Background & Aims: The present study aimed to investigate the lymphocyte subpopulation counts (Th, Tc, B-cell, and NK cell) in SARS-CoV-2 patients (admitted to the ICU) to gain greater insight into the dysregulated immune response found in COVID-19. Materials & Methods: A total of 30 SARS-CoV-2 patients recruited in the intensive care unit (ICU) of Chest Disease (CD) and DRDO hospitals in Srinagar were investigated for lymphocyte subpopulation counts (T cell, B cell, and NK cell) by FACS analysis of blood samples (using the Beckman Coulter (Navios) and FACS Diva software). Results: Correlation analysis of lymphocyte subpopulation counts revealed, in comparison to normal healthy controls, an overall decreased mean T cell subset count, i.e., T-helper (CD3+, CD4+) (1422.5 cell/ul vs 662.4 cell/ul); T-cytotoxic (CD3+CD8+) (973.7 cell/ul Vs 629.2 cell/ul) and B cell count (CD45+CD19+) (442.1 cell/ul Vs. 144.4 cell/ul) with CD4+/CD8+ ratio (1.4 Vs. 1) in SARS-CoV-2 patients. On comparison, Stage 3 Vs Stage 2 patients, the mean T cytotoxic lymphocyte count i.e. CD3+CD8+, was lower (518.9 cells/ul Vs. 849.9 cell/ul) and the T-helper cell count, i.e. CD3+CD4+, was higher (764.9 cell/ul Vs. 457.3 cell/ul) with CD4+/CD8+ = 1.4 Vs. 0.5. Furthermore, the antibody immune response reflected by B-cell count was lower (i.e., CD19+131.9 cell/ul) in Stage 3 patients compared to Stage 2 patients (i.e., CD19+=162.9 cell/ul). ROC analysis with disease outcome revealed raised CD3+CD4+ count (T-helper cell response: AUC = 0.70) and decreased CD19+ count (humoral immune response: AUC = 0.80) and increased NLR (AUC = 0.65) as predictors of poor disease outcome. Conclusion: In conclusion, the study identified increased NLR, T-cell activation (increased T-helper cells), T-cytotoxic exhaustion (decreased T cytotoxic cells), and decreased humoral immune response (decreased CD19+ B cells) as predictive markers of severity and poor disease outcome in ICU-admitted patients with SARS-CoV-2.

Background: The complete blood count (CBC) profile has been found extremely useful in monitoring the growth of SARS-CoV-2 infection; however, predictive CBC parameters that could be used in the management of the disease may vary in different populations. Methods: This study comparatively analyzed the CBC profile of SARS-CoV-2 patients (N = 75; confirmed positive by real-time polymerase chain reaction [PCR]) and healthy individuals (confirmed negative by real-time PCR) from Kashmir (north India). Results: Compared with healthy individuals, most of the CBC parameters (hemoglobin levels [13.43 vs 10.9 g/dL; P = 0.0001], lymphocytes [16.04% vs 30.8%; P = 0.00001], monocytes [5.53% vs 7.53%; P = 0.009], and platelet count [150 vs 186 ×103 µL; P = 0.037]) were significantly low in SARS-CoV-2 infected patients, while neutrophilia was more common in infected patients (76.77% vs 59.26%). Among derived parameters, the neutrophil-to-lymphocyte ratio (NLR; 7.31 vs 2.04; P = 0.001) and derived NLR (d-NLR; 4.43 vs 1.5; P = 0.0002) were significantly high in SARS-CoV-2 patients. Further correlation analysis revealed a significant association of neutrophilia with the severity of the disease in SARS-CoV-2 infected patients. Moreover, receiver operating characteristic (ROC) analysis of derived CBC parameters (NLR, d-NLR, and platelet‐to-lymphocyte ratio [PLR] with disease severity and disease outcome) revealed d-NLR as better predictive marker of disease severity (area under the curve [AUC] = 0.658) and disease outcome (AUC = 0.766) compared to PLR with disease severity (AUC = 0.645) and disease outcome (AUC = 0.693). Conclusion: We therefore conclude, of the CBC parameters neutrophilia as the marker of disease severity and among derived parameters, d-NLR as an early predictive biomarker of both disease severity and poor disease outcome in SARS-CoV-2 patients.

Introduction: Biomarkers of prognostic and predictive relevance are needed for the practical management of COVID-19. Objective: The authors aimed to assess a battery of inflammatory cytokines in patients with SARS-CoV-2 to determine the cytokines of prognostic and predictive relevance in COVID-19. Methods: In a cohort of 100 patients with SARS-CoV-2 (RT-PCR confirmed), hospitalised in Shri Maharaja Hari Singh Hospital associated to Government Medical College Srinagar, India, the level of a battery of cytokines, IL-6, IL-8, IL-10, IL-1α, vascular endothelial growth factor (VEGF), TNF-α, and ferritin were estimated by ELISA on a multimode microplate reader. Results: The deranged levels of these cytokines were mostly found in patients >60 years of age, with cough and pneumonia as the most common symptoms. A significant association was found between IL-6 and IL-8, disease severity (p=0.002; p=0.007), and poor disease outcome (p=0.040; p=0.009), respectively. A significant association was also found between decreased levels of VEGF and poor disease outcome (p=0.020). Further receiver operating characteristic analysis, univariant and multivariant (after adjusting for age, gender, and other inflammatory markers), revealed increased IL-10 (area under the curve [AUC]: 0.72) and IL-6 (AUC: 0.70) as independent markers of both disease severity (p=0.02; p=0.01) and disease outcome (P=0.03; p=0.02), respectively, and decreased VEGF (AUC: 0.69) as an independent marker of disease outcome (p=0.03). A significant association between cough and IL-8 (p=0.01) and IL-10 levels (p=0.03), and of diabetes and raised ferritin levels (p=0.01), with very high ferritin levels (>1500 ng/mL), was found in those who are likely to develop hyperinflammatory phenotype. Conclusion: The authors conclude that ‘IL-6, IL10, VEGF, and IL-8’ are the signature inflammatory cytokine panel/profile in COVID-19, particularly in patients from Kashmir. Increased IL-10 and IL-6 levels proved to be equally significant independent prognosticators of COVID-19 severity and outcome, and decreased VEGF levels were independent predictors of poor disease outcome in patients with SARS-CoV-2. Testing of the signature inflammatory cytokine panel is, therefore, recommended for optimal clinical decision-making in patients with COVID-19 from Kashmir, India.

Inroduction: Blood gases are a measurement of how much oxygen and carbon dioxide is in blood. These determine the acidity of blood. The blood gas testing is generally used for detecting and monitoring lung and kidney problems. The blood gas testing measures partial pressure of oxygen (o2), partial pressure of carbon dioxide (CO2),oxygen saturation(O2Sat), bicarbonate(HCO3) concentration . Materials and Methods: Here in study Patients aged more than 18 years confirmed Covid 19 positive by reverse transcription, PCR (RT-PCR). Patients suffering from moderate to severe Covid 19 as per WHO diagnostic guidelines and underwent at least one ABG were included in the analysis. The ABG test was done on ABG analyzer in department of Biochemistry, SMHS hospital. All the data which was related to study was gathered and recorded in case record forms using files. As well as reports of patients from medical record section. Results: Alkaline pH was found in 57.33% individuals.36% individuals were having normal pH and the percentage of individuals having acidic pH was 6.66%. Low PaO2 was found in 45.33% individuals. Normal PaO2 levels were found in 21.33% and high PaO2 levels were found in 33.33% individuals .Low PaCO2 (<35 mmHg) were found in 56%, normal (35-45mmHg) levels were found in 37.33% and high levels (>45mmHg) were found in 6.66%. Low HCO3- (<22mmol/L) were found in 16%, normal (22-26mmol/L) in 38.66% individuals and high (>26mmol/L) were found in 45.33% individuals would be expected in the case of respiratory alkalosis. Conclusion: Regular ABG monitoring can aid in the early detection of silent hypoxia, and respiratory injury. With early management start-up, many lives can be spared with early diagnosis.

Background: Identifying early predictive biomarkers of disease severity and disease outcome is fundamental for the practical management of Covid -19 patients. Although prognostic value of several Pro- and inflammatory markers have been determined in different population studies, however, it remained to be determined in SARS-CoV-2 patients from Kashmir. Aim: To evaluate the predictive value of ferritin and IL-6 levels in RT- PCR confirmed SARS-CoV-2 patients from Kashmir. Study Design: A Cohort Study. Place and Duration of Study: The study was done at Government Medical College, Srinagar Kashmir, North India between October 2020 to November 2021. Method: Here, we estimated ferritin and IL-6 levels respectively by chemiluminescent method on fully automated immune analyzer and by ELISA in a cohort of 100 RT-PCR confirmed SARS-CoV-2 patients, which were followed twice (14th and 28th day) for a period of one month. Results: Based on estimated ferritin levels, the cohort was categorized into Mild = <500 ng/ml, Moderate = ≥500-<1500, and High = ≥1500ng/ml. Also patients were grouped as Mild = 0-<10pg/ml, Moderate = ≥10-<80pg/ml and High =≥80pg/ml based on Interleukin IL-6 levels. Correlation analysis of SARS-CoV-2 patients of varying ferritin levels with disease severity revealed a percent increase in the number of patients of stage 3 severity as ferritin levels increased from mild, to moderate and high levels. Similarly, a percent increase in the number of SARS-CoV-2 patients of increased severity was found as IL-6 levels increased from mild to moderate and high levels. Further, the ROC analysis of ferritin and IL-6 levels with disease outcome suggested both ferritin and IL-6 as early predictive markers of poor disease outcome. However, IL-6, with AUC =0.70 and sensitivity of 70% and specificity of 62%, is a better early predictive marker of poor disease outcome than ferritin with AUC=0.66 at sensitivity of 60% and specificity of 68% in SARS-CoV-2 patients from Kashmir. Further ROC analysis of patients with very high ferritin levels (>1500ng/ml) alone suggests it as an early predictive marker of patients with hyperinflammatory phenotype. Conclusion: Estimation of ferritin and IL-6 levels as simple complementary early prognostic markers that are helpful in clinical decision-making and selecting appropriate treatment options in SARS-CoV-2 patients from Kashmir, North India.

Background and Objectives: We aimed to analyze the impact of prestorage Inline leukodepletion and storage time on interleukin 8 (IL-8) levels in stored buffy coat-depleted packed red blood cell (PRBC) units in the Kashmiri population setting. Methods: A total of 50 donors of Kashmiri origin from North India equally and randomly distributed between Leukodepleted (LD) and non-LD (NLD) arms were recruited in this study. Leukodepletion of PRBCs units was performed using 3rd Generation integrated LD filters and the residual white blood cell (WBC) count was enumerated by FACS using fluorochrome-tagged CD45+ antibodies and IL-8 levels measured by ELISA. Results: In contrast to NLD arm, leukodepletion in the LD arm significantly reduced total leukocyte count (TLC) from pre-LD TLC of 2.25 ± 0.47 × 109/PRBC unit to post LD cell count of 2.40 ± 0.65 × 106/PRBC unit, P = 0.001, i.e., 3 log reduction, P = 0.0001. Contrary to the LD arm, a significant difference in IL-8 levels in NLD arm was observed with 27.15 ± 30.32 pg/mL on day 0, 45.15 ± 36.15 pg/mL on day 14, and on day 28, 37.98 ± 33.05 pg/mL. Furthermore, significant variance (LD vs. NLD) in IL-8 levels was observed at day 0, 14th, and 28th day of storage, with maximum variance observed on day 14th Fstat = 21.46, P = 0.00, depicting prestorage LD have a significant role in suppressing the IL-8 levels in LD stored PRBC units while as in NLD PRBC units with time IL-8 accumulated as its cell source (WBCs) was intact. Conclusion: Inline prestorage leukodepletion by 3rd generation LD filters was uniformly effective in reducing the residual WBC count to desired levels of <5 × 106/unit of PRBC. The significant decrease in TLC and resultant far less accumulation of cytokine (IL-8) in prestorage LD PRBC units of Kashmiri origin, as observed in this study, would be translated into clinical benefits associated with transfusion of LD-PRBC units.

Proteomics has evolved as a prime tool for large scale analysis of the proteome complement of living organisms. The proteomic studies have enabled the researchers to understand the fundamental molecular mechanisms at cellular level as well as the dysregulations that cause disease phenotypes. Therefore, this technology has resulted in an unprecedented level of progress in the development of applied curative approaches like targeted therapies and personalized medicine. Inevitably, proteomics has also been employed in all the aspects of cancer research ranging from, ascertaining and characterizing the aberrations of cancerous cells at genetic level, to, unraveling the molecular mechanisms in tumor growth and metastasis. Proteomics has helped in classifying each type of cancer based on its heterogeneity and exploring the efficient biomarkers and prospective targets for anti-cancer therapies. The past decade has witnessed generation of vast amount of proteomic data because of the continuous advancement of proteomic techniques and methodologies. As such many cancer databases are available and they are the means of easily accessible information that could be processed and used to obtain beneficial outputs. In this chapter, we discuss the basics of proteomic and its fundamental and practical applications. We particularly present the detailed description of proteomics in cancer research.

According to various reports, allospecific T cell stimulation is a requisite for elimination. Nevertheless, the method of allospecific T cell stimulation is mostly convenient along with recent agents. Appropriately, brief consequences in allotransplantation possess a consistently upgrade demonstration toward the particular consequence of the T cell-centric sight of contemporary remedy. Thus, the area of awareness has twisted about fall behind the lengthy result. Unchangeable chronic graft devastation to pursue to represent clinical transplantation proposes at that place are main features of alloimmunity those are un-mollified by uncomplicated T cell-directed immunosuppression. As a matter of fact, in the previous generations, it has been evident that the comprehensive biological circumstances jointly recorded as non-acceptance included nearly the Gordian web of elements, both provocative and managerial, that form the makeup of allorecognition. T cell responses, counting the T cell reliant allograft response, are circumstantially determined by the condition of innate immunity in that T cells associated with antigen. Organs used for transplantation exist commonly of deceased donors, for the past two generations are obtained by surgical procedure and then positioned into icy protection mixture prior section implantation into the receiver. Brain death, ischemia-reperfusion, hypoxia, and hemostasis-linked injuries significantly command the condition of innate immunity inside the transplant. Normally, each one of these procedures stimulates innate immunity into a pro-inflammatory shape that develops tissue critical forms of adaptive immunity. These pathways and cell types turned out to port mainly untargeted, or at minimal under close, and these points of removal facilitate the center of this matter.

COVID-19 also called corona virus emerged in China in December 2019. This turned into a global pandemic in a short period of time. Covid-19 is a novel strain of corona virus that was not seen earlier in human beings. It is important to study the molecular structure of Covid-19 so as to aid in the development of therapeutic measures. Existing Covid-19 pandemic poses an extraordinary risk to health and healthcare systems worldwide. Corona viruses are made of single stranded RNA present within the coat proteins. The virus has a diameter of nearly 80–120nm. Usually, Covid-19 presents with the signs and symptoms of respiratory illness. Cough commonly dry cough, fever, associated with myalgias and sometimes breathing difficulties due to decrease in oxygen saturation rates are also present in these patients. Some people show fever with body aches, while some are relatively asymptomatic. Corona virus is primarily transmitted in humans through respiratory route and is highly contagious. Mostly old people and those having comorbid illnesses suffer most. After invading into the human body, the virus may lead to a sequence of processes such as viral invasion, replication, and programmed cell death, that is, apoptosis. To control and prevent this viral infection, we need to study the molecular aspects of Covid-19 in detail so as to design therapeutic agents as well as for vaccine formation. The micro-RNA is defined as the single-stranded noncoding RNA molecule. They have a length of about 22 nucleotides approximately and help in the post transcriptional regulation of gene expression. Micro RNAs regulate many types of cancers in addition to Covid-19 and other infections. Viral micro RNA is a newer type of mi-RNA and controls the host cell expression and viral target genes. This was completed by inducing micro-RNA cleavage, breakdown, translation, inhibition, or other mechanisms. The micro-RNAs of Covid-19 are explained to give an authoritative means to study this novel coronavirus. These control the host cell expression and also viral target genes by inducing micro-RNA cleavage, breakdown, translation, inhibition, and also other mechanisms.

EGFRis a transmembrane receptor tyrosine kinase involved in regulating cell proliferation, differentiation and survival. EGFR is actively pursued as a therapeutic target because its aberrant expression or activity has been reported in several cancers. Several studies have reported the nuclear localization of the EGFR in various cell types, however, its exact nuclear functions are not clear yet. In this study, we have generated GFP fusion constructs of EGFR and its mutants to analyze their subcellular localizationin normal and cancer cells and impact of its sub-cellular location on its various activities using immunoblotting, confocal microscopy, reporter assays, loss-of-function EGFR mutants, and EGFR specific small molecule inhibitors. We show that EGFR is involved in modulating TCF dependent β-catenin transcriptional activity in HepG2 cells in a similar fashion as IGF1R tyrosine kinase. Moreover, we show that cytoplasmic and nuclear functions are two independent activities of EGFR.

The oncogenic activation of BRAF is commonly reported in human cancers; however, it is an understudied research area in breast cancer. In this study, we took the initiative to screen breast cancer patients for the most prevalent hotspot BRAFV600E mutation and discuss its clinical implications. Mutational screening was performed using a highly sensitive technique, mutation allele‑specific multiplex PCR (MASMP), the results of which were previously confirmed by sequencing the product and sensitivity compared to direct DNA sequencing. In total, BRAFV600E mutation status was analysed in 50 breast tumour samples and an equal number of adjacent normal tissues. Mutational screening by MASMP revealed its presence in 12% of the breast cancer patients. Association analysis revealed that BRAFV600E mutation was significantly present in oestrogen receptor (ER)/progesterone receptor (PR)‑negative (χ2=4.36, P=0.03) and mostly in triple‑negative breast cancers (TNBCs) (χ2=2.5, P=0.11). In addition, although not significant, BRAFV600E‑positive breast cancers were mostly found in older‑aged (χ2=1.10, P=0.29) and in post‑menopausal women (χ2=1.10, P=0.29). No significant association was found between BRAFV600E‑mutated breast cancers and traditional poor prognostic factors, such as clinical tumour stages III and IV (χ2 0.036, P=0.84) and a poorly differentiated (PD) histopathological grade (χ2 0.04, P=0.82).On the whole, positivity for BRAFV600E was noted in a fraction of elderly post‑menopausal women, predominantly of the ER/PR‑negative and/TNBC molecular subtype. MASMP was found to be a simple, sensitive and effective method for the rapid detection of BRAFV600E‑mutated breast cancers. For these types of breast cancers, BRAF‑targeted therapies in place of endocrine therapy, at least in BRAFV600E‑positive ER/PR‑negative/TNBC, may be considered as possible targeted therapy in the future.

Molecular studies have implicated mutant B-type Raf kinase (BRAFMut) of MAP-kinase signalling pathway in the pathogenesis of several cancers including colorectal cancer. Recently, the prognostic and therapeutic relevance of the most frequent BRAFV600E mutation also has been highlighted in colorectal carcinomas (CRC). Thus, the aim of this study was to investigate the prevalence of BRAFV600E mutation and to determine the correlation between this mutation and indicators of poor prognosis and outcome in patients with CRCs from Kashmir, North India. Here, we developed a highly sensitive technique, mutation allele-specific multiplex PCR (MASMP), for detection of BRAFV600E/BRAFc.1799T>A mutation, the results of which were confirmed by sequencing the product and compared to direct DNA sequencing. In total, BRAFV600E mutation status was analyzed in 57 colorectal tumour samples and an equal number of adjacent normal tissues. A high frequency of BRAFV600E mutation 21% (12/57) was identified in tumour tissues by MASMP compared to only 5.2% by direct DNA sequencing. Statistical analysis indicated that compared to BRAF-negative colorectal tumours, patients with BRAFV600E colorectal tumours were more likely to be >50 years old (61%) (P < 0.03). These tumours were more likely to be of clinical tumour stages III and IV (63%) (P < 0.04) with lymph node metastasis (52%) (P < 0.02) and characterised by a high-grade histology (63%) (P < 0.04). Colorectal patients harbouring BRAFV600E mutation experience more relapse/recurrence (52%) (P < 0.02). We, therefore, conclude that BRAFV600E mutation can be used as an indicator of poor prognosis to predict the outcome for CRC patients from Kashmir. MASMP proved to be a simple, sensitive and reliable technique for screening patients for BRAFV600E mutation. Testing for this mutation may be useful for selecting initial therapy mode and for follow-up monitoring in CRC patients.

Celphos poisoning is a major cause of mortality largely due to nonavailability of its antidote, due to delay in appropriate management and skepticism amongst physicians regarding the outcome. Although different trials has been tried to counter its irreversible toxic effects but hardly with any concrete success. Here we report novel intervention, the protocol of which we have formulated and standardized for last 1.5years, for Celphos poisioning which aims to diminish the production and absorption of phosphine, enhance its excretion and prevent any organ toxicity with appropriate supportive therapy. The management plan involves gastric lavage with an aliquot of coconut oil mixed with NaHCO3 followed by KMNO4 in Normal saline as an essential step in the initial stage. In addition the plan involves appropriate supportive measures that were taken which include Inj. NS-4 units (500ml each) Iv. over 6hrs, inj. Citicholine 500mg Iv. BD (antioxidant to prevent neuronal toxicity), Tab.N-Acetyl cysteine (dispersable) 600mg 1 tab PO BD (antioxidant, replenishing cellular glutathione), broad spectrum antibiotics eg. Inj. Monocef 1gm Iv. BD and inj. Metronidazole 500mg Iv. TID, Magnesium (inj MgSO4 (50%)(4 ampules in 500ml of NS) as cell membrane stabilizer to prevent arrhythmias, dopamine for inotropic support, if required and inj. Pantop -40mg Iv. BD to decrease HCl production and for symptomatic relief. The survival rate of this novel intervention turns out to be 91%(10/11). Early arrival, history of vomiting, early diagnosis, resuscitation, decreasing formation and absorption of phosphine (by gastric and retrograde lavage with coconut oil

Heat shock protein (Hsp) 90 is a key component of the super-chaperone complex that maintains functionally active conformation of various client proteins. Many of these client proteins regulate important nodal points in multiple signalling pathways that promote cancer cell growth and survival. Inhibitors of Hsp90, therefore, have the potential of functioning as anti-cancer agents with pleiotropic effects. Identification of novel Hsp90 inhibitors with more favourable pharmacological properties is a priority in cancer therapy. To achieve this goal, we screened a compound library using a biochemical assay based on refolding of denatured firefly luciferase. The assay revealed high sensitivity, reliability and reproducibility with a Z-factor of 0.81 ± 0.17. Six Hsp90 inhibitory compounds identified by this screening with IC50 values between 1.0 and 6 μM were further characterised for anti-proliferative activity by Cell Titer-Blue Cell Viability Assay using multiple tumour cell lines. Of particular interest was ONO4140 with lowest GI50 values in three different cancer cell lines viz; DU-145, BT-474 and K562 cell lines. This study also revealed that short-term exposure of tumour cells with ONO4140 is sufficient to inhibit the catalytic activity of Hsp90, evaluated through disruption of Hsp90-p23 association by immunoprecipitation. This short term exposure appears to initiate events like degradation of Hsp90 client proteins such as ErbB2/Her-2 and Akt with concomitant inhibition of survival signalling leading to the apoptotic death of tumour cells as seen by western blotting and Caspase Glow-3,7 assay. The study also reveals that apoptosis following Hsp90 inhibition with ONO4140 occurs via Caspase9-Caspase3 intrinsic apoptotic pathway, a process that is likely triggered by inactivation of Akt. In conclusion, we have identified a novel class of synthetic compounds which show potent Hsp90 inhibitory action in preclinical studies. The discovery of this novel class of synthetic Hsp90 inhibitors with simple chemical backbone allows us to conduct further structural modifications to improve their potency and pharmacokinetic properties for use in cancer therapy.

Background: Heat Shock Proteins (HSP’s) are expressed at high levels in wide range of tumors. They are determining factors for tumor cell survival as they promote autonomous cell proliferation, inhibit cell death pathways, delay senescence as well as influence the immune response to tumor cells. Purpose of the study: We designed a large scale case-control study to characterize the frequency of two polymorphisms within the MHC classIII-linked HSP70 genes, Hsp70-2 and Hsp70-hom, in order to find any association of these genotypic variants for predisposition to and clinical outcome of breast carcinoma patients from Kashmir valley in North India. Polymerase Chain Reaction and restriction enzymes were utilized to characterize the frequency of two polymorphisms with in Hsp70-2 and Hsp70-hom genes in 114 breast carcinoma cases and 90 healthy controls from the same population of Kashmir. Association of high frequency allelic/genotypic variants of Hsp70genes with various clinicopathological features of prognostic significance was assessed by Chi-square test using SPSS software. Results: In the present study, allelic frequency of Hsp70-2 A/G heterozygote (0.88) (p=0.008) was found to be significantly high in breast carcinoma cases compared to control (0.744) with a Relative Risk =2.67 fold. Conversely, the allelic frequency of Hsp70-2A/A allele in homozygous condition was significantly low in breast carcinoma cases and worked out to be 0.078 (Vs 0.244 in control) with p=0.001, implicating it as a protective allele against breast cancer in subjects with this genotype. Similarly, significantly high frequency of 0.50 (Vs 0.30 in control) of Hsp70-homC/C allele was found in homozygous condition in breast cancer cases suggestive of a positive relative risk associated with this genotype (RR=2.42) (p=0.003). The overall genotype frequency data analysis of Hsp70-2 and Hsp70-hom genes was significant (χ2=11.46, p=0.003; and χ2=10.56, p=0.005). The study also reveals considerable association of high frequency alleles of HSP70 genes, especially of Hsp70-2A/G or G/G in breast tumors with clinico-pathological features of poor prognosis. Conclusion: These results indicate that the relative risk of breast cancer associated with Hsp70-2 and Hsp70-hom gene polymorphisms is confined to Hsp70-2 A/G or G/G and Hsp70homC/C haplotype in our population. The study, therefore, suggests Hsp70-2A/G orG/G and Hsp70homC/C genotypes as potential susceptibility markers and independent prognostic indicators in breast carcinoma patients in Kashmiri population.