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PurposeTo evaluate the use of the water‐to‐fat (W‐F) value obtained from in vivo proton (1H) MR spectroscopy (MRS) as a response indicator of cytologically confirmed patients with locally advanced breast cancer (LABC), and to monitor the therapeutic response of such patients to neoadjuvant chemotherapy (NACT)Materials and MethodsSerial 1H MR spectra were recorded both before and after the completion of chemotherapy in 33 LABC patients (with infiltrating ductal carcinoma (IDC)) at 1.5T. In addition, spectra from normal breast tissues of 28 healthy volunteers were recorded.ResultsMalignant breast tissues showed elevated W‐F values compared to normal breast tissues of controls. Statistically significant higher pretherapy W‐F value (P < 0.01) was observed in patients compared to controls. In patients who received NACT resulting in the reduction of the primary tumor size, the W‐F value showed a decrease that was statistically significant (P < 0.01). Analysis of the MR data further indicates that the W‐F value had no correlation with the menstrual status of the patients. A comparison of pretherapy W‐F value with pretherapy tumor volume showed a fair correlation (P = 0.05), while the posttherapy W‐F value showed no such correlation with the posttherapy tumor volume.ConclusionThis study demonstrates that simple, conventional in vivo 1H MRS is a useful technique for monitoring the therapeutic response of breast cancer patients. The observed trend in the reduction of W‐F value provides a noninvasive response indicator to monitor the clinical outcome of locally advanced breast cancer patients to NACT J. Magn. Reson. Imaging 2006. © 2006 Wiley‐Liss, Inc.

Non-small cell lung cancer has a devastating prognosis, and markers enabling a precise prediction of therapy response have long remained scarce. Better treatment monitoring would allow an individual's more effective patient adjusted therapy with lesser side effects and good clinical outcomes. In the present study, we monitored the serum cytochrome c levels pre- and post-chemotherapy of non-small cell lung cancer patients. Using highly sensitive enzyme-linked immunosorbent assay, we evaluated cytochrome c levels in serum of 100 non-small cell lung cancer and 100 healthy controls. We observed about threefold lower serum cytochrome c level in newly diagnosed non-small cell lung cancer patients than healthy individuals. Patients in advanced stages and grade 3 histological differentiation showed significantly low level of serum cytochrome c, and the lower levels were associated with worse survival outcome of non-small cell lung cancer patients. In addition, serum cytochrome c level was observed to be more than 13-fold higher after first cycle of conventional chemotherapy, wherein patients with higher level of serum cytochrome c before any therapy showed better response to chemotherapy in terms of significantly higher level of serum cytochrome c after first cycle of chemotherapy than patients with low level of serum cytochrome c at the time of diagnosis. Detection of serum cytochrome c levels at the time of diagnosis may be useful in suggesting disease severity and prognosis of the non-small cell lung cancer patients. Monitoring of serum cytochrome c might also serve as a sensitive apoptotic marker in vivo reflecting chemotherapy-induced cell death burden in patients with non-small cell lung cancer.

The FIF technique can be employed for UAM in place of wedge-based conformal treatment plans.

MDM2 protein is an important regulator of the p53 pathway and has a large effect on the anti-tumorigenic activity of the p53. Presently, we aimed to analyze the possible association of p53 and mdm2 in the development and progression of non-small cell lung cancer. In addition, impact of an important gene promoter polymorphism of MDM2 (T309G, rs 2279744) on its gene expression and ultimately of the TP53 was investigated in non-small cell lung cancer patients. A case-control study using peripheral blood samples of 100 non-small cell lung cancer patients and 100 cancer free healthy controls was conducted. Expression profile of MDM2 and TP53 gene were evaluated by using quantitative real time polymerase chain reaction assay, and MDM2 promoter polymorphism were analyzed by amplification refractory mutation system polymerase chain reaction. Non-small cell lung cancer patients expressed more than 6-fold increased mdm2 and about 7-folds decreased in p53 expression levels compared to healthy controls. Higher fold change increase of mdm2 and/or decrease of p53 were associated with advanced status and poor clinical outcome of the patients. A significant increase in mdm2 of about 14-folds and decrease in p53 of about 16.5-fold were observed among patients with MDM2 (309GG) genotype vs just 2.2-fold increase in mdm2 and 1.9-fold decrease in p53 among patients with MDM2 (309TT) genotype. In conclusion, present study demonstrated that MDM2 (309 T > G) polymorphism may be one of the important factors for the increased expression mdm2, which was associated with down-regulation of p53 at messenger RNA (mRNA) level and ultimately may contribute in the poor clinical outcome of the non-small cell lung cancer patients, thus may prove as a promising target for the treatment of non-small cell lung cancer at molecular level.