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Year : 2013  |  Volume : 9  |  Issue : 7  |  Page : 121-122

Tumor metastasis: What happened to the invading cancer cells?

Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China

Date of Web Publication30-Nov-2013

Correspondence Address:
Qian Liu
Tianjin Key Laboratory of Lung, Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer, Institute, Tianjin Medical University General Hospital, Tianjin 300052
Qinghua Zhou
Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-1482.122502

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How to cite this article:
Liu Q, Zhou Q. Tumor metastasis: What happened to the invading cancer cells?. J Can Res Ther 2013;9, Suppl S2:121-2

How to cite this URL:
Liu Q, Zhou Q. Tumor metastasis: What happened to the invading cancer cells?. J Can Res Ther [serial online] 2013 [cited 2021 Sep 27];9:121-2. Available from: https://www.cancerjournal.net/text.asp?2013/9/7/121/122502

Metastasis is defined as the late stage of tumors and the major cause of death in patients with cancer. The progression of a cancer cell into metastatic status is extremely complicated, in which a cancer cell endows itself with the abilities not only to invade the surrounding tissue and translocate largely through the blood stream to microvessels of distant tissues, but also exist from the bloodstream and finally adapt to the foreign microenvironment of these tissues in ways that facilitate cell proliferation and the formation of a macroscopic secondary tumor. [1]

It is now widely accepted that cancer is attributed to the accumulation of genetic alterations in cells. [2] The malignant lesions are caused either by per se genetic alterations, or by environmental factors, such as viral infection. Indeed, previous studies have revealed that several factors, such as netrin-1, toll-like receptors (TLR), signatures of metastases of certain solid tumors, suggest that many of these cells were already present in the primary tumor. [3-5] These factors are potential molecular targets for the treatment of malignant tumors. Herein, A study by Xu et al. summarized the role of neural-related factors in the metastasis of the gastrointestinal cancer, in which they showed us the function of the neural-related factors and their crosstalk with immune systems. Lu et al. summarized current knowledge on the roles of TLR in microbiota-associated gastrointestinal cancer metastasis, mainly introducing TLR recognition of micorbiota ligands, initiating inflammation and promoting tumorigenesis as well as the therapeutic strategies to target TLR. These reviews also connect the cancer metastasis with immune system, which has become one of the important research focuses recently. The accumulation of genetic alterations is often accompanied by heterogeneity in certain malignant cancer cells, which is also essential for metastasis. [6] In this issue, the role of heterogenous ribonucleoproteins in cancer metastasis is reviewed by Han et al. In fact, a number of genes have been also identified as having functions in inducing or suppressing metastasis in experimental models. Such as Li et al. report that RASSF7 and RASSF8 proteins are predictive factors for development and metastasis in malignant thyroid neoplasms in this issue. However, the association between causative genetic alterations and resulting phenotypic alterations with respect to the metastatic potential of cancer cells is not fully understood. The systemic research in cell microenvironment or even whole body is future trends. Cui et al. here study the immune responsiveness in a mouse model. Growing evidence suggests that human cancers are stem cell diseases. [7] This topic is also addressed in the current issue by Sun et al. They reviewed the recent progress made in the relationship between the epithelial-mesenchymal transition status of cancer stem cells (CSCs) and tumor metastasis and between the localization and chemotaxis of CSCs and the formation of the metastatic colonies. These researches on mechanism of metastasis will give us clues to prognosis or therapy in clinical application.

Although there are few effective treatment options to cure metastatic cancer, several research groups have made effort to offer optimizing regimens to control the cancer progression and improve patients' life qualities. Systemic chemotherapy is proved to be effective and safe in large majority of patients who suffered a relapse after radical surgery or are diagnosed with metastatic disease initially. [8,9] In this issue, Zhang et al. have provided evidence that paclitaxel and capecitabine combination therapy is safe and effective for fluoropyrimidine-platinum-resistant metastatic gastric adenocarcinoma. Moreover, this combination therapy warrants further evaluation in future phase III trials. Another example is conducted in triple-negative breast cancer, in which brain metastasis is very common. Although whole brain radiotherapy for brain metastasis effectively control localized disease and eliminate subclinical lesions to prevent recurrence, it dramatically destroyed brain function, leading to neurocognitive disorder. [10] Recently, precise radiotherapy (including intensity modulated radiation therapy, stereotactic radio surgery and other conformal radiotherapy) combined with whole brain irradiation not only significantly prolongs the survival time in patients, but also makes effective protection of normal brain tissue. [11,12] Herein, Wu's group conducted a retrospective study illustrating the outcome of precise radiotherapy combined with whole brain irradiation, mainly focusing on treatment efficiency, survival time and prognosis of precise radiotherapy of brain cancer metastasis.

Besides combined chemotherapy, combined immunotherapy is another compromise choice against cancer. Adoptive cellular immunotherapy is demonstrated to be a promising therapy against malignant tumor until now, for its wide antitumor spectrum and less side-effects associated with traditional radiotherapy and chemotherapy. [13] Natural killer (NK) cells and dendritic cells (DCs), two distinct components of the protective immune response, play a vital role during immune regulation and in establishing adaptive immune responses [14,15] and also in antitumor responses. [16,17] Cui et al. have assessed their potential application in the immunobiological treatment of malignant tumors and explored the interaction between NK cells and DCs in vivo and this paper was included in the current issue.

Although diverse molecular mechanisms have been revealed to be indispensible to the progression of cancer metastasis, more questions are remained challenged due to the complicated external and internal risk factors, maybe the cell migration in normal tissue prompts some insights that why and how tumoral cells metastasis. This process remains one of the most enigmatic aspects of cancer. The aim of this special issue is to show some latest results and a better understanding on cancer metastasis.

 > References Top

1.Chaffer CL, Weinberg RA. A perspective on cancer cell metastasis. Science 2011;331:1559-64.  Back to cited text no. 1
2.Hanahan D, Weinberg RA. Hallmarks of cancer: The next generation. Cell 2011;144:646-74.  Back to cited text no. 2
3.Mehlen P, Guenebeaud C. Netrin-1 and its dependence receptors as original targets for cancer therapy. Curr Opin Oncol 2010;22:46-54.  Back to cited text no. 3
4.Yamashita T, Wang XW. Cancer stem cells in the development of liver cancer. J Clin Invest 2013;123:1911-8.  Back to cited text no. 4
5.Yu L, Wang L, Chen S. Dual character of Toll-like receptor signaling: Pro-tumorigenic effects and anti-tumor functions. Biochim Biophys Acta 2013;1835:144-54.  Back to cited text no. 5
6.Bhatia S, Frangioni JV, Hoffman RM, Iafrate AJ, Polyak K. The challenges posed by cancer heterogeneity. Nat Biotechnol 2012;30:604-10.  Back to cited text no. 6
7.Clevers H. The cancer stem cell: Premises, promises and challenges. Nat Med 2011;17:313-9.  Back to cited text no. 7
8.Kang YK, Kang WK, Shin DB, Chen J, Xiong J, Wang J, et al. Capecitabine/cisplatin versus 5-fluorouracil/cisplatin as first-line therapy in patients with advanced gastric cancer: A randomised phase III noninferiority trial. Ann Oncol 2009;20:666-73.  Back to cited text no. 8
9.Koizumi W, Narahara H, Hara T, Takagane A, Akiya T, Takagi M, et al. S-1 plus cisplatin versus S-1 alone for first-line treatment of advanced gastric cancer (SPIRITS trial): A phase III trial. Lancet Oncol 2008;9:215-21.  Back to cited text no. 9
10.Patil CG, Pricola K, Sarmiento JM, Garg SK, Bryant A, Black KL. Whole brain radiation therapy (WBRT) alone versus WBRT and radiosurgery for the treatment of brain metastases. Cochrane Database Syst Rev 2012;9:CD006121.  Back to cited text no. 10
11.Aoyama H, Shirato H, Tago M, Nakagawa K, Toyoda T, Hatano K, et al. Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: A randomized controlled trial. JAMA 2006;295:2483-91.  Back to cited text no. 11
12.Park HS, Chiang VL, Knisely JP, Raldow AC, Yu JB. Stereotactic radiosurgery with or without whole-brain radiotherapy for brain metastases: An update. Expert Rev Anticancer Ther 2011;11:1731-8.  Back to cited text no. 12
13.Kalos M, June CH. Adoptive T cell transfer for cancer immunotherapy in the era of synthetic biology. Immunity 2013;39:49-60.  Back to cited text no. 13
14.Beaulieu AM, Bezman NA, Lee JE, Matloubian M, Sun JC, Lanier LL. MicroRNA function in NK-cell biology. Immunol Rev 2013;253:40-52.  Back to cited text no. 14
15.Palucka K, Banchereau J. Dendritic-cell-based therapeutic cancer vaccines. Immunity 2013;39:38-48.  Back to cited text no. 15
16.Fernandez NC, Lozier A, Flament C, Ricciardi-Castagnoli P, Bellet D, Suter M, et al. Dendritic cells directly trigger NK cell functions: Cross-talk relevant in innate anti-tumor immune responses in vivo. Nat Med 1999;5:405-11.  Back to cited text no. 16
17.Andrews DM, Scalzo AA, Yokoyama WM, Smyth MJ, Degli-Esposti MA. Functional interactions between dendritic cells and NK cells during viral infection. Nat Immunol 2003;4:175-81.  Back to cited text no. 17


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