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Results: 4

1.
Figure 2

Figure 2. CA 19-9 restores to normal levels with MMC treatment. From: Personalizing cancer treatment in the age of global genomic analyses: PALB2 gene mutations and the response to DNA damaging agents in pancreatic cancer.

Time-course of CA 19-9 showing disease progression while on gemcitabine and complete normalization with MMC. Y-axis is log-scale of CA19-9 concentration presented in Units/mL;

Maria C. Villarroel, et al. Mol Cancer Ther. ;10(1):3-8.
2.
Figure 3

Figure 3. MMC and cisplatin treatment remarkably suppressed the tumor growth of patient’s pancreatic carcinoma grown in nu/nu mice xenografts. From: Personalizing cancer treatment in the age of global genomic analyses: PALB2 gene mutations and the response to DNA damaging agents in pancreatic cancer.

Tumor growth curves indicating resistance to gemcitabine and remarkable response to MMC and cisplatin in the patient’s own xenografts (JH033). Panc 185, a pancreatic cancer xenograft with wild-type PALB2 wass presented as a control. Mice were treated and tumor volumes were monitored over time (days) as indicated in the materials and methods. Tumor growth is expressed as mean tumor volume ± SEM.

Maria C. Villarroel, et al. Mol Cancer Ther. ;10(1):3-8.
3.
Figure 1

Figure 1. Images of Clinical Outcome. From: Personalizing cancer treatment in the age of global genomic analyses: PALB2 gene mutations and the response to DNA damaging agents in pancreatic cancer.

A) Pet-CT obtained at the first postoperative visit showing an enlarged left supraclavicular lymph node with increase FDG uptake (arrowhead). A biopsy of this lymph node showed metastatic adenocarcinoma; B) CT revealing extensive locoregional recurrent disease after four cycles of gemcitabine; C) Late pulmonary progression with a left upper lesion that developed 22 months of follow up after the initial treatment with MMC (arrowhead); D) Decrease in pulmonary lesion size after two additional courses of MMC (arrowhead).

Maria C. Villarroel, et al. Mol Cancer Ther. ;10(1):3-8.
4.
Figure 4

Figure 4. Mechanistic Studies. From: Personalizing cancer treatment in the age of global genomic analyses: PALB2 gene mutations and the response to DNA damaging agents in pancreatic cancer.

A) Location of somatic mutation in the PALB2 gene. The patient had somatically acquired a transition mutation (C to T) at a canonical splice site for exon 10 (IVS10+2). Exons are represented as black boxes and introns as black lines; B) Co-immunoprecipitation with a monoclonal antibody against BRCA1 of the BRCA1-BRCA2 complex. No complex is identified in the PALB2 mutant tumor JH033 as compared to the wild type Panc185 tumor used as a control; C) Western blot of FANCD2 ubiquitination. The upper band represents the ubiquitinated or long form (PFANCD2 Lys561) and the lower band represents the short, non ubiquitinated form. JH033 has competent proximal FA complex similar to the MMC resistant Panc185 control.

Maria C. Villarroel, et al. Mol Cancer Ther. ;10(1):3-8.

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