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However, we can speculate that insulin may modulate cancer development through both the insulin receptor and insulin like growth factor-1 receptor (IGF-1R).
In the last 20 years, T lymphocytes reactive to antigens expressed by tumor cells have been shown to modulate cancer development in animal models and human cancer patients [1], [2].
They found that functionally significant variability exists among ovarian cancer patients in the ability of the microenvironment to modulate cancer development.
Our results indicate that functionally significant variability exists among ovarian cancer patients in the ability of the microenvironment to modulate cancer development.
Nevertheless, the current results are consistent with the hypothesis that the microenvironment plays a significant role in ovarian cancer development and suggest that functionally significant variability may exist among ovarian cancer patients in the ability of the microenvironment to modulate cancer development.
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Our investigation indicates that mitochondrial haplogroups could have a tissue-specific, population-specific and stage-specific role in modulating cancer development.
Our data indicate that mitochondrial haplogroups could have a tissue-specific, population-specific and stage-specific role in modulating cancer development.
These data suggest that n-3 PUFA can promote BAD-dependent apoptosis to modulate prostate cancer development [ 17].
The purpose of this review is to highlight the recent advances in our understanding of the mechanisms by which n-3 PUFA modulate prostate cancer development.
In order to begin to evaluate a role for systemic inflammation in the etiology of breast cancer, Freund's adjuvant (FA), which is known to induce both local and systemic inflammation [ 8] was evaluated for its ability to modulate breast cancer development in a rat model in which cancer is induced by the neu oncogene.
A full appreciation of the critical role for altered selection in cancer development could significantly impact treatment and prevention strategies by shifting focus toward microenvironmental factors modulating cancer evolution, both for initial tumor development and following therapy.
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