Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on medication adherence

LIVE: Thursday 27th June 2024, 18:00-19:30 (CEST)
Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.
ADVANCED SEARCH
Log in
Top
Cancer and Metastasis Reviews
Published in: Cancer and Metastasis Reviews 3-4/2013

01-12-2013 | NON-THEMATIC REVIEW

The pre-metastatic niche: finding common ground

Authors: Jaclyn Sceneay, Mark J. Smyth, Andreas Möller

Published in: Cancer and Metastasis Reviews | Issue 3-4/2013

Login to get access

Abstract

It is rapidly becoming evident that the formation of tumor-promoting pre-metastatic niches in secondary organs adds a previously unrecognized degree of complexity to the challenge of curing metastatic disease. Primary tumor cells orchestrate pre-metastatic niche formation through secretion of a variety of cytokines and growth factors that promote mobilization and recruitment of bone marrow-derived cells to future metastatic sites. Hypoxia within the primary tumor, and secretion of specific microvesicles termed exosomes, are emerging as important processes and vehicles for tumor-derived factors to modulate pre-metastatic sites. It has also come to light that reduced immune surveillance is a novel mechanism through which primary tumors create favorable niches in secondary organs. This review provides an overview of our current understanding of underlying mechanisms of pre-metastatic niche formation and highlights the common links as well as discrepancies between independent studies. Furthermore, the possible clinical implications, links to metastatic persistence and dormancy, and novel approaches for treatment of metastatic disease through reversal of pre-metastatic niche formation are identified and explored.
Literature
1.
Gupta, G. P., & Massague, J. (2006). Cancer metastasis: building a framework. Cell, 127(4), 679–695.PubMed
2.
Klein, C. A. (2008). Cancer. The metastasis cascade. Science, 321(5897), 1785–1787.PubMed
3.
Joyce, J. A., & Pollard, J. W. (2009). Microenvironmental regulation of metastasis. Nature Reviews. Cancer, 9(4), 239–252.PubMed
4.
Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell, 144(5), 646–674.PubMed
5.
Paget, G. (1889). Remarks on a case of alternate partial anaesthesia. British Medical Journal, 1(1462), 1–3.PubMed
6.
Muller, A., et al. (2001). Involvement of chemokine receptors in breast cancer metastasis. Nature, 410(6824), 50–56.PubMed
7.
Weigelt, B., et al. (2005). No common denominator for breast cancer lymph node metastasis. British Journal of Cancer, 93(8), 924–932.PubMed
8.
Kaplan, R. N., et al. (2005). VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche. Nature, 438(7069), 820–827.PubMed
9.
Psaila, B., & Lyden, D. (2009). The metastatic niche: adapting the foreign soil. Nature Reviews. Cancer, 9(4), 285–293.PubMed
10.
Duda, D. G., & Jain, R. K. (2010). Premetastatic lung “niche”: is vascular endothelial growth factor receptor 1 activation required? Cancer Research, 70(14), 5670–5673.PubMed
11.
Dawson, M. R., et al. (2009). VEGFR1-activity-independent metastasis formation. Nature, 461(7262), E4. Discussion, E5.PubMed
12.
Lin, E. Y., et al. (2006). Macrophages regulate the angiogenic switch in a mouse model of breast cancer. Cancer Research, 66(23), 11238–11246.PubMed
13.
Nozawa, H., Chiu, C., & Hanahan, D. (2006). Infiltrating neutrophils mediate the initial angiogenic switch in a mouse model of multistage carcinogenesis. Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12493–12498.PubMed
14.
Coussens, L. M., et al. (1999). Inflammatory mast cells up-regulate angiogenesis during squamous epithelial carcinogenesis. Genes & Development, 13(11), 1382–1397.
15.
Hiratsuka, S., et al. (2006). Tumour-mediated upregulation of chemoattractants and recruitment of myeloid cells predetermines lung metastasis. Nature Cell Biology, 8(12), 1369–1375.PubMed
16.
Kowanetz, M., et al. (2010). Granulocyte-colony stimulating factor promotes lung metastasis through mobilization of Ly6G + Ly6C + granulocytes. Proceedings of the National Academy of Sciences of the United States of America, 107(50), 21248–21255.PubMed
17.
Harris, A. L. (2002). Hypoxia—a key regulatory factor in tumour growth. Nature Reviews. Cancer, 2(1), 38–47.PubMed
18.
Semenza, G. L. (2012). Hypoxia-inducible factors: mediators of cancer progression and targets for cancer therapy. Trends in Pharmacological Sciences, 33(4), 207–214.PubMed
19.
Bos, R., et al. (2003). Levels of hypoxia-inducible factor-1alpha independently predict prognosis in patients with lymph node negative breast carcinoma. Cancer, 97(6), 1573–1581.PubMed
20.
Dales, J. P., et al. (2005). Overexpression of hypoxia-inducible factor HIF-1alpha predicts early relapse in breast cancer: retrospective study in a series of 745 patients. International Journal of Cancer, 116(5), 734–739.
21.
Erler, J. T., et al. (2009). Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the premetastatic niche. Cancer Cell, 15(1), 35–44.PubMed
22.
Wong, C. C., et al. (2011). Hypoxia-inducible factor 1 is a master regulator of breast cancer metastatic niche formation. Proceedings of the National Academy of Sciences of the United States of America, 108(39), 16369–16374.PubMed
23.
Bondareva, A., et al. (2009). The lysyl oxidase inhibitor, beta-aminopropionitrile, diminishes the metastatic colonization potential of circulating breast cancer cells. PLoS One, 4(5), e5620.PubMed
24.
Sceneay, J., et al. (2012). Primary tumor hypoxia recruits CD11b+/Ly6Cmed/Ly6G+ immune suppressor cells and compromises NK cell cytotoxicity in the premetastatic niche. Cancer Research, 72, 3906–11.PubMed
25.
Chioda, M., et al. (2011). Myeloid cell diversification and complexity: an old concept with new turns in oncology. Cancer Metastasis Reviews, 30(1), 27–43.PubMed
26.
Yan, H. H., et al. (2010). Gr-1 + CD11b + myeloid cells tip the balance of immune protection to tumor promotion in the premetastatic lung. Cancer Research, 70(15), 6139–6149.PubMed
27.
Kim, S., et al. (2009). Carcinoma-produced factors activate myeloid cells through TLR2 to stimulate metastasis. Nature, 457(7225), 102–106.PubMed
28.
Granot, Z., et al. (2011). Tumor entrained neutrophils inhibit seeding in the premetastatic lung. Cancer Cell, 20(3), 300–314.PubMed
29.
Filipazzi, P., et al. (2007). Identification of a new subset of myeloid suppressor cells in peripheral blood of melanoma patients with modulation by a granulocyte-macrophage colony-stimulation factor-based antitumor vaccine. Journal of Clinical Oncology, 25(18), 2546–2553.PubMed
30.
Gabrilovich, D. I., & Nagaraj, S. (2009). Myeloid-derived suppressor cells as regulators of the immune system. Nature Reviews Immunology, 9(3), 162–174.PubMed
31.
Poschke, I., et al. (2010). Immature immunosuppressive CD14+HLA-DR-/low cells in melanoma patients are Stat3hi and overexpress CD80, CD83, and DC-sign. Cancer Research, 70(11), 4335–4345.PubMed
32.
Rodriguez, P. C., & Ochoa, A. C. (2006). T cell dysfunction in cancer: role of myeloid cells and tumor cells regulating amino acid availability and oxidative stress. Seminars in Cancer Biology, 16(1), 66–72.PubMed
33.
Serafini, P., Borrello, I., & Bronte, V. (2006). Myeloid suppressor cells in cancer: recruitment, phenotype, properties, and mechanisms of immune suppression. Seminars in Cancer Biology, 16(1), 53–65.PubMed
34.
Youn, J. I., et al. (2008). Subsets of myeloid-derived suppressor cells in tumor-bearing mice. Journal of Immunology, 181(8), 5791–5802.
35.
Almand, B., et al. (2001). Increased production of immature myeloid cells in cancer patients: a mechanism of immunosuppression in cancer. Journal of Immunology, 166(1), 678–689.
36.
Gabrilovich, D. I., Ostrand-Rosenberg, S., & Bronte, V. (2012). Coordinated regulation of myeloid cells by tumours. Nature Reviews Immunology, 12(4), 253–268.PubMed
37.
Huang, B., et al. (2007). CCL2/CCR2 pathway mediates recruitment of myeloid suppressor cells to cancers. Cancer Letters, 252(1), 86–92.PubMed
38.
Yang, L., et al. (2008). Abrogation of TGF beta signaling in mammary carcinomas recruits Gr-1+CD11b+ myeloid cells that promote metastasis. Cancer Cell, 13(1), 23–35.PubMed
39.
Shojaei, F., et al. (2007). Bv8 regulates myeloid-cell-dependent tumour angiogenesis. Nature, 450(7171), 825–831.PubMed
40.
Sica, A., & Bronte, V. (2007). Altered macrophage differentiation and immune dysfunction in tumor development. The Journal of Clinical Investigation, 117(5), 1155–1166.PubMed
41.
Gao, D., et al. (2012). Myeloid progenitor cells in the premetastatic lung promote metastases by inducing mesenchymal to epithelial transition. Cancer Research, 72(6), 1384–1394.PubMed
42.
Corzo, C. A., et al. (2010). HIF-1α regulates function and differentiation of myeloid-derived suppressor cells in the tumor microenvironment. The Journal of Experimental Medicine, 207(11), 2439–2453.PubMed
43.
Deng, J., et al. (2012). S1PR1-STAT3 signaling is crucial for myeloid cell colonization at future metastatic sites. Cancer Cell, 21(5), 642–654.PubMed
44.
Movahedi, K., et al. (2008). Identification of discrete tumor-induced myeloid-derived suppressor cell subpopulations with distinct T cell-suppressive activity. Blood, 111(8), 4233–4244.PubMed
45.
Dolcetti, L., et al. (2010). Hierarchy of immunosuppressive strength among myeloid-derived suppressor cell subsets is determined by GM-CSF. European Journal of Immunology, 40(1), 22–35.PubMed
46.
Mauti, L. A., et al. (2011). Myeloid-derived suppressor cells are implicated in regulating permissiveness for tumor metastasis during mouse gestation. The Journal of Clinical Investigation, 121(7), 2794–2807.PubMed
47.
Li, H., et al. (2009). Cancer-expanded myeloid-derived suppressor cells induce anergy of NK cells through membrane-bound TGF-beta 1. Journal of Immunology, 182(1), 240–249.
48.
Hoechst, B., et al. (2009). Myeloid derived suppressor cells inhibit natural killer cells in patients with hepatocellular carcinoma via the NKp30 receptor. Hepatology, 50(3), 799–807.PubMed
49.
Zhu, J., Huang, X., & Yang, Y. (2012). Myeloid-derived suppressor cells regulate natural killer cell response to adenovirus-mediated gene transfer. Journal of Virology, 86, 13689–96.PubMed
50.
Liu, C., et al. (2007). Expansion of spleen myeloid suppressor cells represses NK cell cytotoxicity in tumor-bearing host. Blood, 109(10), 4336–4342.PubMed
51.
Nagaraj, S., et al. (2012). Antigen-specific CD4(+) T cells regulate function of myeloid-derived suppressor cells in cancer via retrograde MHC class II signaling. Cancer Research, 72(4), 928–938.PubMed
52.
Doedens, A. L., et al. (2010). Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression. Cancer Research, 70(19), 7465–7475.PubMed
53.
Corzo, C. A., et al. (2010). HIF-1alpha regulates function and differentiation of myeloid-derived suppressor cells in the tumor microenvironment. The Journal of Experimental Medicine, 207(11), 2439–2453.PubMed
54.
Gallina, G., et al. (2006). Tumors induce a subset of inflammatory monocytes with immunosuppressive activity on CD8+ T cells. The Journal of Clinical Investigation, 116(10), 2777–2790.PubMed
55.
Watanabe, S., et al. (2008). Tumor-induced CD11b+Gr-1+ myeloid cells suppress T cell sensitization in tumor-draining lymph nodes. Journal of Immunology, 181(5), 3291–3300.
56.
Nagaraj, S., et al. (2007). Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer. Nature Medicine, 13(7), 828–835.PubMed
57.
Serafini, P., et al. (2008). Myeloid-derived suppressor cells promote cross-tolerance in B-cell lymphoma by expanding regulatory T cells. Cancer Research, 68(13), 5439–5449.PubMed
58.
Huang, B., et al. (2006). Gr-1+CD115+ immature myeloid suppressor cells mediate the development of tumor-induced T regulatory cells and T-cell anergy in tumor-bearing host. Cancer Research, 66(2), 1123–1131.PubMed
59.
Pan, P. Y., et al. (2010). Immune stimulatory receptor CD40 is required for T-cell suppression and T regulatory cell activation mediated by myeloid-derived suppressor cells in cancer. Cancer Research, 70(1), 99–108.PubMed
60.
Paez, D., et al. (2012). Cancer dormancy: a model of early dissemination and late cancer recurrence. Clinical Cancer Research, 18(3), 645–653.PubMed
61.
Pavlidis, N., & Pentheroudakis, G. (2012). Cancer of unknown primary site. Lancet, 379(9824), 1428–1435.PubMed
62.
Uhr, J. W., & Pantel, K. (2011). Controversies in clinical cancer dormancy. Proceedings of the National Academy of Sciences of the United States of America, 108(30), 12396–12400.PubMed
63.
Almog, N. (2010). Molecular mechanisms underlying tumor dormancy. Cancer Letters, 294(2), 139–146.PubMed
64.
Ringel, M. D. (2011). Metastatic dormancy and progression in thyroid cancer: targeting cells in the metastatic frontier. Thyroid, 21(5), 487–492.PubMed
65.
Chaput, N., & Thery, C. (2011). Exosomes: immune properties and potential clinical implementations. Seminars in Immunopathology, 33(5), 419–440.PubMed
66.
Ratajczak, J., et al. (2006). Membrane-derived microvesicles: important and underappreciated mediators of cell-to-cell communication. Leukemia, 20(9), 1487–1495.PubMed
67.
Peinado, H., Lavotshkin, S., & Lyden, D. (2011). The secreted factors responsible for pre-metastatic niche formation: old sayings and new thoughts. Seminars in Cancer Biology, 21(2), 139–146.PubMed
68.
Peinado, H., et al. (2012). Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. Nature Medicine, 18, 883–91.PubMed
69.
Jung, T., et al. (2009). CD44v6 dependence of premetastatic niche preparation by exosomes. Neoplasia, 11(10), 1093–1105.PubMed
70.
Grange, C., et al. (2011). Microvesicles released from human renal cancer stem cells stimulate angiogenesis and formation of lung premetastatic niche. Cancer Research, 71(15), 5346–5356.PubMed
71.
Gabrilovich, D. (2004). Mechanisms and functional significance of tumour-induced dendritic-cell defects. Nature Reviews Immunology, 4(12), 941–952.PubMed
72.
Do, T. H., et al. (2004). Impaired circulating myeloid DCs from myeloma patients. Cytotherapy, 6(3), 196–203.PubMed
73.
Liu, C., et al. (2006). Murine mammary carcinoma exosomes promote tumor growth by suppression of NK cell function. Journal of Immunology, 176(3), 1375–1385.
74.
Huber, V., et al. (2005). Human colorectal cancer cells induce T-cell death through release of proapoptotic microvesicles: role in immune escape. Gastroenterology, 128(7), 1796–1804.PubMed
75.
Valenti, R., et al. (2006). Human tumor-released microvesicles promote the differentiation of myeloid cells with transforming growth factor-β-mediated suppressive activity on T lymphocytes. Cancer Research, 66(18), 9290–9298.PubMed
76.
Xiang, X., et al. (2009). Induction of myeloid-derived suppressor cells by tumor exosomes. International Journal of Cancer, 124(11), 2621–2633.
77.
Liu, Y., et al. (2010). Contribution of MyD88 to the tumor exosome-mediated induction of myeloid derived suppressor cells. The American Journal of Pathology, 176(5), 2490–2499.PubMed
78.
Yu, S., et al. (2007). Tumor exosomes inhibit differentiation of bone marrow dendritic cells. Journal of Immunology, 178(11), 6867–6875.
79.
Park, J. E., et al. (2010). Hypoxic tumor cell modulates its microenvironment to enhance angiogenic and metastatic potential by secretion of proteins and exosomes. Molecular & Cellular Proteomics, 9(6), 1085–1099.
80.
Wong, C. C., et al. (2012). Inhibitors of hypoxia-inducible factor 1 block breast cancer metastatic niche formation and lung metastasis. Journal of Molecular Medicine (Berlin), 90, 803–15.
81.
Hiratsuka, S., et al. (2008). The S100A8-serum amyloid A3-TLR4 paracrine cascade establishes a pre-metastatic phase. Nature Cell Biology, 10(11), 1349–1355.PubMed
82.
Skog, J., et al. (2008). Glioblastoma microvesicles transport RNA and proteins that promote tumour growth and provide diagnostic biomarkers. Nature Cell Biology, 10(12), 1470–1476.PubMed
83.
Noerholm, M., et al. (2012). RNA expression patterns in serum microvesicles from patients with glioblastoma multiforme and controls. BMC Cancer, 12, 22.PubMed
84.
Khan, S., et al. (2012). Plasma-derived exosomal survivin, a plausible biomarker for early detection of prostate cancer. PLoS One, 7(10), e46737.PubMed
85.
Chen, T., et al. (2011). Chemokine-containing exosomes are released from heat-stressed tumor cells via lipid raft-dependent pathway and act as efficient tumor vaccine. Journal of Immunology, 186(4), 2219–2228.
86.
Levy, E. M., Roberti, M. P., & Mordoh, J. (2011). Natural killer cells in human cancer: from biological functions to clinical applications. Journal of Biomedicine and Biotechnology, 2011, 676198.PubMed
87.
Jinushi, M., et al. (2008). MHC class I chain-related protein A antibodies and shedding are associated with the progression of multiple myeloma. Proceedings of the National Academy of Sciences of the United States of America, 105(4), 1285–1290.PubMed
88.
Sibbitt, W. L., Jr., et al. (1984). Defects in natural killer cell activity and interferon response in human lung carcinoma and malignant melanoma. Cancer Research, 44(2), 852–856.PubMed
89.
Konjevic, G., et al. (2009). Biomarkers of suppressed natural killer (NK) cell function in metastatic melanoma: decreased NKG2D and increased CD158a receptors on CD3-CD16+ NK cells. Biomarkers, 14(4), 258–270.PubMed
90.
Konjevic, G., et al. (2007). Low expression of CD161 and NKG2D activating NK receptor is associated with impaired NK cell cytotoxicity in metastatic melanoma patients. Clinical & Experimental Metastasis, 24(1), 1–11.
91.
Gill, S., Olson, J. A., & Negrin, R. S. (2009). Natural killer cells in allogeneic transplantation: effect on engraftment, graft- versus-tumor, and graft-versus-host responses. Biology of Blood and Marrow Transplantation, 15(7), 765–776.PubMed
92.
Burke, S., et al. (2010). New views on natural killer cell-based immunotherapy for melanoma treatment. Trends in Immunology, 31(9), 339–345.PubMed
93.
Koehn, T. A., et al. (2012). Increasing the clinical efficacy of NK and antibody-mediated cancer immunotherapy: potential predictors of successful clinical outcome based on observations in high-risk neuroblastoma. Frontiers in Pharmacology, 3, 91.PubMed
94.
Sawanobori, Y., et al. (2008). Chemokine-mediated rapid turnover of myeloid-derived suppressor cells in tumor-bearing mice. Blood, 111(12), 5457–5466.PubMed
95.
Shojaei, F., et al. (2009). G-CSF-initiated myeloid cell mobilization and angiogenesis mediate tumor refractoriness to anti-VEGF therapy in mouse models. Proceedings of the National Academy of Sciences, 106(16), 6742–6747.
96.
Mazzoni, A., et al. (2002). Myeloid suppressor lines inhibit T cell responses by an NO-dependent mechanism. The Journal of Immunology, 168(2), 689–695.PubMed
97.
Yang, L., et al. (2004). Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. Cancer Cell, 6(4), 409–421.PubMed
98.
Melani, C., et al. (2007). Amino-biphosphonate-mediated MMP-9 inhibition breaks the tumor-bone marrow axis responsible for myeloid-derived suppressor cell expansion and macrophage infiltration in tumor stroma. Cancer Research, 67(23), 11438–11446.PubMed
99.
Sinha, P., et al. (2008). Proinflammatory S100 proteins regulate the accumulation of myeloid-derived suppressor cells. The Journal of Immunology, 181(7), 4666–4675.PubMed
100.
Cheng, P., et al. (2008). Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein. The Journal of Experimental Medicine, 205(10), 2235–2249.PubMed
101.
Terabe, M., et al. (2003). Transforming growth factor-β production and myeloid cells are an effector mechanism through which CD1d-restricted T cells block cytotoxic T lymphocyte-mediated tumor immunosurveillance. The Journal of Experimental Medicine, 198(11), 1741–1752.PubMed
102.
Xiang, X., et al. (2009). Induction of myeloid-derived suppressor cells by tumor exosomes. International Journal of Cancer, 124(11), 2621–2633.
103.
Gabrilovich, D., et al. (1998). Vascular endothelial growth factor inhibits the development of dendritic cells and dramatically affects the differentiation of multiple hematopoietic lineages in vivo. Blood, 92(11), 4150–4166.PubMed
104.
Kusmartsev, S., et al. (2008). Oxidative stress regulates expression of VEGFR1 in myeloid cells: link to tumor-induced immune suppression in renal cell carcinoma. Journal of Immunology, 181(1), 346–353.
105.
Shojaei, F., et al. (2007). Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells. Nature Biotechnology, 25(8), 911–920.PubMed
106.
van Cruijsen, H., et al. (2007). Defective differentiation of myeloid and plasmacytoid dendritic cells in advanced cancer patients is not normalized by tyrosine kinase inhibition of the vascular endothelial growth factor receptor. Clinical & Developmental Immunology, 2007, 17315–17315.
107.
Hiratsuka, S., et al. (2011). Endothelial focal adhesion kinase mediates cancer cell homing to discrete regions of the lungs via E-selectin up-regulation. Proceedings of the National Academy of Sciences of the United States of America, 108(9), 3725–3730.PubMed
108.
Schelter, F., et al. (2011). Tissue inhibitor of metalloproteinases-1-induced scattered liver metastasis is mediated by hypoxia-inducible factor-1alpha. Clinical & Experimental Metastasis, 28(2), 91–99.
109.
Gil-Bernabé, A. M., et al. (2012). Recruitment of monocytes/macrophages by tissue factor-mediated coagulation is essential for metastatic cell survival and premetastatic niche establishment in mice. Blood, 119, 3164–75.PubMed
Metadata
Title
The pre-metastatic niche: finding common ground
Authors
Jaclyn Sceneay
Mark J. Smyth
Andreas Möller
Publication date
01-12-2013
Publisher
Springer US
Published in
Cancer and Metastasis Reviews / Issue 3-4/2013
Print ISSN: 0167-7659
Electronic ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-013-9420-1

Other articles of this Issue 3-4/2013

Cancer and Metastasis Reviews 3-4/2013 Go to the issue

CLINICAL

Adverse reactions to targeted and non-targeted chemotherapeutic drugs with emphasis on hypersensitivity responses and the invasive metastatic switch

OriginalPaper

Aneuploidy and chromosomal instability: a vicious cycle driving cellular evolution and cancer genome chaos

NON-THEMATIC REVIEW

Central and peripheral nervous systems: master controllers in cancer metastasis

OriginalPaper

Do mutator mutations fuel tumorigenesis?

NON-THEMATIC REVIEW

Targeting MAPK pathway in melanoma therapy

OriginalPaper

Chromosomal instability (CIN): what it is and why it is crucial to cancer evolution
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits