; one that promotes tumor growth and another that inhibits it, with the former being more common and contributing to tumor development and therapy resistance through various mechanisms. Various subpopulations of CAFs have been identified across different cancer types. In breast cancer, for example, studies using 955:

as well as replicate rapidly and homogenously, making them potentially very effective as a cancer-therapy. Since the tumor microenvironment has several barriers that limit the ability of CAR T cells to infiltrate the tumor, several strategies have been developed to address this. Localized delivery of

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Tumor-infiltrating lymphocytes are lymphocytes, including T cells, B cells and natural killer cells, that penetrate the tumor and have the ability to recognize and kill cancer cells. A high concentration is generally positively correlated with good prognosis (802). This type of immune cells can also

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that regulate functions and mechanical properties. However, in tumors, the ECM plays an important role in shaping the tumor microenvironment and influences cancer progression, metastasis, and therapeutic response. This process is called extracellular matrix remodeling and is characterized by changes

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Experiments in mice have mainly shown that tumor-associated neutrophils exhibit tumor-promoting functions, but a smaller number of studies show that neutrophils can also inhibit tumor growth. Tumor associated neutrophils can be divided into N1- and N2-polarized neutrophils. N1-polarized neutrophils

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from tumor cells. Stromal cells contribute to tumor initiation, progression and drug resistance, and the stroma is known to evolve as the tumor develops. Understanding the interactions between cancer cells and stromal cells is essential for developing effective cancer treatments. Alterations in the

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Hypoxia causes the upregulation of hypoxia induced factors (HIFs), which are transcription factors that decides how cells respond to a lack of oxygen. HIFs induces the transcription of thousands of genes, some of which induces angiogenesis or furthers metastasis, leading, for instance, to increased

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genetic variants can significantly influence the composition of the tumor microenvironment. These germline variants affect the number of infiltrating CD8 T cells and regulatory T cells within tumors, thereby impacting immune evasion and responses to immunotherapy. Notably, studies published in the

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analysis and single-cell RNA sequencing have shed more light on the diverse characteristics of CAFs, revealing distinct and sometimes contradictory functions. Their functions appear to be context dependent. This diversity in stomal composition not only shapes the tumor microenvironment, but also

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T cells must replicate after arriving at the tumor site to effectively kill the cancer cells, survive hostile elements and migrate through the stroma to the cancer cells. This is affected by the tumor microenvironment. The draining lymph nodes are the likely location for cancer specific T cell

449:. The transmission of signals from the ECM to the cell interior involves various pathways. One primary way is direct transduction mediated by transmembrane proteins like integrins. Integrins is the most studied ECM binding receptor and mediate ECM remodeling and regular cellular processes like 582:

activation allows for the smoldering inflammation seen in cancer. Unlike normal macrophages, tumor-associated macrophages lack cytotoxic activity. Monocyte derived macrophages are divided into inflammatory M1-polarized macrophages and anti-inflammatory M2-polarized macrophages. M1-polarized

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Tumor-associated immune cells can be tumor-antagonizing or tumor-promoting, meaning that they can suppress or promote tumor growth. Because of the effects of hypoxia, the anti-tumor abilities of many tumor-antagonizing immune cells, such as cytotoxic T cells and natural killer cells, become

613:. Neutrophils can accumulate in tumors and in some cancers, such as lung adenocarcinoma, their abundance at the tumor site is associated with worsened disease prognosis. Neutrophil numbers (and myeloid cell precursors) in the blood can be increased in some patients with solid tumors. 102:

factors of the vascular connection, with tumor cells more likely to be trapped in the first connected organ. This viewpoint suggested that certain properties or mutations within cancer cells might dictate their metastatic potential, independent of the surrounding tissue environment.

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of a particular type of cancer ("the seed") often metastasizes to certain sites ("the soil") based on the similarity of the original and secondary tumor sites. In other words, just as seeds need fertile soil to grow, cancer cells require a supportive microenvironment to metastasize.

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The enhanced permeability and retention effect is the observation that the vasculature of tumors tend to accumulate macromolecules in the blood stream to a greater extent than in normal tissue. This is due to the "leaky" nature of the vasculature around tumors, and a lacking

85:'s "seed and soil" theory introduced the important role of TME in cancer metastasis, highlighting the intricate relationship between tumors and their surrounding microenvironment. The theory indicated that cancer cells have tendencies when spreading. Paget proposed that the 500:

and acid deposition. Additionally, the restructured ECM and its degradation fragments (matrikines) impacts signaling pathways via cell-surface receptor interactions, leading to dysregulated stromal cell behavior and the emergence of an oncogenic microenvironment.

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Targeting CAF has emerged as a promising strategy for improving cancer treatment, but the research faces several challenges. These include gaps in our understanding of CAF origins and their diverse functions, some of which may be helpful in combating tumors.

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CAFs are one of the most common components of the tumor stroma and are particularly found in the interstitial spaces of breast, prostate, and pancreatic cancer. They interact with cancer cells by secreting a variety of extracellular matrix components or

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macrophages phagocytize tumor cells and are considered tumor-antagonizing. M2-polarized macrophages are, on the other hand, tumor-promoting, because they promote tumor progression by suppressing immunosurveillance, aiding angiogenesis by secreting

203:. The permeable vasculature allows for easier delivery of therapeutic drugs to the tumor, and the lacking lymphatic vessels contribute to an increased retention. The permeable vasculature is thought to have several causes, including insufficient 257:

pathways. This genetic instability leads to a high number of mutated cells, and is associated with cancer progression. Periods of mild and acute hypoxia and reoxygenation can lead cancer cells to adapt and grow into more aggressive phenotypes.

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stroma, including the activation of fibroblasts into carcinoma-associated fibroblasts (CAFs) and remodeling of the extracellular matrix (ECM), are recognized as important in cancer progression and potential targets for therapy and diagnosis.

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Unezaki S, Maruyama K, Hosoda JI, Nagae I, Koyanagi Y, Nakata M, et al. (22 November 1996). "Direct measurement of the extravasation of polyethyleneglycol-coated liposomes into solid tumor tissue by in vivo fluorescence microscopy".

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Zhang W, Wang L, Zhou D, Cui Q, Zhao D, Wu Y (January 2011). "Expression of tumor-associated macrophages and vascular endothelial growth factor correlates with poor prognosis of peripheral T-cell lymphoma, not otherwise specified".

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Cancer is a complex disease involving both tumor cells and surrounding stromal cells. In cancer biology, the stroma is defined as the nonmalignant cells found in the supportive tissue surrounding tumors. These cells include

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T cells reach tumor sites via the vascular system, where the tumor microenvironment appears to preferentially recruit other immune cells over T cells. One such discriminating mechanism is the release of cell-type specific

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formulated a complementary hypothesis in the 1970s, where he proposed that while the mechanical aspects of blood flow is important, metastatic colonization specifically targets certain organs, known as organotropism.

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and immune-suppressive properties. However, their cytotoxic activity was found to be lower compared to lymphocytes from distant sites, likely due to the overall immunosuppressive state in tumor-bearing individuals.

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A tumor's vasculature is important to its growth, as blood vessels deliver oxygen, nutrients, and growth factors to the tumor. Tumors smaller than 1–2 mm in diameter are delivered oxygen and nutrients through

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challenged Paget's theory with his own perspective on cancer metastasis. Ewing proposed that the ability of cancer cells to metastasize was primarily influenced by mechanical mechanisms such as anatomical and

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vehicles (~20–200 nm in diameter) can transport drugs and other therapeutic molecules. These therapies can be targeted to selectively extravasate through tumor vasculature. These efforts include protein

663:(Tregs). CD8+ cells are tumor-antagonizing cells that recognize tumor antigens and targets cancer cells for destruction. In addition, CD8+ cells slow tumor progression and suppress angiogenesis by releasing 587:(VEGF) and remodeling the extracellular matrix. The tumor microenvironment promotes the M2-polarized macrophages, and an increased amount of tumor-associated macrophages is associated with worse prognosis. 932:(PTKs). This show promise in modulating the tumor microenvironment, resulting in cancer regression. Understanding how TKIs modulates the tumor microenvironment may offer another form of cancer treatment. 3949:

Zhang BC, Gao J, Wang J, Rao ZG, Wang BC, Gao JF (December 2011). "Tumor-associated macrophages infiltration is associated with peritumoral lymphangiogenesis and poor prognosis in lung adenocarcinoma".

344:, which is important in regulating the biological behavior of tumors. These regulations are particularly important for tumor development and influence cancer cell growth, invasion, inflammation, and 617:

accumulate in the tumor in its early stages and support with tumor cell death. In later stages N2-polarized neutrophils promotes angiogenesis by secreting vascular endothelial growth factor (VEGF).

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into chemical signals. Integrins can sense differences between simple, rigid two-dimensional surfaces and complex, malleable three-dimensional environments, altering cellular signaling accordingly.

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Stromal cells within the tumor microenvironment represent an important cellular component in cancer development, influencing tumor metabolism, growth, metastasis, immune evasion, and resistance to

687:(FasL) in the vasculature of ovarian, colon, prostate, breast, bladder and renal tumors. Tumors with a high expression of FasL has been shown to contain an abundancy of Tregs, but few CD8+ cells. 274:". HIFs also regulate immune cells, and an increased expression can lead to the inactivation of anti-tumor functions. This furthers the survival of tumor cells and hinders anti-tumor treatment. 635:

Tumor-infiltrating lymphocytes can become tumor-promoting due to the immunosuppressive mechanisms of the tumor microenvironment. Cancer cells induce apoptosis of activated T cells by secreting

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While ECM remodeling is tightly regulated under normal physiological conditions, it also modulates many of the tumor cell behaviors associated with cancer progression. This includes evasion of

476:. These receptors interact with various ECM components and create diverse cellular processes that contribute both to normal physiological functions and pathological conditions like cancer. 5061:

Feng Y, Liao Z, Zhang H, Xie X, You F, Liao X, et al. (January 2023). "Emerging nanomedicines strategies focused on tumor microenvironment against cancer recurrence and metastasis".

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and cell-matrix alterations. ECM remodeling involves dynamic alterations in ECM composition, organization, and biomechanical properties. ECM remodeling is induced by factors such as

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of oxygen is below 5 mmHg in over 50% of locally advanced solid tumors, compared to venous blood which has a partial pressure of oxygen at 40-60 mmHg. A hypoxic environment leads to

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Lei X, Lei Y, Li JK, Du WX, Li RG, Yang J, et al. (2020-02-01). "Immune cells within the tumor microenvironment: Biological functions and roles in cancer immunotherapy".

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Korneev KV, Atretkhany KN, Drutskaya MS, Grivennikov SI, Kuprash DV, Nedospasov SA (January 2017). "TLR-signaling and proinflammatory cytokines as drivers of tumorigenesis".

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cell migration and matrix remodeling. An increased HIF expression can lead tumor cells to shift their metabolism from aerobic to anaerobic, where they obtain energy through

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Danhier F, Feron O, Préat V (December 2010). "To exploit the tumor microenvironment: Passive and active tumor targeting of nanocarriers for anti-cancer drug delivery".

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in the microenvironment and is present in all tissue. The ECM is a highly dynamic structure and is essential for tissue development, repair, support, and

4188:"Prognostic value of pretreatment circulating neutrophils, monocytes, and lymphocytes in oropharyngeal cancer stratified by human papillomavirus status" 3731:

Mathias RA, Gopal SK, Simpson RJ (January 2013). "Contribution of cells undergoing epithelial-mesenchymal transition to the tumour microenvironment".

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Component of the tumor microenvironment (TME). The tumor microenvironment is a complex system of various tumor cells, stromal cells, and immune cells.

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inhibited. Tumor-promoting immune cells such as regulatory T cells and myeloid derived suppressor cells will, on the other hand, become upregulated.

145:. In larger tumors the center becomes too far away from the existing blood supply, leading the tumor microenvironment to become hypoxic and acidic. 3809:"A distinct and unique transcriptional program expressed by tumor-associated macrophages (defective NF-kappaB and enhanced IRF-3/STAT1 activation)" 906:

are potent, specific and target abnormal kinases while minimizing toxicity. Kinase inhibitors have expanded treatment options for various cancers.

1458: 270:, which decreases the pH in the microenvironment from a neutral and healthy 7.35-7.45 to an acidic 6.3-7.0. This phenomenon is described as the " 104: 5484:

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suggested improvement of CAR T cell trafficking. As this therapy expands to other diseases, managing its unique toxicity profile, including

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have revealed distinct phenotypes, including vascular CAFs, matrix CAFs, cycling CAFs, and developmental CAFs. Studies using

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Alasvand N, Urbanska AM, Rahmati M, Saeidifar M, Gungor-Ozkerim PS, Sefat F, et al. (2017-01-01), Grumezescu AM (ed.),

724:. 3D tumor models have been developed as a more spatially representative model of the TME. Spheroid cultures, scaffolds and 720:

have been long used in order to study various tumors. They are quick to set up and inexpensive, but simplistic and prone to

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containing death ligands such as FasL and TRAIL, and via the same method, turn off the normal cytotoxic response of

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Multiple factors determine whether tumor cells will be eliminated by the immune system or will escape detection.

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within the tumor microenvironment. Reports emerged detailing the presence and activities of tumor-infiltrating

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and other common genetic variants in modulating the tumor immune landscape and driving therapeutic outcomes.

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In later stages of tumor progression endothelial cells can differentiate into carcinoma associated

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Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models

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Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models

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suppresses tumor growth by inducing transition of macrophages to proinflammatory types.

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suggested improved anti-tumor activity and engineering these cells to overexpress

651:

There are several types of T cells that are important to tumorigenesis, including

575: 336:(ETM), or endothelial cells trough endothelial to mesenchymal transition (EndMT). 5693: 5676: 5497: 4981:"STAT3-enhancing germline mutations contribute to tumor-extrinsic immune evasion" 3919: 3629: 3324: 2458: 1474: 1364: 1347: 1299:"Pan-Cancer Analysis of Ligand-Receptor Cross-talk in the Tumor Microenvironment" 1240: 1188: 902:

are common in cancer cells, making them attractive targets for anticancer drugs.

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and are much better at recreating the tumour architecture than 2D cell cultures.

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Tumor-associated macrophages are a central component in the strong link between

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origin that are considered tumor promoting. They have the potential to repress

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Targeting immunoregulatory membrane receptors succeeded in some patients with

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Immune checkpoints of immunosuppressive actions associated with breast cancer

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is clinically approved in the US to treat a variety of cancers by targeting

453:, survival, migration, and invasion in response to ECM changes. They act as 5710: 5661: 5605: 5578: 5513: 5470: 5406: 5380: 5329: 5253: 5204: 5141: 4965: 4906: 4871: 4836: 4795: 4746: 4657: 4608: 4551: 4494: 4435: 4386: 4329: 4270: 4213: 4164: 4129: 4072: 4030: 3971: 3927: 3891: 3834: 3793: 3752: 3706: 3645: 3587: 3528: 3471: 3412: 3350: 3293: 3242: 3196: 3137: 3078: 3019: 2962: 2905: 2837: 2785: 2728: 2666: 2607: 2548: 2484: 2424: 2373: 2307: 2265: 2250: 2191: 2107: 2050: 1993: 1931: 1872: 1786: 1729: 1682: 1623: 1564: 1490: 1438: 1324: 1283: 1248: 1206: 1154: 1100: 1081: 1046: 968:(CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and 957: 853: 780: 560: 458: 401: 389: 345: 301: 283: 170: 149:

is upregulated to feed the cancer cells and is linked to tumor malignancy.

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The concept of the tumor microenvironment (TME) dates back to 1863 when

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are polymorphonuclear immune cells that are critical components of the

571:

with the M2 phenotype are considered myeloid-derived suppressor cells.

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In the late 1970s, attention shifted towards understanding the role of

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in protein content and enzymatic activity which influences signal

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Myeloid-derived suppressor cells and tumor-associated macrophages

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Surroundings of tumors including nearby cells and blood vessels

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do not usually develop with the tumor, leading to increased

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In hypoxic environments the tissue sends out signals called

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Human germline genetic variants and tumor microenvironment

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replication, although this also occurs within the tumor.

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into cancerous cells, specifically breast cancer cells.

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Tumor-associated macrophages are associated with using

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In addition to integrins, other cell receptors like

457:

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1942: 1933: 1929: 1924: 1919: 1915: 1911: 1906: 1901: 1897: 1893: 1889: 1882: 1874: 1870: 1865: 1860: 1856: 1852: 1848: 1844: 1840: 1836: 1832: 1828: 1824: 1817: 1815: 1813: 1811: 1809: 1807: 1805: 1803: 1801: 1799: 1797: 1788: 1784: 1780: 1776: 1771: 1766: 1762: 1758: 1754: 1747: 1739: 1735: 1731: 1727: 1723: 1719: 1715: 1711: 1707: 1703: 1699: 1692: 1684: 1680: 1675: 1670: 1666: 1662: 1657: 1652: 1648: 1644: 1640: 1633: 1625: 1621: 1616: 1611: 1607: 1603: 1598: 1593: 1589: 1585: 1581: 1574: 1566: 1562: 1557: 1552: 1548: 1544: 1540: 1536: 1532: 1528: 1524: 1517: 1515: 1513: 1511: 1509: 1500: 1496: 1492: 1488: 1484: 1480: 1476: 1472: 1468: 1464: 1460: 1453: 1451: 1449: 1440: 1436: 1431: 1426: 1422: 1418: 1414: 1410: 1406: 1402: 1398: 1391: 1383: 1379: 1375: 1371: 1366: 1361: 1357: 1353: 1349: 1342: 1334: 1330: 1326: 1322: 1317: 1312: 1308: 1304: 1300: 1293: 1285: 1281: 1277: 1273: 1269: 1265: 1258: 1250: 1246: 1242: 1238: 1234: 1230: 1223: 1221: 1219: 1217: 1208: 1204: 1199: 1194: 1190: 1186: 1182: 1178: 1174: 1167: 1165: 1156: 1152: 1147: 1142: 1138: 1134: 1130: 1126: 1122: 1115: 1113: 1111: 1102: 1098: 1093: 1088: 1083: 1078: 1074: 1070: 1066: 1059: 1057: 1048: 1044: 1039: 1034: 1030: 1026: 1021: 1016: 1012: 1008: 1004: 997: 993: 983: 980: 979: 973: 971: 967: 963: 959: 954: 950: 949:T lymphocytes 946: 945:immunotherapy 942: 933: 931: 927: 923: 919: 915: 911: 907: 905: 901: 891: 889: 886: 882: 878: 874: 870: 866: 861: 859: 855: 851: 847: 843: 839: 825: 823: 819: 815: 811: 807: 802: 798: 794: 790: 786: 782: 778: 774: 770: 760: 758: 754: 750: 745: 735: 733: 732: 727: 723: 722:genetic drift 719: 715: 711: 707: 692: 688: 686: 682: 678: 672: 670: 669:interleukin-2 666: 662: 658: 654: 644: 642: 638: 633: 628: 618: 614: 612: 608: 599: 597: 593: 588: 586: 581: 577: 572: 570: 566: 562: 558: 554: 550: 537: 529: 521: 517: 512: 502: 499: 495: 486: 477: 475: 471: 467: 462: 460: 456: 452: 451:proliferation 448: 444: 440: 436: 426: 424: 420: 416: 412: 407: 403: 402:glycoproteins 399: 395: 391: 390:proteoglycans 387: 378: 369: 365: 362: 358: 354: 353:tumorigenesis 349: 347: 343: 337: 335: 331: 327: 319: 310: 307: 303: 298: 296: 292: 285: 278:Stromal cells 275: 273: 269: 265: 259: 256: 252: 248: 244: 240: 236: 227: 222: 221:Tumor hypoxia 212: 210: 206: 202: 195: 185: 183: 179: 174: 172: 168: 164: 160: 150: 148: 144: 133: 130: 126: 123:, as well as 122: 121:B lymphocytes 118: 114: 109: 106: 105:Isaiah Fidler 101: 96: 91: 88: 84: 83:Stephen Paget 80: 70: 68: 64: 61:and inducing 60: 56: 52: 48: 44: 40: 39:blood vessels 36: 32: 23: 19: 5687:(1): 34–48. 5684: 5680: 5670: 5636:(1): 31–44. 5633: 5629: 5619: 5609:, retrieved 5597: 5587: 5544: 5540: 5530: 5489: 5485: 5479: 5434: 5430: 5420: 5410:, retrieved 5398: 5389: 5352: 5348: 5338: 5303: 5299: 5289: 5272: 5268: 5262: 5227: 5223: 5213: 5188: 5184: 5178: 5164:(1): 11–17. 5161: 5157: 5150: 5113: 5109: 5099: 5066: 5062: 5056: 5029: 5025: 5015: 4988: 4984: 4974: 4940:(18): 4610. 4937: 4933: 4923: 4890: 4886: 4880: 4855: 4851: 4845: 4818: 4814: 4804: 4769: 4765: 4755: 4702: 4680:. Retrieved 4678:. 2011-02-02 4675: 4666: 4631: 4627: 4617: 4574: 4570: 4560: 4517: 4513: 4503: 4458: 4454: 4444: 4409: 4405: 4395: 4352: 4348: 4338: 4293: 4289: 4279: 4244: 4240: 4230: 4195: 4191: 4181: 4148: 4144: 4138: 4103: 4099: 4089: 4056: 4052: 4039: 4005:(117): 117. 4002: 3998: 3988: 3955: 3951: 3944: 3914:(1): 46–52. 3911: 3907: 3900: 3868:(1): 39–51. 3865: 3861: 3851: 3816: 3812: 3802: 3775: 3771: 3761: 3736: 3732: 3672: 3668: 3662: 3621: 3617: 3551: 3547: 3537: 3494: 3490: 3480: 3435: 3431: 3421: 3376: 3372: 3316: 3312: 3302: 3269: 3265: 3259: 3218: 3214: 3160: 3156: 3146: 3101: 3097: 3087: 3042: 3038: 3028: 2985: 2981: 2971: 2928: 2924: 2914: 2863: 2859: 2813: 2809: 2751: 2747: 2737: 2695:(16): 3906. 2692: 2688: 2630: 2626: 2616: 2574:(14): 3466. 2571: 2567: 2557: 2514: 2510: 2450: 2446: 2396: 2392: 2382: 2337: 2333: 2273: 2269: 2259: 2214: 2210: 2200: 2175: 2171: 2148:, retrieved 2126: 2116: 2073: 2069: 2059: 2016: 2012: 2002: 1959: 1955: 1895: 1891: 1881: 1830: 1826: 1760: 1756: 1746: 1705: 1701: 1691: 1649:(10): 2617. 1646: 1642: 1632: 1587: 1583: 1573: 1530: 1526: 1469:(1): 69–74. 1466: 1462: 1404: 1400: 1390: 1355: 1351: 1341: 1306: 1302: 1292: 1267: 1263: 1257: 1232: 1228: 1180: 1176: 1128: 1124: 1072: 1068: 1013:(17): 4131. 1010: 1006: 996: 958:glioblastoma 939: 908: 897: 862: 854:angiogenesis 836: 781:angiogenesis 766: 752: 748: 741: 729: 709: 705: 703: 689: 673: 650: 634: 630: 615: 605: 589: 573: 561:angiogenesis 547: 514: 505:Immune cells 491: 463: 459:cytoskeleton 445:(DDRs), and 432: 411:transduction 383: 366: 350: 346:angiogenesis 338: 324: 302:chemotherapy 299: 287: 284:Stromal cell 260: 232: 197: 175: 171:angiogenesis 156: 147:Angiogenesis 139: 129:cytotoxicity 110: 92: 76: 43:immune cells 30: 28: 18: 4772:: 341–360. 4628:Cancer Cell 3772:Cancer Cell 3739:: 545–557. 3698:2434/145688 3624:: 126–133. 3373:Biomimetics 3221:: 192–200. 3098:Biomimetics 2866:(1): 4294. 2399:(6): 1616. 2070:Cancer Cell 1407:(4): 1–15. 1270:: 127–135. 838:Bevacizumab 814:endothelium 801:Nanocarrier 797:ferumoxytol 791:(ECM), and 607:Neutrophils 602:Neutrophils 569:macrophages 553:myelogenous 394:homeostasis 291:fibroblasts 178:fibroblasts 136:Vasculature 113:lymphocytes 100:hemodynamic 95:James Ewing 47:fibroblasts 5611:2024-02-20 5598:StatPearls 5492:: 106087. 5412:2024-02-20 5355:(1): 116. 5306:: 102017. 5116:(1): 274. 5069:: 139506. 4682:2024-02-19 4241:Oncotarget 3554:(1): 238. 3379:(2): 146. 2517:(9): 587. 2150:2024-02-19 1898:(1): 204. 1763:: 100422. 1590:(1): 176. 1358:: 100017. 988:References 970:cytopenias 873:urothelial 833:Antibodies 773:metastasis 685:Fas ligand 677:chemokines 657:T helper 1 264:glycolysis 247:DNA repair 182:metastasis 87:metastases 53:) and the 5703:0923-7534 5561:2372-7705 5547:: 69–77. 5522:237943611 5506:1357-2725 5453:1476-4598 5437:(1): 43. 5322:0305-7372 5091:252676223 4729:1664-431X 3654:208063582 3638:0304-3835 3570:2072-6694 3511:1059-1524 3454:2073-4409 3438:(2): 81. 3395:2313-7673 3333:1878-1551 3286:0955-0674 3251:202571768 3235:1044-579X 3179:2234-943X 3120:2313-7673 3104:(3): 87. 3061:2296-889X 3002:1471-0080 2945:1474-1768 2888:2041-1723 2830:1476-5500 2768:2092-6413 2711:2072-6694 2649:2234-943X 2590:2072-6694 2531:2041-4889 2467:1540-336X 2356:2234-943X 2290:0021-9738 2233:2296-634X 2090:1535-6108 2033:1432-1335 1976:1533-0346 1914:1756-9966 1855:0960-9822 1779:2468-2942 1722:1474-1768 1665:2073-4409 1606:1476-4598 1547:1573-7233 1483:1072-4109 1421:1021-335X 1382:244452599 1374:2667-3940 1333:232432582 1183:: 41–48. 1029:1422-0067 924:, target 922:gefitinib 918:lapatinib 914:erlotinib 828:Therapies 810:liposomes 726:organoids 681:apoptosis 494:apoptosis 447:syndecans 439:integrins 423:proteases 398:collagens 361:proteomic 205:pericytes 93:In 1928, 67:cancerous 5725:Category 5711:33098993 5662:29103912 5606:30725979 5579:35434273 5514:34563698 5471:29455663 5407:31643906 5381:32680511 5330:32335505 5254:23323560 5205:22827162 5142:35701781 5047:10182072 4966:34572836 4915:20557369 4907:26020501 4872:15885603 4837:17409393 4796:21954698 4747:35165861 4658:21907922 4609:25985180 4552:26649828 4495:25624500 4436:29191879 4387:25822788 4330:24591638 4271:25865224 4214:25336438 4173:21924175 4165:27339708 4130:26193342 4073:27282249 4031:21939504 3980:24840259 3972:20676804 3936:26116121 3928:21077742 3892:20371344 3835:16269622 3794:15766659 3753:23099347 3707:18650914 3646:31730903 3588:35008401 3529:30091653 3472:30678058 3413:37092398 3404:10123695 3351:31063753 3294:16919434 3243:31518697 3197:32351878 3138:35892357 3079:35558554 3020:25415508 2963:31980749 2906:37463917 2897:10354071 2838:33712707 2786:37394578 2777:10394065 2729:36010899 2667:33763348 2608:34298680 2549:37666813 2540:10477351 2485:26222075 2425:32570870 2374:36212414 2308:35642641 2251:33796526 2192:20797419 2108:36917953 2099:10202656 2051:34613483 1994:34350796 1932:32993787 1873:32810447 1787:34147821 1738:13777357 1730:29700396 1683:34685596 1624:29197379 1565:23114846 1499:53010974 1491:30339548 1439:37615187 1430:10485805 1325:33547160 1284:26854213 1264:Cytokine 1249:21963199 1207:26938687 1155:25838376 1101:24310355 1047:31450598 976:See also 898:Mutated 865:melanoma 787:(CAFs), 744:germline 706:in vitro 704:Several 695:Research 683:inducer 655:(CD8+), 637:exosomes 596:microRNA 592:exosomes 419:acidosis 5653:5763077 5570:8980704 5462:5817793 5372:7367382 5281:3555767 5245:3584330 5133:9195263 5071:Bibcode 5006:5919827 4957:8468887 4934:Cancers 4787:3578602 4738:9113058 4649:3172582 4600:4594765 4579:Bibcode 4543:4700594 4522:Bibcode 4486:4330753 4463:Bibcode 4427:6343476 4406:Science 4378:4475637 4357:Bibcode 4321:3964061 4298:Bibcode 4262:4496237 4121:4852857 4081:4393159 4022:3190352 3883:4994190 3843:5884781 3715:4429118 3677:Bibcode 3579:8750014 3548:Cancers 3520:6233061 3463:6406979 3342:6527347 3188:7174611 3163:: 397. 3129:9326521 3070:9086898 3011:4316204 2954:7046529 2868:Bibcode 2720:9405783 2689:Cancers 2658:7982455 2599:8303391 2568:Cancers 2476:4963227 2416:7352839 2393:Cancers 2365:9545774 2299:9151701 2242:8007910 2042:8557138 1985:8358492 1923:7526376 1864:8194051 1835:Bibcode 1674:8533895 1615:5712107 1556:4432936 1198:4975620 1133:Bibcode 1125:Science 1092:3756368 1069:Cancers 1038:6747260 900:kinases 806:capsids 777:hypoxia 731:ex vivo 710:in vivo 647:T cells 415:hypoxia 268:lactate 235:hypoxia 215:Hypoxia 73:History 69:cells. 5709: 5701: 5660: 5650: 5604: 5577: 5567: 5559: 5520: 5512: 5504: 5469: 5459: 5451: 5405: 5379: 5369: 5328: 5320: 5279: 5252: 5242: 5203: 5140: 5130: 5089: 5044: 5003: 4964: 4954: 4913: 4905: 4870: 4835: 4794: 4784: 4745: 4735: 4727: 4717: 4656: 4646: 4607: 4597: 4571:Nature 4550: 4540: 4514:Nature 4493: 4483: 4434: 4424: 4385: 4375: 4349:Nature 4328: 4318: 4269: 4259: 4222:926930 4220: 4212: 4192:Cancer 4171: 4163: 4128: 4118: 4079: 4071: 4029: 4019: 3978: 3970: 3934: 3926: 3890: 3880: 3841: 3833: 3792: 3751: 3713: 3705: 3669:Nature 3652: 3644: 3636: 3586: 3576: 3568: 3527: 3517: 3509: 3470: 3460: 3452: 3411: 3401: 3393: 3349: 3339: 3331: 3292: 3284: 3249: 3241: 3233: 3195: 3185: 3177: 3136: 3126: 3118: 3077: 3067: 3059: 3018: 3008: 3000: 2961: 2951: 2943: 2904: 2894: 2886: 2836: 2828: 2784: 2774: 2766: 2727: 2717: 2709: 2665: 2655: 2647: 2606: 2596: 2588: 2547: 2537: 2529: 2483: 2473: 2465: 2423: 2413: 2372: 2362: 2354: 2306: 2296: 2288: 2276:(11). 2249: 2239: 2231: 2190: 2141: 2106: 2096: 2088: 2049: 2039: 2031: 1992: 1982: 1974: 1930: 1920: 1912: 1871: 1861: 1853: 1785: 1777: 1736: 1728: 1720: 1681: 1671: 1663: 1622: 1612: 1604: 1563: 1553: 1545: 1497: 1489: 1481: 1437: 1427: 1419: 1380: 1372: 1331: 1323: 1282: 1247: 1205: 1195: 1153: 1099: 1089: 1045: 1035: 1027: 920:, and 881:CTLA-4 842:VEGF-A 700:Models 557:T cell 404:, and 5731:Tumor 5518:S2CID 5087:S2CID 5032:(1). 4911:S2CID 4218:S2CID 4169:S2CID 4077:S2CID 4049:(PDF) 3976:S2CID 3932:S2CID 3839:S2CID 3813:Blood 3711:S2CID 3650:S2CID 3432:Cells 3247:S2CID 1734:S2CID 1643:Cells 1495:S2CID 1378:S2CID 1329:S2CID 885:FOXP3 580:NF-κB 437:like 35:tumor 5707:PMID 5699:ISSN 5658:PMID 5602:PMID 5575:PMID 5557:ISSN 5510:PMID 5502:ISSN 5467:PMID 5449:ISSN 5403:PMID 5377:PMID 5326:PMID 5318:ISSN 5277:PMID 5250:PMID 5201:PMID 5138:PMID 4962:PMID 4903:PMID 4868:PMID 4833:PMID 4792:PMID 4743:PMID 4725:ISSN 4715:ISBN 4654:PMID 4605:PMID 4548:PMID 4491:PMID 4432:PMID 4383:PMID 4326:PMID 4267:PMID 4210:PMID 4161:PMID 4126:PMID 4069:PMID 4027:PMID 3968:PMID 3924:PMID 3888:PMID 3862:Cell 3831:PMID 3790:PMID 3749:PMID 3703:PMID 3642:PMID 3634:ISSN 3584:PMID 3566:ISSN 3525:PMID 3507:ISSN 3468:PMID 3450:ISSN 3409:PMID 3391:ISSN 3347:PMID 3329:ISSN 3290:PMID 3282:ISSN 3239:PMID 3231:ISSN 3193:PMID 3175:ISSN 3134:PMID 3116:ISSN 3075:PMID 3057:ISSN 3016:PMID 2998:ISSN 2959:PMID 2941:ISSN 2902:PMID 2884:ISSN 2834:PMID 2826:ISSN 2782:PMID 2764:ISSN 2725:PMID 2707:ISSN 2663:PMID 2645:ISSN 2604:PMID 2586:ISSN 2545:PMID 2527:ISSN 2481:PMID 2463:ISSN 2421:PMID 2370:PMID 2352:ISSN 2304:PMID 2286:ISSN 2247:PMID 2229:ISSN 2188:PMID 2139:ISBN 2104:PMID 2086:ISSN 2047:PMID 2029:ISSN 1990:PMID 1972:ISSN 1928:PMID 1910:ISSN 1869:PMID 1851:ISSN 1783:PMID 1775:ISSN 1726:PMID 1718:ISSN 1679:PMID 1661:ISSN 1620:PMID 1602:ISSN 1561:PMID 1543:ISSN 1487:PMID 1479:ISSN 1435:PMID 1417:ISSN 1370:ISSN 1321:PMID 1280:PMID 1245:PMID 1203:PMID 1151:PMID 1097:PMID 1043:PMID 1025:ISSN 848:and 808:and 751:and 716:and 708:and 472:and 384:The 253:and 119:and 49:and 29:The 5689:doi 5648:PMC 5638:doi 5565:PMC 5549:doi 5494:doi 5490:140 5457:PMC 5439:doi 5367:PMC 5357:doi 5308:doi 5240:PMC 5232:doi 5193:doi 5189:134 5166:doi 5162:144 5128:PMC 5118:doi 5079:doi 5067:452 5042:PMC 5034:doi 5001:PMC 4993:doi 4989:128 4952:PMC 4942:doi 4895:doi 4860:doi 4823:doi 4782:PMC 4774:doi 4733:PMC 4707:doi 4644:PMC 4636:doi 4595:PMC 4587:doi 4575:522 4538:PMC 4530:doi 4518:528 4481:PMC 4471:doi 4459:112 4422:PMC 4414:doi 4410:358 4373:PMC 4365:doi 4353:522 4316:PMC 4306:doi 4294:111 4257:PMC 4249:doi 4200:doi 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