A CpG oligodeoxynucleotide potentiates the anti-tumor effect of HSP65-Her2 fusion protein against Her2 positive B16 melanoma in mice

Yan, Youyou; Cao, Zhao; Yang, Ming; Li, He; Wei, Hongfei; Fu, Yao; Song, Dandan; Wang, Liying; Yu, Yongli

doi:10.1016/j.intimp.2011.12.013

Cited by 5 publications

(4 citation statements)

References 30 publications

(16 reference statements)

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“…We initially chose the B16 V600E model given previous validation of B16 for vaccine testing in the literature [30][31][32][33]. Although inducible models of BRAF V600E have been described and used to test therapeutic agents [39,45,46], variability in tumor expression of current inducible transgenic BRAF models and random development of spontaneous tumors have precluded widespread use of these transgenic models up to this point.…”

Section: Discussionmentioning

confidence: 99%

Type I-polarized BRAF-pulsed dendritic cells induce antigen-specific CD8+ T cells that impact BRAF-mutant murine melanoma

Cintolo

Datta

et al. 2016

Melanoma Research

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Existing therapies targeting the mutated BRAF oncodriver (BRAF(V600E)) successfully treat melanoma but are susceptible to resistance. This study assessed the potential of a dendritic cell-based BRAF(V600E) vaccine for the treatment of BRAF(V600E)-mutant melanoma. Type 1-polarized dendritic cells (DC1) pulsed with affinity-modified BRAF(V600E) peptide were administered to C57Bl/6 mice both before (prevention) and twice weekly after (treatment) the development of established tumor with B16 melanoma transfected to express BRAF(V600E) (B16(V600E)). The efficacy of the BRAF(V600E)-pulsed DC1 vaccine was corroborated in a novel transplantable BRAF(V600E)-mutant murine melanoma model (BRAF(V600E-/+); PTEN(-/-); CDK2NA(-/-)). Three-dimensional tumor measurements and survival were determined. Induction of BRAF(V600E)-specific CD8(+) T-cell responses after brief in-vitro sensitization was assessed by interferon-γ enzyme-linked immunosorbent assay and/or enzyme-linked immunospot. Mice receiving BRAF(V600E)-pulsed DC1 vaccines before B16(V600E) tumor challenge demonstrated increased tumor-doubling times (P<0.001) and improved survival (P=0.0186) compared with those that received ovalbumin (control)-pulsed DC1 vaccines. In mice bearing established B16(V600E) tumors (mean 32 mm(3)), BRAF-pulsed DC1 vaccines delayed tumor growth (P<0.001) and improved survival (P=0.0008), compared with untreated mice. Likewise, in mice bearing BRAF(V600E-/+); PTEN(-/-); CDK2NA(-/-) tumors, compared with controls, BRAF-DC1 vaccination recapitulated these effects by delaying tumor growth (P<0.001) and improving survival (P=0.002). Vaccination elicited specific CD8(+) T-cell recognition of BRAF(V600E)-pulsed antigen-presenting cells (P<0.05), as well as BRAF(V600E)-expressing cancer cells (P<0.001), measured by interferon-γ release in vitro. BRAF-(V600E)pulsed DC1 vaccines induce oncogene-specific CD8(+) T-cell immune responses that impact tumor growth and survival in preclinical models of BRAF(V600E)-mutant melanoma. Exploration of BRAF(V600E)-targeted vaccines, in combination with BRAF-targeted therapies and checkpoint inhibitors, is warranted.

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Section: Discussionmentioning

confidence: 99%

Type I-polarized BRAF-pulsed dendritic cells induce antigen-specific CD8+ T cells that impact BRAF-mutant murine melanoma

Cintolo

Datta

et al. 2016

Melanoma Research

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“…Another HSP tested for melanoma was BCG HSP65. Cytosine-guanosine nucleotide (CpG) enhanced the antitumor effect of BCG HSP65 when anchored to tumor antigens Her2 [ 55 ] or tumor-associated antigen Mucin 1 (MUC1) [ 56 , 57 ], both expressed in melanoma cells. In fact, mycobacterial DNA alone was also shown to have therapeutic properties against melanoma.…”

Section: Melanoma and Mycobacteriamentioning

confidence: 99%

Mycobacteria-Based Vaccines as Immunotherapy for Non-urological Cancers

Noguera-Ortega

Guallar-Garrido

Julián

2020

Cancers

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The arsenal against different types of cancers has increased impressively in the last decade. The detailed knowledge of the tumor microenvironment enables it to be manipulated in order to help the immune system fight against tumor cells by using specific checkpoint inhibitors, cell-based treatments, targeted antibodies, and immune stimulants. In fact, it is widely known that the first immunotherapeutic tools as immune stimulants for cancer treatment were bacteria and still are; specifically, the use of Mycobacterium bovis bacillus Calmette-Guérin (BCG) continues to be the treatment of choice for preventing cancer recurrence and progression in non-invasive bladder cancer. BCG and also other mycobacteria or their components are currently under study for the immunotherapeutic treatment of different malignancies. This review focuses on the preclinical and clinical assays using mycobacteria to treat non-urological cancers, providing a wide knowledge of the beneficial applications of these microorganisms to manipulate the tumor microenvironment aiming at tumor clearance.

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“…For instance, the researchers have shown that a B-class CpG ODN (BW006) as a TLR9 agonist, could enhance anti-tumor activity of the recombinant HSP65-Her2 fusion protein, accompanied with improved HSP65-Her2 specific Th1 response in mice bearing Her2 (+) B16 melanoma. 29 Following this investigation, the researchers have examined if N-terminally fusion of Her2/neu to HSP70 can improve efficiency of Her2/neu DNA vaccine. Surprisingly, HSP70 fusion to N-terminal of rat Her2/neu led to tumor progression.…”

Section: Dna-based Vaccinesmentioning

confidence: 99%