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Cancer as a mitochondrial metabolic disease.

Seyfried TN - Front Cell Dev Biol (2015)

Bottom Line: This view persists despite the numerous inconsistencies associated with the somatic mutation theory.In contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto Warburg.The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Boston College Chestnut Hill, MA, USA.

ABSTRACT
Cancer is widely considered a genetic disease involving nuclear mutations in oncogenes and tumor suppressor genes. This view persists despite the numerous inconsistencies associated with the somatic mutation theory. In contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto Warburg. The findings are reviewed from nuclear cytoplasm transfer experiments that relate to the origin of cancer. The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease.

No MeSH data available.


Related in: MedlinePlus

Nuclei from brain tumors support normal mouse embryonic development. (A) H&E staining of a mouse embryo (embryonic day, E-7.5) derived from a cell containing the transplanted “nucleus” from a medulloblastoma tumor. (B) the boxed area in (A) (at a higher magnification) showing the three germ layers; ecto-placental cone (pla); embryonic endoderm (end); embryonic mesoderm (mes,); embryonic ectoderm (ect), Scale bar, 20 μm. The cytoplasm will contain normal mitochondria. The results show that a nucleus derived from a brain tumor can direct normal embryonic development when implanted into normal cytoplasm. Reprinted with permission from Li et al. (2003).
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Figure 1: Nuclei from brain tumors support normal mouse embryonic development. (A) H&E staining of a mouse embryo (embryonic day, E-7.5) derived from a cell containing the transplanted “nucleus” from a medulloblastoma tumor. (B) the boxed area in (A) (at a higher magnification) showing the three germ layers; ecto-placental cone (pla); embryonic endoderm (end); embryonic mesoderm (mes,); embryonic ectoderm (ect), Scale bar, 20 μm. The cytoplasm will contain normal mitochondria. The results show that a nucleus derived from a brain tumor can direct normal embryonic development when implanted into normal cytoplasm. Reprinted with permission from Li et al. (2003).

Mentions: Findings similar to those obtained with the Lucke frog renal tumor were also obtained following nuclear transfer in mouse tumors. Morgan and colleagues showed that nuclei from a mouse brain tumor, arising from cerebellar granule cells (medulloblastoma), could direct normal development when the tumor nuclei were transplanted into enucleated somatic cells (Li et al., 2003). Figure 1 from their study shows that normal embryonic tissues and germ cell layers can be formed from cells containing the tumor nuclei. These investigators showed that the transfer of the tumor cell nucleus into normal cytoplasm suppressed the tumorigenic phenotype despite the continued presence of the mutant nuclear gene (Patched) that was thought responsible for the original tumorigenic phenotype (Li et al., 2003; Seyfried, 2012d). The transplanted medulloblastoma nuclei produced post-implantation embryos that underwent normal tissue differentiation and early stage organogenesis. Importantly, no malignancies or abnormal cell growth were seen in any of the recipient mice. Normal proliferation control was observed in cultured blastocysts indicating that nuclear somatic mutations alone were not likely responsible for the original tumorigenic phenotype (Li et al., 2003).


Cancer as a mitochondrial metabolic disease.

Seyfried TN - Front Cell Dev Biol (2015)

Nuclei from brain tumors support normal mouse embryonic development. (A) H&E staining of a mouse embryo (embryonic day, E-7.5) derived from a cell containing the transplanted “nucleus” from a medulloblastoma tumor. (B) the boxed area in (A) (at a higher magnification) showing the three germ layers; ecto-placental cone (pla); embryonic endoderm (end); embryonic mesoderm (mes,); embryonic ectoderm (ect), Scale bar, 20 μm. The cytoplasm will contain normal mitochondria. The results show that a nucleus derived from a brain tumor can direct normal embryonic development when implanted into normal cytoplasm. Reprinted with permission from Li et al. (2003).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493566&req=5

Figure 1: Nuclei from brain tumors support normal mouse embryonic development. (A) H&E staining of a mouse embryo (embryonic day, E-7.5) derived from a cell containing the transplanted “nucleus” from a medulloblastoma tumor. (B) the boxed area in (A) (at a higher magnification) showing the three germ layers; ecto-placental cone (pla); embryonic endoderm (end); embryonic mesoderm (mes,); embryonic ectoderm (ect), Scale bar, 20 μm. The cytoplasm will contain normal mitochondria. The results show that a nucleus derived from a brain tumor can direct normal embryonic development when implanted into normal cytoplasm. Reprinted with permission from Li et al. (2003).
Mentions: Findings similar to those obtained with the Lucke frog renal tumor were also obtained following nuclear transfer in mouse tumors. Morgan and colleagues showed that nuclei from a mouse brain tumor, arising from cerebellar granule cells (medulloblastoma), could direct normal development when the tumor nuclei were transplanted into enucleated somatic cells (Li et al., 2003). Figure 1 from their study shows that normal embryonic tissues and germ cell layers can be formed from cells containing the tumor nuclei. These investigators showed that the transfer of the tumor cell nucleus into normal cytoplasm suppressed the tumorigenic phenotype despite the continued presence of the mutant nuclear gene (Patched) that was thought responsible for the original tumorigenic phenotype (Li et al., 2003; Seyfried, 2012d). The transplanted medulloblastoma nuclei produced post-implantation embryos that underwent normal tissue differentiation and early stage organogenesis. Importantly, no malignancies or abnormal cell growth were seen in any of the recipient mice. Normal proliferation control was observed in cultured blastocysts indicating that nuclear somatic mutations alone were not likely responsible for the original tumorigenic phenotype (Li et al., 2003).

Bottom Line: This view persists despite the numerous inconsistencies associated with the somatic mutation theory.In contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto Warburg.The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Boston College Chestnut Hill, MA, USA.

ABSTRACT
Cancer is widely considered a genetic disease involving nuclear mutations in oncogenes and tumor suppressor genes. This view persists despite the numerous inconsistencies associated with the somatic mutation theory. In contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto Warburg. The findings are reviewed from nuclear cytoplasm transfer experiments that relate to the origin of cancer. The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease.

No MeSH data available.


Related in: MedlinePlus