Generation of Autologous Tumor-specific T Cell Clones From a Patient With Adenosquamous Carcinoma of the Lung

Saito, Tomoko; Takenoyama, Mitsuhiro; Sugaya, Masakazu; Yasuda, Manabu; Eifuku, Ryozo; Yoshimatsu, Takashi; Hanagiri, Takeshi; Oyama, Tsunehiro; Kodate, Mantaro; Osaki, Toshihiro; Yasumoto, Kosei

doi:10.1093/jjco/hye062

Cited by 8 publications

(16 citation statements)

References 30 publications

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“…One week after the third stimulation, the RLNLs were harvested, washed, and tested for their CTL activity. To establish CTL clones from CTL lines, a limiting dilution method was done as reported previously (20).…”

Section: Methodsmentioning

confidence: 99%

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Haplotype Loss of HLA Class I Antigen as an Escape Mechanism from Immune Attack in Lung Cancer

Takenoyama

Mizukami

et al. 2005

Cancer Research

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One of tumor escape mechanisms from the host's immunosurveillance system (i.e., a haplotype loss of HLA class I antigens) has been detected in various tumor cells. We hypothesize that the majority of tumor cells with normal HLA class I expression were attacked and eradicated by CTLs, and only a minority with an abnormal expression of HLA class I antigens could escape the host's immunosurveillance system. Using HLA class I-transfected tumor variants as stimulators in A904L lung cancer cell line, which has a haplotype loss of HLA class I antigens, both the transfected HLA-A26 and HLA-B39-restricted CTL lines were induced from autologous lymphocytes. However, only one HLA-B39-restricted CTL clone (CTL G3b) was established, and it was then used to identify the antigen. SGT1B [suppressor of G2 allele of SKP1 (SGT1), suppressor of kinetochore protein (SKP1)] was identified as the antigen recognized by CTL G3b. Further experiments using 13 subclones from a primary culture of A904L were found to confirm our above-mentioned hypothesis.

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Section: Methodsmentioning

confidence: 99%

“…16). In a blocking assay, one fourth of diluted culture supernatant of hybridomas was added to the coculture of CTLs and tumor cells (20).…”

Section: Methodsmentioning

confidence: 99%

Haplotype Loss of HLA Class I Antigen as an Escape Mechanism from Immune Attack in Lung Cancer

Takenoyama

Mizukami

et al. 2005

Cancer Research

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“…We reported that tumor-specific CTL clones could be induced from regional lymph node lymphocytes in lung cancer patients (9)(10)(11)(12)(13). In this study, we identified a new cancer/germline antigen recognized by CTL using cDNA expression cloning method.…”

Section: Introductionmentioning

confidence: 98%

Identification of a New Cancer/Germline Gene,KK-LC-1, Encoding an Antigen Recognized by Autologous CTL Induced on Human Lung Adenocarcinoma

et al. 2006

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The purpose of our present study is to identify a tumorspecific antigen capable of inducing a specific cellular immune response in lung cancer patients. We established a lung adenocarcinoma cell line, designated as F1121L, and induced tumor-specific CTL clone H1 from regional lymph node lymphocytes of patient F1121. CTL clone H1 lysed autologous tumor cells in an HLA-B*1507-restricted manner, but not autologous EBV-B, phytohemagglutinin-blast cells, and K562. The CTL clone also recognized allogeneic HLA-B*1501-or 1507-positive lung cancer cell lines in the HLArestricted manner. Using the CTL clone, we identified an antigen-coding gene by cDNA expression cloning technique. The gene consisted of 556 bp, including an open reading frame consisted of 113 amino acids, designated as Kita-kyushu lung cancer antigen 1 (KK-LC-1). A 9-mer peptide (KK-LC-1 76-84 ; RQKRILVNL) was identified as an epitope peptide. The genomic DNA of this antigen was located in chromosome Xq22. A reverse transcription-PCR analysis revealed that the mRNA of this gene was only expressed in the testis among normal tissues. It was expressed in 9 of 18 (50%) allogeneic non-small-cell lung cancer cell lines and in 40 of 100 (40%) non-small-cell lung cancer tissues. We thus identified a new tumor antigen-coding gene categorized as a cancer/germline gene by an autologous lung cancer and CTL system. The new cancer/germline gene was located in Xq22, which is apparently different from the locations of previously reported cancer/germline genes. (Cancer Res 2006; 66(9): 4922-8)

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“…To establish T-cell clones, a limited dilution method was performed on the bulk CTL line, as reported previously. 31 …”

Section: Induction Of Bulk Ctls and Generation Of Ctl Clonesmentioning

confidence: 99%

“…In the blocking assay, a one-quarterdiluted culture supernatant of hybridomas was added to the coculture of CTLs and tumor cells, as reported previously. 31,33 …”

Section: Measurement Of Interferon ␥ Production By Ctlsmentioning

confidence: 99%

A different pattern of cytotoxic T lymphocyte recognition against primary and metastatic tumor cells in a patient with nonsmall cell lung carcinoma

Takenoyama

Ichiki

et al. 2004

Cancer

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BACKGROUNDLung carcinoma represents the most frequent cause of cancer death worldwide because of tumor metastases. The objective of the current study was to analyze the immunologic response during the progress of lung carcinoma metastasis.METHODSThe authors established two tumor cell lines that were derived from primary and metastatic lesions in a patient with lung carcinoma (Patient G603). One cell line (G603L) was established from the primary lesion, and the other cell line (G603AD) was established from a metastatic lesion in the right adrenal gland 7 months after the patient underwent surgery for the primary lesion. Autologous regional lymph node lymphocytes were stimulated with CD80‐transfected G603L cells, then cytotoxic T lymphocytes (CTLs) were induced against both lung carcinoma cell lines.RESULTSBoth G603L cells and G603AD cells expressed Class I human leukocyte antigen, intracellular cell adhesion molecule 1, and lymphocyte‐associated antigen type 3 (LFA‐3), but not Fas or Fas ligand on their surfaces. By stimulation with CD80‐transfected G603L cells, 2 CTL clones (H2/17 and H2/36) were established from the bulk CTLs. CTL clone H2/17 lysed G603L cells but not G603AD cells, suggesting that the antigen recognized by CTL clone H2/17 was abrogated during the process of metastasis. In contrast, CTL clone H2/36 lysed both G603L cells and G603AD cells, indicating that the antigen recognized by CTL clone H2/36 was maintained in the tumor cells throughout tumor progression.CONCLUSIONSThe results demonstrated the possibility that some tumor‐associated antigens may be abrogated during the process of metastasis, although others are maintained. The identification of these antigens will lead to a better understanding of their immunologic role during disease progression in patients with lung carcinoma. Cancer 2005. © 2004 American Cancer Society.

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Generation of Autologous Tumor-specific T Cell Clones From a Patient With Adenosquamous Carcinoma of the Lung

Abstract: These results are the first demonstration of a successful induction of AT-specific T cell clones from a patient with lung adenosquamous carcinoma. It may therefore supply a possible way to apply specific immunotherapy to this type of lung cancer.

Cited by 8 publications

References 30 publications

Haplotype Loss of HLA Class I Antigen as an Escape Mechanism from Immune Attack in Lung Cancer

Haplotype Loss of HLA Class I Antigen as an Escape Mechanism from Immune Attack in Lung Cancer

Identification of a New Cancer/Germline Gene,KK-LC-1, Encoding an Antigen Recognized by Autologous CTL Induced on Human Lung Adenocarcinoma

A different pattern of cytotoxic T lymphocyte recognition against primary and metastatic tumor cells in a patient with nonsmall cell lung carcinoma

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