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. 2001 Mar 19;193(6):727–740. doi: 10.1084/jem.193.6.727

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Progression of mammary tumor to malignancy was accelerated in CSF-1–transgenic Csf1^op/Csf1^op PyMT mice. (A, a) Schematic diagram of CSF-1 transgenic construct. CSF-1 cDNA was ligated downstream of a CMV promoter controlled by tetracycline operators, TetO. SV40An, polyadenylation site from SV40 small t antigen; X, restriction site for XbaI, Bam, restriction site for BamHI; Bgl, restriction site for BglII. (A, b) RT-PCR analysis of transgenic CSF-1 expression in mammary glands. RNA samples were analyzed from four nontransgenic control (lanes 3–6), two CSF-1–transgenic (lanes 7 and 8), and the same CSF-1–transgenic PyMT mice without reverse transcriptase (lanes 1 and 2). Lane 9, genomic DNA from a CSF-1–transgenic mouse. CSF-1 Tg, positive 300-bp band. (B) Histopathological distribution of primary mammary tumors in CSF-1–transgenic and control Csf1^op/Csf1^opPyMT mice at 18 wk of age. Data are presented as the percentile distribution of four histopathological stages of primary mammary tumors in CSF-1–transgenic (Tg+, n = 6) and control (Tg−, n = 10) Csf1^op/Csf1^opPyMT mice. Asterisk indicates a significant difference in the frequency of late carcinoma stage tumors between CSF-1–transgenic and control Csf1^op/Csf1^opPyMT mice (Fisher's exact test, P = 0.039). (C) Pulmonary metastasis of mammary tumors in CSF-1–transgenic Csf1^op/Csf1^op and control PyMT mice at 18 wk of age were compared by Northern analysis of PyMT mRNA expression in lung. Data are presented as the mean ± SE of at least five mice/point. Asterisks indicate significant differences for both CSF-1–transgenic Csf1^op/Csf1^op(Tg+, n = 6) and control +/Csf1^op PyMT mice (n = 5) when compared with control Csf1^op/Csf1^op PyMT mice (n = 6) (Mann-Whitney test, P = 0.03 and 0.008, respectively). No significant difference was found between CSF-1–transgenic Csf1^op/Csf1^opand control +/Csf1^op PyMT mice at the same age (Mann-Whitney test, P = 0.33). (D–G) Histology of mammary tumors from CSF-1–transgenic (E and G) and control (D and F) Csf1^op/Csf1^op PyMT mice at 18 wk of age. Stained with hematoxylin and eosin (D and E) and with anti-F4/80 antibody (F and G; original magnification: ×250).

Progression of mammary tumor to malignancy was accelerated in CSF-1–transgenic Csf1^op/Csf1^op PyMT mice. (A, a) Schematic diagram of CSF-1 transgenic construct. CSF-1 cDNA was ligated downstream of a CMV promoter controlled by tetracycline operators, TetO. SV40An, polyadenylation site from SV40 small t antigen; X, restriction site for XbaI, Bam, restriction site for BamHI; Bgl, restriction site for BglII. (A, b) RT-PCR analysis of transgenic CSF-1 expression in mammary glands. RNA samples were analyzed from four nontransgenic control (lanes 3–6), two CSF-1–transgenic (lanes 7 and 8), and the same CSF-1–transgenic PyMT mice without reverse transcriptase (lanes 1 and 2). Lane 9, genomic DNA from a CSF-1–transgenic mouse. CSF-1 Tg, positive 300-bp band. (B) Histopathological distribution of primary mammary tumors in CSF-1–transgenic and control Csf1^op/Csf1^opPyMT mice at 18 wk of age. Data are presented as the percentile distribution of four histopathological stages of primary mammary tumors in CSF-1–transgenic (Tg+, n = 6) and control (Tg−, n = 10) Csf1^op/Csf1^opPyMT mice. Asterisk indicates a significant difference in the frequency of late carcinoma stage tumors between CSF-1–transgenic and control Csf1^op/Csf1^opPyMT mice (Fisher's exact test, P = 0.039). (C) Pulmonary metastasis of mammary tumors in CSF-1–transgenic Csf1^op/Csf1^op and control PyMT mice at 18 wk of age were compared by Northern analysis of PyMT mRNA expression in lung. Data are presented as the mean ± SE of at least five mice/point. Asterisks indicate significant differences for both CSF-1–transgenic Csf1^op/Csf1^op(Tg+, n = 6) and control +/Csf1^op PyMT mice (n = 5) when compared with control Csf1^op/Csf1^op PyMT mice (n = 6) (Mann-Whitney test, P = 0.03 and 0.008, respectively). No significant difference was found between CSF-1–transgenic Csf1^op/Csf1^opand control +/Csf1^op PyMT mice at the same age (Mann-Whitney test, P = 0.33). (D–G) Histology of mammary tumors from CSF-1–transgenic (E and G) and control (D and F) Csf1^op/Csf1^op PyMT mice at 18 wk of age. Stained with hematoxylin and eosin (D and E) and with anti-F4/80 antibody (F and G; original magnification: ×250).