IntroductionKi-67 is a nuclear antigen present in the synthesis phase of the cell cycle. Studies have shown that a high value of Ki-67 results in greater response to chemotherapy with higher incidence of complete pathological response, which ultimately results in improved overall survival. Methods and materialsThe objective of the study was to determine the frequency of high Ki-67 levels in breast cancer patients and to find the correlation of complete pathological response in breast cancer with Ki-67 levels. It is a descriptive case series with a correlational study design done at Fauji Foundation Hospital Rawalpindi. Eighty patients with locally advanced breast cancer who underwent neoadjuvant chemotherapy followed by surgery were recruited. Their Ki-67 levels were determined on trucut biopsy. Pathological response in the post-op sample was correlated with Ki-67 levels. ResultsThe results showed 27 (33%) patients out of the 80 had high Ki-67 values. Among them 17 (63%) had complete pathological response, seven (26%) showed partial pathological response whereas three (11%) had disease progression. In contrast, out of the 53 patients having low Ki-67 values, only nine (17%) had complete pathological response, 31 (58%) showed partial pathological response and 13 (25%) had progressive disease. A Chi-square test was applied which showed significant correlation between Ki-67 and complete pathological response, with a p value of 0.00018. ConclusionTherefore high Ki-67 values in patients with breast cancer correlated well with attainment of complete pathological response. We can incorporate Ki-67 in the initial clinical assessment of breast cancer patients to help predict effectiveness as well as response to chemotherapy.

Background: Chemotherapy induced peripheral neuropathy (CIPN) is one of the commonest and disabling side effect of chemotherapy drugs like taxanes , platinum compounds, vinca alkaloids, thalidomide and bortezomib.It often leads to dose reduction and discontinuation of treatment. Many agents like Vitamin E, glutathione, glutamate, acetyl L carnityle have been evaluated for their role in prevention of CIPN without any significant success Hence, CIPN is an important area of research due to lack of effective agent to prevent CIPN. Methodology: Un-blind double arm interventional study Results: Forty patients were distributed in two groups; intervention (vitamin E supplemented n=20) and control (n=20) arms. The TNSn scores were comparable at baseline and immediately after chemotherapy among both groups. However, after 3 months of chemotherapy the mean TNSn was comparatively low in the intervention arm (0.95 versus 1.64) which was not statistically significant. In subset analysis of Paclitaxel-Cisplatin combination chemotherapy subgroup, TNSn scores of two arms immediately post chemotherapy and at 3 months showed maximum difference between the arms (p-value, <0.001). In subset of Paclitaxel group, TNSn score at baseline and after chemotherapy were comparable. However, TNSn score measured after 3 months of chemotherapy in Intervention arm normalized, in contrast to non-intervention arm which still had a mean TNS of 1 with a p-value of 0.001 Conclusions: Our study showed a protective role of vitamin E profoundly in patients receiving single agent paclitaxel followed by paclitaxel and cisplatin regimen where the recovery from CIPN was much better as compared to control arm.

Background:Tamoxifen acts as a selective estrogen receptor modulator by binding to the estrogenreceptors on mammary epithelium andblockingtheproliferative action of estrogen on mammaryepithelium. In contrast to that it has a weak estrogen agonistic effect on bone, liver and endometrium.Tamoxifen therapy has favorable effects on serum lipid profile by decreasing serum levels of Total cholesterol and low density lipoprotein (LDL), while its effect on high density lipoprotein (HDL) and triglyceride (TG)is still controversial. So this study is to evaluate the effects of tamoxifenTherapy on fasting serum lipid profile in patients with breast cancer. Results: Mean age was 43.56±3.53yrs , most common BMI was 30-34.9. Patient serum TG levels were raised from baseline after 3 months of tamoxifen with p values of (0.000) which was statistically significant while HDL levels were raised but with p value of (0.008 ) which was statistically insignificant. Serum LDL and total cholesterol were reduced from baseline after 3 month with p value of (0.000) and (0.000) respectively. Conclusion: This study concludes that tamoxifen has effects on serum lipid profile by increasing TG levels and lowering TC and LDL levels so this should be in consideration while prescribing tamoxifen to the patients having other risk factors for cardiovascular abnormalities.

Background: According to WHO, breast cancer is the most common cancer in the women worldwide, soearly diagnosis is the best way to reduce its morbidity and mortality. Among various risk factors, the relationship between serum lipid profile and breast cancer is still unclear. Therefore, this study was conducted to evaluate this relationship. Methodology: Prospective, descriptive observational study with a comparative study designconducted at Fauji Foundation Hospital, Rawalpindi between November 2018 to April 2019. Results: 140 patients were divided into two groups i.e. cases and controls. Both groups were equally sub divided based on menstrual status. Independent student t-test was applied for comparison between the groups. BMI was significantly higher in the study group as compared to control group (p=0.002). Serum TG and LDL levels were higher in breast cancer patients (p= 0.032 and p=0.07 respectively). Cholesterol level was not statistically different in any group (p= >0.05). Higher HDL levels were seen in pre-menopausal cases (p=0.004) but there was no statistical difference when studied across cases and control groups. Conclusion: As breast cancer is the most common tumor in females, so early diagnosis is the key to reduce its morbidity and mortality. In this study, higher BMI, TG and LDL levels were seen in breast cancer patients as compared to controls. So, it may be concluded that BMI and dyslipidemia have some role in the etiology of breast cancer.

During the last few decades, overall survival of cancer patients has improved. Now more cancer survivors reach old age, in which cardiovascular diseases remain the leading cause of mortality. [1] Cardio toxicity secondary to chemotherapy also puts cancer survivors at high risk of death secondary to cardiovascular events. [2] Anthracyclines (Doxorubicin, Daunorubicin, Idarubicin, Epirubicin and Mitoxantrone) are the class of chemotherapeutic agents that are potentially cardio toxic. [3] Cardio toxicity caused by anthracyclines can present as acute and chronic cardiotoxicity. Acute cardiotoxicity is seen in <1% of the patients which is usually reversible and self-limiting. [4] Chronic toxicity however can have two presentations, either as early onset chronic toxicity and or late onset chronic toxicity. [5] Early onset chronic cardio toxicity happens within first 12 months of chemotherapy, with peak incidence documented in the initial three months. [6] Late onset cardio toxicity develops after 12 months of chemotherapy and can manifest as late as 1-2 decades after chemotherapy. The late onset cardio toxicities are not reversible. [4] Anthracycline are assumed to cause cardiomyocyte impairment by forming free radicles and reactive oxygen species which contribute to oxidative stress resulting in mitochondrial damage and cell death [7]. Moreover, calcium and iron hemostasis is also affected by anthracycline which contribute to cardiomyocyte damage. Topoisomerase 2 ß is another mechanism of causing injury to non-proliferative cells like cardiomyocyte. [7][8] These different mechanisms are thought to be causing the cardiac cell death. Early detection of cardio toxicity in patients treated with anthracyclines remains an important topic for research. Different biomarkers like troponins, brain natriuretic peptide (BNP), C reactive protein (CRP), myeloperoxidase (MPO), galectin-3 and nitrous oxide have been studied for detecting cardiotoxicity caused by anthracyclines. [3][6][9][10] Azher et al reported high levels of Troponin I in patients who developed cardiotoxicity after Anthracycline based chemotherapy. [6] Lipshultz et al found high CRP values in pediatric cancer survivors. In addition to these studied biomarkers certain other markers are also under evaluation and have been evaluated in a couple of studies. Myeloperoxidase is pro inflammatory enzyme. Ky et al found that high MPO levels were related to risk of cardiotoxicity after anthracycline based chemo therapeutic agents at 15 months follow up. Nitrous oxide is another marker that plays a vital role in cardiomyocyte contractility. Guler at al noticed high nitrous oxide values in pediatric patients who received with doxorubicin with post chemotherapy low left ventricular ejection fraction (LVEF) and fractional shortening. [9] A correlational analysis by Annop et al noticed that high pro b-type natriuretic peptide (ProBNP) levels were associated with fractional shortening. [3]