The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果及结肠癌基因的小鼠发生肠道肿瘤的机率比那些没有额外的108个基因而仅有结肠癌基因的小鼠44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位基因丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新癌基因，但其在肿瘤中的表达调控机制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上基会导致人类出现癌症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善基因组上的全面去基化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠的小鼠发生肠道肿瘤的率比那些没有携带额外的108个而仅携带有结肠的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新，但其在肿瘤中的表达调控不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲会导致人类出现症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善组上的全面去甲化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠癌基因小鼠发生肠道肿率比那些没有携带额外108个基因而仅携带有结肠癌基因小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿形态学上极相似，是1号染色短臂上等位基因丢失肿比没有丢失药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族一个新成员，可能是人类一种新癌基因，肿中表达调控制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲基会导致人类出现癌症想法，还只是个假说，肿学家手头上也没有任何药物，可以用来改善基因组上全面去甲基化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠基因的小鼠发生肠道肿瘤的机率比那些没有携带额外的108个基因而仅携带有结肠基因的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位基因丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新基因，但其在肿瘤中的表达调控机制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲基会导致人类症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善基因组上的全面去甲基化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠的小鼠发生肠道肿瘤的率比那些没有携带额外的108个而仅携带有结肠的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新，但其在肿瘤中的表达调控不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲会导致人类出现症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善组上的全面去甲化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠癌基因的小鼠发生肠道肿瘤的机率比那些没有携带额外的108个基因而仅携带有结肠癌基因的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学极其相似，但1色短位基因丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)lipocalin家族的一个新成员，可能人类的一种新癌基因，但其在肿瘤中的表达调控机制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA缺少甲基会导致人类出现癌症的想法，还只个假说，肿瘤学家手头也没有任何药物，可以用来改善基因组的全面去甲基化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果携带三及结肠癌的小鼠发生肠道肿瘤的那些没有携带额外的108个而仅携带有结肠癌的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，是1号染色短臂上等位丢失的肿瘤没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新癌，其在肿瘤中的表达调控制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲会导致人类出现癌症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善组上的全面去甲化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

结果带三及结肠癌基因的小鼠发生肠道肿瘤的机率比那些没有带额外的108基因带有结肠癌基因的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位基因丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的成员，可能是人类的种癌基因，但其在肿瘤中的表达调控机制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲基会导致人类出现癌症的想法，还只是假说，肿瘤学家手头上也没有任何药物，可以用来改善基因组上的全面去甲基化。

The trisomic, colon cancer mice had 44% fewer intestinal tumors than the colon cancer mice that did not have the extra 108 genes.

果携带三及肠癌基因的小鼠发生肠道肿瘤的机率比那些没有携带额外的108个基因而仅携带有肠癌基因的小鼠少44%。

Despite a high morphological similarity, tumors with allelic loss on the short arm of chromosome 1 (1pLOH) are more chemosensitive than those without 1pLOH.

尽管两种肿瘤在形态学上极其相似，但是1号染色短臂上等位基因丢失的肿瘤比没有丢失的药物敏感性要高得多。

Neutrophil gelatinase-associated lipocalin(NGAL) is a novel member of the lipocalin family and may be a new human oncogene, but the regulation mechanism of NGAL was not clear in the cancer.

NGAL(neutrophil gelatinase-associated lipocalin)是lipocalin家族的一个新成员，可能是人类的一种新癌基因，但其在肿瘤中的表达调控机制尚不清楚。

The idea that a lack of methyl on the DNA can lead to human cancer is still just a hypothesis, and in any case oncologists have no drugs that can correct genome-wide undermethylation.

DNA上缺少甲基人类出现癌症的想法，还只是个假说，肿瘤学家手头上也没有任何药物，可以用来改善基因组上的全面去甲基化。